expository essay on breast cancer

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Personal Essay: My Mom Beat Breast Cancer, and It Changed My Life

I learned all about breast cancer after my mom, Bridget Bocchino Hochstuhl, was diagnosed with the disease in 2010. I was only three years old at the time, but over the years, as I became old enough to understand, I learned that breast cancer is the most common cancer found in women in the United States, second only to skin cancer. I learned that each year in the United States, there are an estimated 240,000 diagnosed cases of breast cancer in women and around 2,100 in men. And I learned that the disease occurs when the DNA in breast cells mutates, creating cancerous cells that destroy the normal ones.

I also learned that while Breast Cancer Awareness Month is October, breast cancer awareness should exist year-round. This is because early detection is key to beating the disease, so it’s critical that women get regular mammograms, X-rays of the breast, according to the guidelines set by their doctors and the American Cancer Society (ACS). Being diagnosed with cancer is not always a death sentence; my mom is living proof of that. And she wanted to share her own story of survival in the hopes of helping others do the same.

It has been 13 years since my mom’s diagnosis. She survived breast cancer, and she’s the strongest person I know. She says she fought to survive in order to raise her kids and be here for her family. I love my mom with my entire heart.”

— Emily Hochstuhl

When my mom was first diagnosed in 2010, she was an otherwise healthy and fit 38-year-old. She had just lost 30 of the 50 pounds she had gained while pregnant with my younger brother, whom she was breastfeeding at the time.

When she first felt the lump in her breast, she thought it was a clogged milk duct. After all, she used to get them when she was breastfeeding her first child, me. At the urging of her coworkers, however, she got a mammogram just to be sure. Luckily, the health insurance company where she worked had a mobile mammogram machine on site to make it easier for employees to get the diagnostic test while at work.

She was officially diagnosed with breast cancer on Aug. 5, 2010, while throwing my brother’s first birthday party. She told my dad and her own mother, my grandmother, about the cancer, but she kept it a secret from most people in her life because she needed privacy and time to process the information.

After the diagnosis, things moved quickly, and my mother had a double mastectomy the following month, on Sept. 15, 2010. The pathology results showed that the cancer had spread to 28 lymph nodes in her armpit, thereby classifying it as a stage IV breast cancer diagnosis.

In the fight to save her life, my mother began the first of what she thought would be 12 rounds of a chemotherapy regimen, which was estimated would take six months to finish. However, the 12 rounds quickly turned into 30, and six months stretched to over one and a half years, due to the anaphylactic reaction she had to the treatment. After the chemotherapy treatments, she underwent 52 rounds of radiation. By the time she had finished all the chemo and radiation, she was in a severely weakened state.

The medical procedures didn’t end there, however. From 2010 to 2023, my mother underwent 18 breast reconstruction surgeries, which included adding and adjusting expanders, then adding and adjusting implants.

Other complications arose during her treatments. For one, the excessive radiation she’d undergone caused her to experience chronic cellulitis. She also suffered from multiple side effects due to staying on a chemo pill that had acted as an estrogen blocker for 10 years. At one point, an oncologist saved my mom’s life when she suffered a pulmonary embolism. At the time, she was estimated to only have about three weeks left to live, but she beat the odds and survived.

It has been 13 years since my mom’s diagnosis. She survived breast cancer, and she’s the strongest person I know. She says she fought to survive in order to raise her kids and be here for her family. I love my mom with my entire heart; she is the kindest, sweetest, most generous person who could ever exist. She puts everyone else above herself, no matter what she is going through.

Ever since I was old enough to do so, I have supported her on her 13-year-long journey toward becoming a survivor of the disease. Breast cancer is a serious issue that often goes unnoticed, which in turn, can cost people their lives. Screening tests in the form of mammograms are the best defense; they can detect cancer early, way before a person has symptoms. According to the American Cancer Society (ACS), women should consider starting annual mammograms at age 40, or even earlier if there is a family history of the disease. At age 45, the ACS recommends that all women start getting annual mammograms. People who have cancer in their family can also get genetic testing before this age to see if they carry genes for the disease.

During her breast cancer journey, my mother taught me life lessons that I’ll carry with me always. I learned about being strong, the healing power of love and the importance of protecting my health. I learned about breast cancer prevention strategies, and the importance of getting regular screenings for early detection of the disease. Who knows, from all I’ve learned, I might save my own life one day. All of this is thanks to what I learned from my beloved mom, breast cancer survivor Bridget Bocchino Hochstuhl.

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Cindy Burrini • Dec 7, 2023 at 4:51 pm

Emily, what a brave and courageous and heartfelt thing to do, sharing your Mom’s story of her battle with breast cancer. I remember that time well. Your Mom dealt with every complication imaginable as she also dealt with work and her family, especially two babies. Your Mom is a true warrior and an absolute inspiration to anyone going through or who will be diagnosed with breast cancer. Cancer is not a death sentence, and as your Mom says, “Storms always lose to the sun.” YOU and your Mom are rays of sunshine that will always rise above the “storm” I love you guys!

Jeanine • Dec 6, 2023 at 7:54 pm

This is incredible Emily. I’m so proud of your courage. Your mom is the strongest woman I know, and let me tell you, she fought so hard because of you! Her beautiful family! Thanks for sharing this and acknowledging your mom is a true hero. Her words–storms always lose to the sun ☀️ XOXO Jeanine

Melissa Ferraro • Dec 6, 2023 at 11:30 am

Absolutely Beautiful Emily. The love you have for your mother and her strength is inspiring. Your mother is a gift.

Andrea Seiden • Dec 5, 2023 at 6:44 pm

Beautiful story, Emily. Your mom’s strength is an inspiration to all of us. Lovely and engaging writing. Thank you for sharing, Emily!

Emily • Dec 6, 2023 at 10:05 am

Thank you!!!!!

Denise O • Dec 5, 2023 at 6:34 pm

Beautifully written tribute to your mom, Emily. Great reminder to get your mammogram.

Erich Guy Hochstuhl • Dec 5, 2023 at 6:18 pm

Great writing, Emily. I’m proud to be your Dad. I love you.

Melinda Seger • Dec 5, 2023 at 5:21 pm

This is such a touching story of such a great love and admiration between a mother and daughter…absolutely priceless.

Jill • Dec 5, 2023 at 5:21 pm

Emily, your Mom is a strong woman. Your story is a tribute to her and your love for her.

Theresa Puljic • Dec 5, 2023 at 2:21 pm

Emily wrote a wonderful piece on her hero, and I’m overwhelmed with admiration and love for this piece. Love to you all, and thank God that Bridget was able to beat this!

Anna Hankin • Dec 5, 2023 at 11:34 am

What an amazing, loving daughter! This is absolutely a beautiful story! Mom is a true warrior; her story will encourage others to never give up!! Such a beautiful tribute to a wonderful Mom! Thank you for sharing this! Xo

Danee DeCarlo • Dec 5, 2023 at 10:54 am

Thank you for sharing this beautiful story. As a mom with a young baby, it was very informational and thought provoking. Great job of taking the courage to share something so personal. I wish you and your family all the best in all the years to come

Martha Conte • Dec 5, 2023 at 10:27 am

A truly beautiful article Emily. How you articulate the entire journey is so impressive. Keep up the great work!

Bridget Bocchino Hochstuhl • Dec 5, 2023 at 10:13 am

My beautiful daughter, my precious gem, such a heartfelt article, and I thank you from the bottom of my heart for being my rock, my strength and one of the rays in my sunshine. You’re a strong woman of substance. Don’t let anybody tell you differently. I love you. Great job on the article. Love, Mom.

Tina B • Dec 2, 2023 at 7:56 am

What an incredible article. The author’s writing created the perfect blend of education and adoration. I could feel the strength her mother had, and the love and gratitude she has for that courage. Well done! Thanks for sharing this very motivational story.

Dana Wallock • Dec 7, 2023 at 12:25 pm

Your mom is a true warrior – thank you for sharing her story with your beautiful words! Loved how your reflected on your journey as her daughter.

Linda Venturini • Dec 2, 2023 at 7:41 am

Thank you for allowing all of us to see what a strong and beautiful Mom you have. Your story of all she has been through is going to help many others to get checked out sooner rather than later. Your Mom is a true warrior but after reading this, so are you. Thank you for sharing this.

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117 Breast Cancer Essay Topic Ideas & Examples

Inside This Article

Breast cancer is a prevalent and life-threatening disease that affects millions of individuals worldwide. It is important to raise awareness about breast cancer, its causes, prevention methods, and treatment options. Writing an essay on breast cancer can help educate others, spread awareness, and provide support to those affected by the disease. To help you get started, here are 117 breast cancer essay topic ideas and examples:

• The history of breast cancer research.
• Understanding breast cancer: Causes, risk factors, and prevention.
• The impact of genetics on breast cancer development.
• Exploring the different types and stages of breast cancer.
• The role of hormonal imbalances in breast cancer.
• Environmental factors and their link to breast cancer.
• The importance of regular breast self-examinations.
• The significance of early detection in breast cancer survival rates.
• The impact of breast cancer on mental health.
• The emotional journey of breast cancer survivors.
• The role of support groups in the breast cancer community.
• Breast cancer in men: Understanding the challenges and misconceptions.
• The importance of mammograms in breast cancer screening.
• The role of lifestyle choices in breast cancer prevention.
• Exploring the various treatment options for breast cancer.
• The impact of chemotherapy on breast cancer patients.
• Radiation therapy: Benefits and side effects.
• Surgical interventions for breast cancer: Mastectomy vs. lumpectomy.
• Breast reconstruction surgery: A personal choice after breast cancer.
• The role of targeted therapies in breast cancer treatment.
• The impact of hormone therapy on breast cancer patients.
• The role of immunotherapy in advanced breast cancer cases.
• The psychological effects of breast cancer on patients' relationships.
• Coping strategies for dealing with the emotional toll of breast cancer.
• The role of nutrition in supporting breast cancer treatment.
• The importance of exercise during and after breast cancer treatment.
• Alternative and complementary therapies for breast cancer patients.
• The financial burden of breast cancer treatment.
• Breast cancer advocacy: The fight for better research and resources.
• The role of technology in advancing breast cancer detection methods.
• Breast cancer awareness campaigns: Their impact on public perception.
• Breast cancer in developing countries: Challenges and solutions.
• The impact of breast cancer on fertility and reproductive choices.
• The role of genetic testing in breast cancer risk assessment.
• The relationship between obesity and breast cancer.
• The impact of race and ethnicity on breast cancer outcomes.
• The importance of early education about breast health.
• Breast cancer in young women: Unique challenges and considerations.
• The role of social media in raising breast cancer awareness.
• Breast cancer and pregnancy: Navigating treatment decisions.
• The impact of breast cancer on sexual health and intimacy.
• The role of survivorship programs in supporting breast cancer patients.
• The impact of breast cancer on workplace dynamics and discrimination.
• Breast cancer and the LGBTQ+ community: Unique experiences and challenges.
• The importance of clinical trials in advancing breast cancer research.
• Breast cancer and the role of epigenetics.
• The impact of stress and emotional trauma on breast cancer outcomes.
• The role of advocacy organizations in supporting breast cancer patients.
• Breast cancer and the role of spirituality in coping.
• The impact of hormone replacement therapy on breast cancer risk.
• The role of patient navigation programs in improving breast cancer outcomes.
• Breast cancer and the impact on body image and self-esteem.
• The significance of breast cancer education in schools and colleges.
• The role of art therapy in supporting breast cancer patients.
• Breast cancer recurrence: Challenges and treatment options.
• The impact of breast cancer on caregivers and their mental health.
• The role of exercise in reducing the risk of breast cancer recurrence.
• Exploring the relationship between breast cancer and autoimmune diseases.
• Breast cancer and the impact on fertility preservation options.
• The role of palliative care in supporting advanced breast cancer patients.
• The impact of breast cancer on survivorship and quality of life.
• The role of community-based organizations in supporting breast cancer patients.
• Breast cancer and the impact on body image in the media.
• The importance of peer support in the breast cancer community.
• Breast cancer and the role of spirituality in healing and recovery.
• The impact of breast cancer on families and children.
• The role of mindfulness-based interventions in supporting breast cancer patients.
• Breast cancer in the elderly population: Challenges and considerations.
• The importance of clinical breast exams in early detection.
• Breast cancer and the impact on sexual orientation and gender identity.
• The role of survivorship care plans in supporting breast cancer survivors.
• Breast cancer and the impact on fertility preservation options for transgender individuals.
• The significance of dietary supplements in breast cancer prevention.
• The impact of breast cancer on body image and self-acceptance.
• Breast cancer and the role of spirituality in coping with treatment side effects.
• The importance of breast cancer education in underserved communities.
• Breast cancer and the impact on mental health in marginalized populations.
• The role of music therapy in supporting breast cancer patients.
• Breast cancer and the impact on access to healthcare in rural areas.
• The significance of breastfeeding in reducing the risk of breast cancer.
• Breast cancer and the role of integrative medicine in treatment.
• The impact of breast cancer on sexual identity and gender dysphoria.
• The role of survivorship clinics in addressing long-term effects of breast cancer treatment.
• Breast cancer and the impact on body image in different cultures.
• The importance of mentorship programs for young breast cancer survivors.
• Breast cancer and the role of spiritual practices in coping with treatment side effects.
• The impact of breast cancer on mental health in refugee populations.
• The significance of art therapy in supporting breast cancer patients during treatment.
• Breast cancer and the impact on healthcare disparities in minority communities.
• The role of laughter therapy in improving the well-being of breast cancer patients.
• Breast cancer and the importance of culturally sensitive healthcare practices.
• The impact of breast cancer on mental health in adolescent survivors.
• The significance of dance therapy in improving physical and emotional well-being of breast cancer patients.
• Breast cancer and the role of mobile health applications in self-management.
• The impact of breast cancer on mental health in immigrant populations.
• The importance of peer mentoring programs for breast cancer survivors.
• Breast cancer and the role of mindfulness meditation in managing treatment side effects.
• The impact of breast cancer on mental health in the LGBTQ+ community.
• The significance of pet therapy in providing emotional support to breast cancer patients.
• Breast cancer and the role of community health workers in improving access to care.
• The impact of breast cancer on mental health in rural populations.
• The importance of gardening therapy in promoting well-being among breast cancer survivors.
• Breast cancer and the impact on mental health in older adults.
• The role of equine therapy in supporting emotional well-being of breast cancer patients.
• The significance of telehealth in improving access to healthcare for breast cancer patients.
• Breast cancer and the impact on mental health in low-income populations.
• The importance of aromatherapy in managing treatment-related symptoms for breast cancer patients.
• The impact of breast cancer on mental health in individuals with disabilities.
• The role of horticultural therapy in promoting emotional healing among breast cancer survivors.
• Breast cancer and the significance of patient navigators in improving health outcomes.
• The impact of breast cancer on mental health in incarcerated populations.
• The importance of acupuncture in managing treatment side effects for breast cancer patients.
• Breast cancer and the impact on mental health in military veterans.
• The role of aquatic therapy in improving physical and emotional well-being of breast cancer patients.
• The significance of technology-based interventions in supporting breast cancer survivors.
• Breast cancer and the impact on mental health in individuals with substance use disorders.
• The importance of laughter yoga in promoting emotional well-being among breast cancer patients.

These essay topic ideas provide a diverse range of perspectives on breast cancer, allowing you to choose a topic that resonates with you. Remember to conduct thorough research, use credible sources, and share compelling stories to make your essay impactful and informative. Together, we can continue to raise awareness and support those affected by breast cancer.

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Breast Cancer - Free Essay Examples And Topic Ideas

Breast cancer is a type of cancer that develops from breast tissue. Essays on this topic could explore the causes, diagnosis, treatment, and prevention of breast cancer. Additionally, discussions might delve into the psychological and social impact of breast cancer on patients and their families, the ongoing research towards finding a cure, and the broader societal awareness and support systems available for those affected. We have collected a large number of free essay examples about Breast Cancer you can find at Papersowl. You can use our samples for inspiration to write your own essay, research paper, or just to explore a new topic for yourself.

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Corporate Social Responsibility against Cancer

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New Healthcare Inventions on Breast Cancer

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The human body is made up of cells. When a cell dies the body automatically replaces it with a new healthy cell, but sometimes the cell is not healthy and grows out of control. These cells group together and form a lump that can be seen on an x-ray. Breast cancer is a tumor in the cells of person’s breast. It can spread throughout the breast to the person’s lymph nodes and other parts of the body. Sometimes it occurs […]

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Essays About Breast Cancer Breast Cancer is one of the most common cancers in women and is a disease by which the cells in the breast area grow out of control. Breast cancer tends to begin in the ducts or lobules of a breast and there are different types of cancer. In the US alone 1 in 8 women will develop breast cancer at some stage in their lives. In many academic fields; from science to medicine the study of breast cancer and essays about breast cancer are required as part of the curriculum. An essay on breast cancer can seem daunting due to the amount of research and several varying scientific approaches used to talk about the topic. We offer essay examples, or research paper guidance and free essay samples.  These can be used to gauge how to approach the topic and are an informative look at all factors that contribute to breast cancer and prevention. We also factor breast cancer awareness into our essay samples and ensure essays for both university and college build a strong foundation to understanding the disease, but also draw criticism when necessary and a strong conclusion on whatever element of breast cancer the focus of the essay is on.

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125 Breast Cancer Essay Topic Ideas & Examples

🏆 best breast cancer topic ideas & essay examples, 💡 most interesting breast cancer topics to write about, 📌 simple & easy breast cancer essay titles, 👍 good essay topics on breast cancer.

• Best Practices in Breast Cancer Care Based on this, the final stage of therapy should include comprehensive support for patients with breast cancer as one of the main health care practices within the framework of current treatment guidelines.
• Breast Cancer: Concept Map and Case Study Each member of the interdisciplinary team involved in treating patients with cancer and heart disease should focus on educational priorities such as:
• Health Psychology: Going Through a Breast Cancer Diagnosis He is unaware that she has been diagnosed with depression and that she is going for breast screening Stress from work is also a contributing factor to her condition.
• Genes Cause Breast Cancer Evidence suggests the role of BRCA1 in DNA repair is more expansive than that of BRCA2 and involves many pathways. Therefore, it is suggested that BRCT ambit containing proteins are involved in DNA repair and […]
• Breast Cancer and Its Population Burden The other objectives that are central to this paper are highlighted below: To determine which group is at a high risk of breast cancer To elucidate the impact of breast cancer on elderly women and […]
• Mindfulness Practice During Adjuvant Chemotherapy for Breast Cancer She discusses the significance of the study to the nursing field and how nurses can use the findings to help their patients cope with stress.
• Breast Cancer: The Effective Care Domain Information about how the patient is seen, how often the patient is seen, and whether she will return for mammograms can be collected and analyzed to verify the successful intervention to extend consistency with mammograms.
• Garden Pesticide and Breast Cancer Therefore, taking into account the basic formula, the 1000 person-years case, the number of culture-positive cases of 500, and culture-negative of 10000, the incidence rate will be 20 new cases.
• Breast Cancer as a Genetic Red Flag It is important to note that the genetic red flags in Figure 1 depicted above include heart disease, hypertension, and breast cancer.
• Breast Cancer Surveillance Consortium Analysis Simultaneously, the resource is beneficial because it aims to “improve the delivery and quality of breast cancer screening and related outcomes in the United States”.
• Drinking Green Tea: Breast Cancer Patients Therefore, drinking green tea regularly is just a necessity- it will contribute to good health and physical vigor throughout the day and prevent severe diseases.
• Breast Cancer Prevention: Ethical and Scientific Issues Such information can potentially impact the patient and decide in favor of sharing the information about the current condition and risks correlating with the family history.
• Breast Cancer: Epidemiology, Risks, and Prevention In that way, the authors discuss the topics of breast cancer and obesity and the existing methods of prevention while addressing the ethnic disparities persistent in the issue.
• Breast Cancer Development in Black Women With consideration of the mentioned variables and target population, the research question can be formulated: what is the effect of nutrition and lifestyle maintained on breast cancer development in black women?
• Breast Cancer in Miami Florida The situation with the diagnosis of breast cancer is directly related to the availability of medicine in the state and the general awareness of the non-population.
• Breast Cancer: Genetics and Malignancy In the presence of such conditions, the formation of atypical cells is possible in the mammary gland. In the described case, this aspect is the most significant since it includes various details of the patient’s […]
• Breast Cancer. Service Management The trial specifically looks at the effect on breast-cancer mortality of inviting women to screening from age 40 years compared with invitation from age 50 years as in the current NHS breast-screening programme.
• Fibrocystic Breast Condition or Breast Cancer? The presence of the fibrocystic breast condition means that the tissue of the breast is fibrous, and cysts are filled with the liquid or fluid. The main characteristic feature of this cancer is that it […]
• Coping With Stress in Breast Cancer Patients Therefore, it is important for research experts to ensure and guarantee adherence to methodologies and guidelines that define scientific inquiry. However, various discrepancies manifest with regard to the initiation and propagation of research studies.
• Breast Self-Examination and Breast Cancer Mortality Though it is harsh to dismiss self-exams entirely due to studies that indicate little in deaths of women who performed self-exams and those who did not, the self-exams should not be relied on exclusively as […]
• Breast Self-Exams Curbing Breast Cancer Mortality The results of the study were consistent with the findings of other studies of the same nature on the effectiveness of breast self-examination in detecting and curbing breast cancer.
• Taxol Effectiveness in Inhibiting Breast Cancer Cells The following were the objectives of this experiment: To determine the effectiveness of Taxol in inhibiting breast cancer cells and ovarian cancer cells using culture method.
• Control Breast Cancer: Nursing Phenomenon, Ontology and Epistemology of Health Management Then, the evidence received is presented in an expert way leading to implementation of the decision on the management of the disease.
• Breast Cancer: Effects of Breast Health Education The design of the research focused on research variables like skills, performance, self-efficacy, and knowledge as the researchers aimed at examining the effectiveness of these variables among young women who underwent training in breast cancer […]
• Community Nursing Role in Breast Cancer Prevention However, early detection still remains important in the prevention and treatment of breast cancer. The community has thus undertaken activities aimed at funding the awareness, treatment and research in order to reduce the number of […]
• Self-Examination and Knowledge of Breast Cancer Among Female Students Shin, Park & Mijung found that a quarter of the participants practiced breast self-examination and a half had knowledge regarding breast cancer.
• “Tracking Breast Cancer Cells on the Move” by Gomis The article serves the purpose of examining the role of NOG, a gene that is essential in bone development and its role in breast cancer.
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• Gaining Ground on Breast Cancer: Advances in Treatment The article by Esteva and Hortobagyi discusses breast cancer from the aspect of increased survival rates, the novel treatments that have necessitated this and the promise in even more enhanced management of breast cancer.
• Effects of Hypoxia, Surrounding Fibroblasts, and p16 Expression on Breast Cancer The study was conducted to determine whether migration and invasion of breast cancer cells were stimulated by hypoxia, as well as determining whether the expression of p16 ectopically had the potential to modulate the cell […]
• Breast Cancer: Preventing, Diagnosing, Addressing the Issue In contrast to the MRI, which presupposes that the image of the tissue should be retrieved with the help of magnetic fields, the mammography tool involves the use of x-rays.
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• The Detection and Diagnosis of Breast Cancer The severity of cancer depends on the movement of the cancerous cells in the body and the division and growth or cancerous cells.
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• Breast Cancer Genetics & Chromosomal Analysis In this paper, the chromosomal analysis of breast cancer will be assessed, and the causes of the disorder will be detailed.
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• Breast Cancer: Causes and Treatment According to Iversen et al this situation is comparable to the finding of abnormal cells on the surface of the cervix, curable by excision or vaporization of the tissue.
• Monoclonal Antibodies in Treating Breast Cancer The most important function of the lymph glands is that their tissue fluid carries the cancer cells that have been detached from the tumour to the closely located lymph gland.
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• Screening for Breast Cancer The main goal of this paper is to describe the specific set of clinical circumstances under which the application of screening is the most beneficial for women aged 40 to 74 years.
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• Breast Cancer Patients’ Functions and Suitable Jobs The key symptom of breast cancer is the occurrence of a protuberance in the breast. A screening mammography, scrutiny of the patient’s family history and a breast examination help in the diagnosis of breast cancer.
• Jordanian Breast Cancer Survival Rates in 1997-2002 This objective came from the realization that the best way to test the efficacy of breast cancer treatment and to uncover intervening factors influencing the efficacy of these treatments was to investigate the rates of […]
• Breast Cancer Awareness Among African Americans There are reasons that motivate women to seek mammography for example the belief that early detection will enable them treat the cancer in early stages, and their trust for the safety of mammogram. Social marketing […]
• Breast Cancer Screening Among Non-Adherent Women This is one of the aspects that can be identified. This is one of the short-comings that can be singled out, and this particular model may not be fully appropriate in this context.
• Breast Cancer: Treatment and Rehabilitation Options Depending on the site of occurrence, breast cancer can form ductal carcinomas and lobular carcinomas if they occur in the ducts and lobules of the breast, respectively. Breast cancer and treatment methods have significant effects […]
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• Health Information Seeking and Breast Cancer Diagnosis Emotional support is also concerned with the kind of information given to patients and how the information is conveyed. It is equally significant to underscore the role of information in handling breast cancer patients immediately […]
• Current Standing of Breast Cancer and Its Effects on the Society It then places particular focus on the testing and treatment of breast cancer, the effects and conditions associated with it, from a financial point of view, and the possible improvements worth making in service or […]
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• Treatment Options for Breast Cancer This type of breast cancer manifests itself in the tubes/ducts which form the channel for transporting milk from the breast to the nipple.”Lobular carcinoma: this type of cancer usually begins in the milk producing regions […]
• Risk Factors, Staging, and Treatment of Breast Cancer This is so because huge amounts of resources have been used in the research and the development of the breast cancer drugs that in effect help the body to combat the cancer by providing additional […]
• Case Management for Breast Cancer Patients In this respect, preventive measures should be taken in order to decrease the mortality rates all over the world in terms of cancer illness and breast cancer in particular.
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• The Treatment and Management Options for Breast Cancer Patients
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Behind the Breakthroughs: How Can We Better Treat Younger Breast Cancer Patients?

BCRF investigator Dr. Sherene Loi talks about the landmark SOFT trial, international collaboration, and how breast cancer is affecting younger women

When younger women are diagnosed with breast cancer, they generally have poorer outcomes than older women. Incidence is on the rise for young women in the U.S.: In the last 10 years alone, there has been an eight percent increase in diagnoses in women under 40—underscoring the need for research focused on these patients. 

Researchers like Dr. Sherene Loi , a BCRF investigator since 2015, are working to uncover why this is happening—and how we can better treat the disease, reduce recurrence, and prevent it entirely. Through the landmark BCRF-supported SOFT trial, Dr. Loi and her colleagues have already developed treatment strategies that have improved outcomes for women under 40. Now, she’s working to understand the immune microenvironment of breasts cancers in younger women—including the role of tumor-infiltrating lymphocytes—and continue to improve treatment.

Below is an edited transcript of Dr. Loi’s conversation with BCRF staffer and breast cancer thriver Sadia Zapp.

Let's start with tumor-infiltrating lymphocytes (TILs), a major focus of your research. What are they?

TILs are immune cells. When a pathologist looks down the microscope they can see the breast cancer and all the surrounding tissue in a row that surrounds the breast cancer. And they can also see lots of different cells apart from cancer cells, and some of these cells are immune cells. And we call these cells tumor-infiltrating lymphocytes or TILs.

How are TILs being used in breast cancer?

A long time ago we looked at the quantity of immune cells [for people with cancer] and correlated that to whether they had recurrences from their breast cancer in the future. And it was actually quite remarkable, because we did find in these first studies that the amount of immune cells did predict whether you did better from your breast cancer. So, the more immune cells you had, we [realized] that your immune system was actively fighting the cancer. And then once you remove the tumor, your immune system was able to, with the one or the other treatment you receive, mop up the rest of the cancer cells and protect you from cancer recurrence in the long term. So that's subsequently been reproduced by many other investigators, and it really seems to be particular for patients with triple-negative breast cancer (TNBC) , [which is more common in younger patients]. This also seems to be the case with certain types of hormone receptor–positive breast cancer. We're exploring that in more detail, using the [BCRF-supported] SOFT trial .

But getting back to TNBC. We’re in an era now of immunotherapy. We've done quite a lot of work with other investigators that we know that your level of TIL does suggest that you might have a higher rate of pathological complete response [with a drug called] Keytruda and a shorter duration of chemotherapy. So, my belief at the moment is that if we can see your immune system is active, we can enhance that with agents such as Keytruda. And ultimately, we will be able to safely shorten the type of chemotherapy that you require. At the moment, everyone requires a big, intensive chemotherapy regimen. But I think for patients who have existing immune cells or evidence that the immune systems are really active, then they won't need that much additional chemotherapy. The Keytruda will kind of do the job for us.

Why is hormone-receptor positive cancer more aggressive in younger women?

I have a number of theories. So, for younger people to develop cancer, it has to be a little bit more aggressive to get through the natural barriers that we all have to prevent cancer from occurring. For women who are young, they're potentially of childbearing age. They'd have very strong menstrual cycle, and the breast changes during that cycle. So, you have your menstrual cycles, and every month you've got this growth in your breast. And then you have cells die, but a cell that's learned to not die every month is getting this strong growth signal. Naturally women’s fertility drops after the age of 40. We see that breast cancers seem to be a little bit less aggressive in women as they reach their mid-40s and move into a natural menopause.

There are other things that we don't really know, but we suspect. In countries such as America and Australia, women are having children later. There are also some issues with obesity, alcohol, etc. So that probably contributes as well. They're not breastfeeding for long, and we know that breastfeeding particularly does attenuate the risk of triple-negative breast cancer. And other things that we don't really understand like pollution or our environment may be contributing to some of the increased rates or younger onset breast cancer we're seeing. And also, maybe why they're a little bit more aggressive. So, there's potentially lots of reasons there. And no one really knows the answer. It's probably multifactorial, unfortunately, but with trying to study the individual parts to see if making a difference to one of those parts will help a lot.

The SOFT trial and its sister trial TEXT are happening on this massive international scale with more than 5,000 women enrolled from across 500 hospitals and 27 countries. Why is global collaboration so important in breast cancer research?

These studies, which were managed by the International Breast Cancer Study Group are a collaboration between Europe, America, Australia, and many countries in the world. It was really a remarkable feat for the global breast cancer community to answer an important question that is still highly relevant today. Most premenopausal women will receive concurrent ovarian function [to suppress estrogen]. If a woman’s cancer is high risk, that makes a huge difference to their outcomes, even though we are trying to obviously deal with some of the side effects. International collaboration is essential for all good breast cancer research. Getting people together in the one room is really important, and BCRF does that well.

What is your biggest hope for your work and for the future of breast cancer?

I'm hoping in the future, we might incorporate more biomarkers, because I feel we have a lot of biomarkers, but we don't really look to incorporate [them all] in routine practice. I'm hoping in the future, we will be able to incorporate TIL, tumor size, liquid biopsies and more to really understand who needs lesser treatment. We'll be able to individualize therapies for our patients in the future. And, I really do think that hopefully, we will understand a lot more about how we can prevent breast cancer in the future with some of the factors I’ve been talking about. We don't want to just treat, we want to prevent.

Why is BCRF funding specifically so important to your work?

BCRF gives you a lot of freedom to try out some riskier ideas. Fortunately for me, we did one of the first papers on single-cell RNA sequencing. And that was very successful, but at the time, it was extremely expensive. So, BCRF allowed us to work that technique up and apply that to human TILs. So that was very labor intensive and very expensive. But if I didn't have BCRF funding, no one would have given me money to do that. So that was really very helpful and helped us understand a lot about the TIL and certain subsets of the TIL. The whole community is lovely, and there's lots of interaction and networking and discussion about science. The annual meetings are really very motivational. From a scientific and research point of view, you really come back thinking, “I need to do this and this and this.” And [BCRF] gives you the freedom to explore a few things that you think might pay off. I've been very grateful for the support of BCRF. They're just such a fantastic organization.

If there's one takeaway from our conversation, or if there's one thing you hope patients walk away with, what would that be?

I think the cure is near for breast cancer. So hopefully the next generation of women won't have to suffer as much as ours.

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View sample cancer research paper on breast cancer. Browse other research paper examples for more inspiration. If you need a thorough research paper written according to all the academic standards, you can always turn to our experienced writers for help. This is how your paper can get an A! Feel free to contact our writing service for professional assistance. We offer high-quality assignments for reasonable rates.

Breast cancer is one of the major public health problems. Every year some 1.2 million new cases of breast cancer are diagnosed and some 400 000 women die from it. Worldwide, some 50 million women are living after a previous breast cancer experience. Approximately 200 000 deaths from breast cancer occur in developed countries and 200 000 in developing countries. In Europe, there were an estimated 370 000 new cases and 130 000 deaths in 2004. Mortality rates rose from 1951 to about 1990 but have fallen since then in most European countries, noticeably in the UK (Figure 1(a)), but mortality rates in Central and Eastern European countries have been rising (Figure 1(b)). Although rates in Hong Kong and Japan have been lower than those in Europe, they have also been increasing (Figure 1(b)). Rates in North and South America have been similar to those in Western Europe (Figure 1(c)).

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The decline in mortality rates in Western Europe, Australia, and the Americas may be due to widespread mammographic screening, good diagnosis, and increased numbers of women receiving the best treatment, including hormonal drugs (Ferlay et al., 2004).

Causes of Breast Cancer

Family history.

In countries where breast cancer is common, the lifetime excess incidence of breast cancer is 5.5% for women with one first-degree relative who has had breast cancer and 13.3% for women with two. Eight out of nine women who develop the disease do not have an affected mother, sister, or daughter, however. Only 3–4% of women with breast carcinoma have a genetic mutation (BRCA1 or BRCA2), although these are the most strongly associated risk factors: Affected women have a 50–70% risk of developing breast carcinoma during their lifetime.

Pregnancy-Related And Hormone-Related Factors

Women who have their first full-term birth at an early age have a lifetime reduction in risk. Increased parity is associated with a long-term risk reduction, even when the age at first birth is controlled for; the additional, long-lasting protective effect of a young age at subsequent full-term pregnancies is not as strong as that for the first full-term pregnancy; a nulliparous woman has roughly the same risk as a woman who has her first full-term birth aged about 30 years; the risk is transiently increased after a full-term pregnancy. Long duration of lactation confers a small, additional reduction in risk after the age at pregnancy and the number of full-term pregnancies is controlled for. Breast cancer risk factors are set out in Table 1.

The decision not to breastfeed or a very short lifetime duration of breastfeeding, typical of women in developed countries, contributes substantially to the high incidence of breast cancer in these areas. The risk is significantly reduced by breastfeeding, in addition to the reduction for every birth. Breastfeeding practices can be modified and promoted usefully as a strategy to prevent breast cancer.

There is no pronounced excess risk of diagnosis in women 10 or more years after the cessation of oral contraceptive use. The cancers diagnosed in women who have used combined oral contraceptives tend to be less advanced clinically than those diagnosed in women who have never used them. The risk of breast cancer is raised in women using hormone-replacement therapy and increases with duration of use. This effect declines after cessation of hormone-replacement therapy and largely disappears after about 5 years; the benefits and risks associated with this hormone treatment should be taken into account.

After adjustment for known risk factors, induced abortion is not associated with an increased risk of breast cancer. Pregnancies that end as a spontaneous or induced abortion have been shown not to increase a woman’s risk of developing breast cancer (Veronesi et al., 2005).

Anthropometric Indices And Physical Activity

With pooled data from seven prospective studies (337 819 women and 4385 incident breast cancer cases in total) and after adjustment for reproductive, dietary, and other risk factors, the pooled relative risk of breast cancer per height increment of 5 cm was 1.02 (95% CI 0.96–1.10) in premenopausal women and 1.07 (1.03–1.12) in postmenopausal women. The body mass index showed substantial inverse and positive associations with the disease in premenopausal and postmenopausal women, respectively. Height is an independent risk factor for breast cancer after menopause but not in premenopausal women.

In postmenopausal women not taking exogenous hormones, general obesity is an important predictor of breast cancer. In premenopausal women, weight and body mass index showed nonsignificant inverse associations with breast cancer.

Increased physical activity seems to be inversely related to the risk of breast cancer, although the findings are inconsistent. Physical activity and weight control can be recommended at present, although further research may highlight additional benefits.

Dietary Factors

A pooled analysis of eight prospective studies showed relative risks for an increment of 5% of energy intake were 1.09 for saturated fat, 0.93 for monounsaturated fat, and 1.05 for polyunsaturated fat, compared with equivalent energy intake from carbohydrates.

The Nurses’ Health Study II (Cho et al., 2003) showed that intake of animal fat, mainly from red meat, before menopause, was associated with an increased risk of breast cancer. To assess the risk of invasive breast cancer associated with total and beverage-specific alcohol consumption and to establish whether dietary and nondietary factors change such an association, data from six prospective studies were examined. Alcohol consumption correlated with breast cancer incidence in women. A reduction of consumption among women who drink alcohol regularly could reduce their risk of breast cancer. Cigarette smoking, frequently analyzed with alcohol consumption in etiological studies, does not seem to be related to risk.

Environmental Exposures

An increased risk of breast cancer in women exposed to ionizing radiation, particularly during puberty, has been widely accepted even with low-dose exposure. Environmental exposure to organochlorines has been examined as a potential risk factor for breast cancer. Based on current evidence, the association between risk and exposure to organochlorine pesticides and their residues seems to be small, if it exists at all. The combined evidence from five large U.S. studies that assessed the link between breast cancer risk and concentrations of 1,1-dichloro-2,2-bis (p-chlorophenyl) ethylene and polychlorinated biphenyls in blood plasma does not support such an association (Cuzick et al., 2003).

Possibilities Of Chemoprevention

The pharmacological prevention of cancer represents a comparatively novel field in clinical oncology, but it offers a very promising approach to reducing the burden of cancer and its incidence. In cardiology, it is common practice to treat subjects at higher risk for cardiovascular disease long before clinical evidence of the disease can be detected. This has made a definite contribution to lower mortality. A similar strategy could be adopted for cancer prevention in subjects ‘at higher risk’ (Hong and Sporn, 1997).

The peculiarity of carcinogenesis is that it is a multistep, multipath, and multifocal process, involving a series of genetic and epigenetic alterations that develop from genomic instability all the way to the final development of cancer. This is the key notion lying behind the rationale for intervention in the initial steps of the process, by employing natural or synthetic agents capable of delaying, arresting, or even reversing the pathogenesis of cancer. Since the process is generally very long (10–20 years, sometimes more), there is potentially a great deal of time to assess the true risk and intervene with nutrients and/or pharmacological agents that may interrupt the chain of molecular events long before the onset of clinical symptoms. This may prove of particular use where solid tumors are concerned, since they are often characterized by multifocality and metachronous growth. Recently, a number of compounds have been shown to be clinically effective in breast carcinoma, covering all three settings into which prevention may be typically divided. In primary prevention, the goal is to prevent the onset of the disease, selecting healthy cohorts who are at high risk because of their environment, lifestyle, or familial/ genetic factors. Secondary prevention (screening) is aimed at detecting and treating persons with a premalignant condition or an in situ malignancy, thus blocking its evolution to an invasive cancer. Tertiary prevention is a term that can be applied to the protection of individuals who have previously been treated for cancer from developing a second primary tumor (Figures 2 and 3; Table 2).

Pathogenesis of Breast Cancer

Progression from healthy tissue to invasive carcinoma.

In contrast to the position for adenocarcinoma of the colon, no definitive model of progression from the common benign proliferative lesions of the breast to invasive malignancy has been identified. Cytological or architectural dysplastic changes can be identified in various nonmalignant breast diseases, such as florid and columnar duct hyperplasia, adenosis, and papilloma, but their true precancerous potential remains undefined.

Atypical duct hyperplasia has been regarded as the missing link between healthy duct hyperplasia and low-grade, ductal neoplasia in situ (DIN). Morphological features of atypical duct hyperplasia, which are intermediates of those in healthy and malignant tissues, and the substantially raised risk for subsequent carcinoma in affected women, have been claimed as sufficient proof of a precancerous nature. However, genetic changes in atypical duct hyperplasia are identical to changes in fully developed DIN, which raises questions about whether atypical duct hyperplasia is a distinct entity from low-grade intraductal neoplasia.

Novel approaches such as gene-expression profiling will increasingly be used to ascertain the occurrence of true preneoplastic lesions in the breast. Precise identification of these precursor lesions will be vital for planning interventions in women at high risk of breast cancer and to assess the effectiveness of prevention trials.

Ductal lavage is currently undergoing investigation. In this procedure, luminal cells from the ductal tree are obtained by cannulation of the lactiferous ducts and gentle massage of the breast. Harvested cells can then be examined not only for morphological changes but also for the expression of early markers of cell transformation that will eventually be identified. This procedure is being tested for validation as an additional research instrument to identify patients at high risk of developing breast carcinoma (O’Shaughnessy et al., 2002).

In view of the uncertainty of the occurrence of true preneoplastic lesions of the breast, the morphologically identifiable initial phases of neoplastic transformation remain in situ neoplasia, either ductal or lobular. However, this encompasses various lesions, ranging from low-grade to high-grade neoplasms, with remarkably different modes of presentation, histopathological features, genetic alterations, risk of relapse and of progression to invasive carcinoma.

To emphasize the non-life-threatening nature of in situ lesions and reduce any psychological effect caused by the use of carcinoma as a description, the term ductal intraepithelial neoplasia has been suggested to define these cell masses. This has been revised to encompass candidate preneoplastic lesions: Flat epithelial atypia and atypical duct hyperplasia (Tavassoli and Devilee, 2003). The same procedure has been done for noninvasive lobular neoplasms (atypical lobular hyperplasia and lobular carcinoma in situ), which have been classified into a three-tiered system of lobular intraepithelial neoplasia.

Invasion and metastasis are the hallmarks of fully developed breast carcinoma. Extensive histopathological examination of axillary sentinel lymph nodes by complete and serial sectioning at very close cutting intervals (e.g., at least 60 serial sections at 50-mm intervals, as used at the European Institute of Oncology, Milan, Italy) has greatly improved the detection rate of axillary lymphnode association (Veronesi et al., 2003). Detection is strongly associated with the definitive features of the primary breast cancer, such as tumor size and type, occurrence of peritumoral vascular invasion, and multifocality.

Randomized trials (Veronesi et al., 2003) have shown that the recorded number of patients with clinically overt axillary progression of breast cancer is much lower than expected, based on the false-negative rate of the sentinel lymph-node biopsy. This difference suggests that metastatic cells may not progress to clinical disease in all patients and that only some cells are able to sustain tumor progression, which is consistent with the hypothesis that the growth, progression, and clinical outcome of a cancer depend on the activation of tumorigenic stem/ progenitor cells.

This redefinition of the malignancy of breast cancer is recognized in the new pTNM classification, whereby minimum nodal invasion (1 mm or less) is classed as pT1mic (indicating microinvasive cancer) and isolated tumor cells or tumor-cell clusters (0.2 mm or less) in the regional lymph node are no longer regarded as metastatic, and qualify as pN0(iþ). These new classifications are designed to prevent overstaging of the disease and hence overtreatment for the patient.

Systemic adjuvant therapy is currently offered to patients according to selected clinicopathological features of the primary tumor, which include the status of estrogen and progesterone receptors and expression of human epidermal-growth-factor receptor 2 (HER2/neu); such treatment is undertaken independently of the axillary node status, with an equivalent survival benefit.

Quantification of tumor cells circulating in the blood of patients with breast cancer may also be a predictor of the duration of survival.

Gene-expression profiling of breast carcinoma has already shown that differential expression of specific genes is a more powerful prognostic indicator than traditional determinants such as tumor size and lymph-node status. These molecular assays now await clinical validation by prospective randomized trials before being introduced into routine clinical practice.

Breast Cancer Diagnosis and Staging

Organized screening, education programs, and improved consciousness of the female population have substantially changed the type of patients seen nowadays compared with those a few decades ago. The revolution in diagnostic imaging over the past 20 years has also profoundly modified diagnostic strategies in breast cancer.

Diagnostic Procedures

Procedures commonly used for the diagnosis of breast cancer include mammography, ultrasonography, MRI (magnetic resonance imaging), and PET (positron emission tomography). Physical examination of the breast remains important, however, because a substantial minority (11%) of breast cancers are not seen on mammography.

Mammography remains the most important diagnostic tool in women whose breast tissue is not dense. After menopause, mammography is generally the best method to discover tiny, nonpalpable lesions. By contrast, ultrasonography is the most effective procedure to diagnose small tumors in women with dense breast tissue and to differentiate solid lesions from cystic lesions. Although mammography can identify suspicious microcalcifications, it is not good at distinguishing between breast densities and has difficulty in identifying certain lobular invasive carcinomas, Paget’s disease of the nipple, inflammatory carcinoma, and particularly peripheral, small carcinomas.

MRI is mainly used as a problem-solving method after conventional diagnostic procedures. It is highly sensitive and is used mainly to screen high-risk, BRCA-positive patients. In dynamic, contrast-enhanced MRI, images are acquired before and after patients are given a substance to improve contrast when imaging the lesion. Malignant lesions are generally highly permeable, with rapid uptake and elimination of contrast, whereas benign lesions have slow-rising, persistent-enhancement kinetics. Although MRI has good diagnostic accuracy, the false-positive detection rate is still high and MRI findings should not be the sole indication for breast surgery.

PET is currently used to detect metastatic foci in any distant organ or to assess the status of axillary nodes in preoperative staging. However, PET may fail to identify low-grade lesions and tumors smaller than 5 mm.

The use of imaging techniques to detect unknown breast cancers in women who had no symptoms (i.e., screening) was inaugurated by the Health Insurance Plan of New York in the 1960s. In many randomized studies and population studies, mammography has been confirmed as the only screening test that can reduce breast cancer mortality if a large proportion of the population uses the procedure.

However, ultrasonography seems promising for women with dense breast tissue, such as those before menopause, and MRI has been valuable in the screening of women at high risk of breast cancer who are younger than 50 years.

The TNM (tumor-nodes-metastasis) system defines the extent of disease. It is the language used to compare different cases from various centers. With respect to the primary carcinoma (T), T1 can be divided into three subgroups (T1a, T1b, T1c), depending on the size of the primary lesion. However, with new subdivisions, most instances arise in one subcategory (e.g., T1c). In the era of computerized data analysis, classification is thought to be less necessary, whereas precise description of specific cases is regarded as essential and functional to the different needs of statisticians. Therefore, the T classification will probably be determined by a continuous metric description of the size (cm) of the carcinoma (e.g., T0.9, T2.4). The same system could apply to nodes (N) in which the numbers of involved and examined nodes will define the patient’s condition (e.g., N2/18 for two lymph nodes with tumor out of 18 sampled).

Finally, we believe that the TNM system should rely more on biological characteristics (e.g., hormonal receptors, proliferation rates) and biomolecular aspects (e.g., gene expression profile) of tumors. The present biometric, anatomical description will probably be replaced by molecular staging.

Breast Cancer Surgery

Once a diagnostic procedure indicates a tumor in the breast, cytological or histological confirmation is vital before further treatment is given. Cytology is effective in solid lesions, especially if sonographically guided. The histology of the lesion, which can be obtained by a core biopsy, is most useful for surgeons. This is the simplest method for palpable lesions that are easily reached, whereas a vacuum-assisted needle biopsy can obtain enough material for a good histological diagnosis in nonpalpable or deep lesions (Burbank et al., 1996). Excision biopsy a few days before definitive surgery is no longer done, because it creates a local anatomical distortion that makes conservative treatment difficult.

The sophisticated technique of sentinel lymph node biopsy provides knowledge about the condition of the axillary nodes without the need for dissection, when lymph nodes are not affected. Internal mammary nodes can also be easily reached during surgery, to complete the staging procedure. With respect to distant, occult metastases, PET will help identify occult foci of cancer cells anywhere in the body.

Breast conservation is the most popular treatment because most carcinomas have a restricted size and large primary tumors can be reduced in size by primary (neoadjuvant) chemotherapy before surgery. In most breast cancer centers, conservative surgery (lumpectomy) accounts for 75–85% of all operations. Total removal of the mammary gland (mastectomy) is required for multicentric invasive carcinoma, extensive intraduct carcinoma, inflammatory carcinoma, and large primary carcinomas that have not been sufficiently shrunk by neoadjuvant chemotherapy. Early recurrences or even a second ipsilateral carcinoma of restricted size can also be treated with conservative surgery.

Several options are available for reconstruction of the breast, from simple positioning of an expander to the use of musculocutaneous flaps (such as the thoracodorsal or abdominal flap, TRAM). One method becoming widely used is the skin-sparing mastectomy that conserves an extensive section of skin, as well as the more recent skin and nipple-sparing mastectomy, which preserves the nipple-areolar complex.

Identical 5-year survival has been recorded in women with axillary dissection and in women who underwent axillary dissection only if the sentinel lymph node was affected by tumor, although other clinical trials of the long-term effect on survival are ongoing. The histological diagnosis of the sentinel node should be immediately available. The traditional frozen-section procedure (which takes three or four sections of the node) often fails to detect micrometastases. As a consequence, surgeons should completely and definitively examine the sentinel node during surgery, and accurately section the node (up to 60–80 sections) to avoid missing even very small micrometastases. In about 85% of cases in which a micrometastatic sentinel node is found, other axillary nodes are not implicated. Therefore, many surgeons now consider the option of simply monitoring patients carefully with ultrasonography and PET.

In situ lesions are mainly treated with mammary resection. Since axillary metastases are rare, both lymph node dissection and biopsy are optional.

In situ neoplasia should not be incorporated in the TNM classification. Instead, it should be described with the new ductal-intraepithelial-neoplasia system proposed by Tavassoli (Tavassoli et al., 2003).

Radiotherapy in Breast Cancer

Radiotherapy in breast conservation.

The current standard of care for patients with early-stage breast cancer consists of breast-conserving surgery, followed by 5–6 weeks’ postoperative radiotherapy. The need for radiotherapy in breast conservation is still debated. Some subgroups of patients may be expected to have a low risk of local recurrence, and radiotherapy could therefore be avoided. Attempts have been made to identify these populations, which might include individuals with small, low-grade tumors that are estrogenrecept-or-positive, or elderly patients resected with wide tumor-free margins, but no subgroup has been identified that would be adequately treated by breast-conserving surgery alone.

Radiotherapy is used on the whole breast. Some data support the effectiveness of an additional dose applied to the tumor bed (i.e., boost irradiation) to reduce local recurrence. The EORTC study results suggest that the patients deemed to receive the greatest absolute benefit from boost doses are those younger than 50 years and at higher risk of local recurrence (large tumor size or positive or small tumor-free margins in the surgical specimen).

Different radiation treatment schedules with rapid fractionation have been used for years in centers in the UK and Canada. Results from a randomized trial support delivery of a reduced total dose in a shortened schedule (42.5 Gy in 16 fractions for 22 days) in patients with lymph-node-negative breast cancer treated by lumpectomy. A short schedule (20 fractions) with concurrent use of the boost dose is currently used at the European Institute of Oncology Milan after quadrantectomy. In patients younger than 48 years who receive an intraoperative boost dose of 12 Gy, a rapid course of external radiotherapy is used (13 fractions of 2.85 Gy each).

Partial Breast Irradiation

The rationale for partial breast irradiation (restricted to the excision site and adjacent tissues) instead of the conventional approach is based on the finding that most recurrences arise near the primary tumor location. Partial breast irradiation can be delivered by different techniques, such as low or high-dose-rate brachytherapy (delivered interstitially or with an intracavitary balloon), conformal external-beam irradiation (including intensity-modulated radiotherapy), and intraoperative radiotherapy.

Intraoperative Radiotherapy

ELIOT (ELectron Intra Operative Therapy) refers to the application of a high dose of radiation during surgical intervention, after removal of the tumor.

ELIOT is currently used in early-stage breast cancer as the only treatment at the European Institute of Oncology, and a prospective randomized trial is ongoing. Two miniaturized mobile-linear accelerators producing a variable range of electron energies are available. Apart from low costs, ELIOT is advantageous because it potentially overcomes problems related to the accessibility of radiotherapy centers after surgery and has a beneficial impact on the patient’s quality of life. ELIOT does not irradiate the skin or the other breast, and irradiation to the lung and the heart is greatly reduced. ELIOT can also be used to give boost doses: One boost of 10–15Gy in an intraoperative session will extend surgery by just 10–20 min and reduces the time for external treatment by 2 weeks. The TARGIT (TARGeted Intraoperative radio-Therapy) trial is based on the use of a low-energy radiography source to compare one fraction of radiotherapy with a conventional postoperative approach.

Radiotherapy For Ductal Carcinoma In Situ

The role of radiotherapy in ductal carcinoma in situ (DCIS) managed with conservative treatment has been defined by results from three randomized trials. Addition of radiotherapy reduced the local recurrence rate by about 50%, with no effect on survival, and women with positive margins benefited the most. Despite these positive data, the best management of DCIS is still controversial. In fact, according to an analysis of a database of more than 25 000 patients treated between 1992 and 1999, almost half the women did not undergo postoperative radiotherapy after breast-conserving surgery.

Development In Radiation Techniques

Nowadays, the target volume can be tailored to individuals, which reduces the dose to the lung on the same side as the affected breast, and to the heart, the other breast, and surrounding soft tissue. Intensity-modulated beam arrangement ensures a more homogeneous dose delivery. The increasing use of optic or electronic devices (or both) to monitor organ motion and daily setup variations guarantees the accuracy and safety of the delivery system.

Radiotherapy In Locally Advanced Carcinoma

Breast-conserving surgery followed by radiotherapy can be offered to patients with locally advanced disease who respond to induction chemotherapy. A study of 340 patients given this combined treatment had a total locoregional recurrence rate of only 9% at 5-year follow-up. Breast reconstruction after mastectomy has become a standard procedure, and postmastectomy radiotherapy might represent an obstacle to good aesthetic results because of radiation-related fibrosis. The use of radiotherapy after mastectomy is still controversial.

Radiotherapy Of Metastases

With metastases in the skeleton, short courses of irradiation can palliate symptoms and prevent fractures. Radiotherapy and diphosphonates can improve the efficacy of the treatment. Brain metastases or carcinomatous meningitis can be treated successfully: Radiotherapy after complete surgical resection can substantially improve control. Patients with one brain metastasis who can be treated with more aggressive therapies, including surgery and high-precision radiotherapy, are especially challenging. Stereotactic radiotherapy is also used in other secondary tumor sites such as the liver, lung, and soft tissues.

Systemic Treatment of Breast Cancer

Treatment of locally advanced disease.

The presence of estrogen and progesterone receptors in tumor cells shown by immunohistochemical staining is a good predictor of endocrine-responsiveness. Staining for either receptor indicates a response to endocrine therapies. Chemotherapy is also effective in endocrineresponsive disease, but the chances of more extensive cell killing are lower for these tumors than for tumors that are unresponsive.

The distinction between disease lacking expression of steroid-hormone receptors and disease showing some presence of these receptors is associated with gene-expression profiling and with the clinical course. Recognition of such a distinction will require a fundamental shift away from reporting whether the receptor status is positive or negative, which is current practice in many laboratories, to the quantitative reporting of receptor determinations.

Overexpression of the epithelial growth factor receptor HER2/neu on tumor-cell membranes is a strong predictor for response to trastuzumab (Tripathy et al., 2004). Overexpression of both steroid-hormone receptors and HER2/neu has been postulated as a condition for selective resistance to tamoxifen, but less so to aromatase inhibitors in postmenopausal women, and not to tamoxifen combined with suppression of ovarian endocrine function.

Adjuvant Treatments

Adjuvant systemic therapy is given to attempt eradication of micrometastatic disease, which may still be present in all patients with invasive breast cancer. It aims to reduce relapse and increase survival. Postoperative adjuvant therapies cannot be checked for efficacy except with respect to long-term outcomes in a randomized trial. In contrast, the efficacy of systemic treatment given either before surgery (i.e., primary treatments for operable or locally advanced breast cancer) or for metastases, should enable evaluation of the effect of treatment after short-term treatment.

Adjuvant systemic treatments are usually offered to reduce the risk of relapse. An expected 10-year survival below 90% would justify the use of adjuvant chemotherapy. The major concern about adjuvant cytotoxic treatments is that they are offered to a large proportion of patients who are either cured by local treatments or who might have their small risk of relapse reduced by endocrine drugs alone.

Selection of adjuvant treatments is based on the distinction between endocrine-unresponsive and endocrineresponsive breast cancer.

Patients with endocrine-responsive disease are offered adjuvant systemic therapy based on endocrine treatments. High risk of relapse (with metastatic lymph nodes in the operated axilla or vascular invasion) can justify some chemotherapy being given before endocrine treatment in adjuvant therapy.

Premenopausal women with endocrine-responsive disease are usually offered tamoxifen, with or without suppression of ovarian function. Use of cytotoxic drugs before endocrine therapy is recommended only if the risk of relapse is very high. However, the role of both ovarian function suppression and chemotherapy is still uncertain for many of these patients, and trials are in progress. Aromatase inhibitors, which need ovarian function suppression, represent an additional treatment choice.

Women with endocrine-responsive disease after menopause are usually offered endocrine therapy with tamoxifen and increasingly with aromatase inhibitors. Efficacy in reduction of recurrence and mortality well beyond 5 years’ treatment (carryover effect) is the reason for its standard use. When prescribed, chemotherapy should be given before the start of tamoxifen treatment.

New alternatives for tamoxifen are available to treat postmenopausal women with endocrine-responsive disease after surgery, after 2–3 years of tamoxifen to complete standard duration, or after 5 years to further reduce risk of relapse (especially for patients at high risk of relapse) (Coombes et al., 2004). These alternatives include nonsteroidal (anastrozole and letrozole) and steroidal (exemestane) aromatase inhibitors. The IBCSG (International Breast Cancer Study Group) trial 18–98 or BIG 1–98, which compares tamoxifen and letrozole alone or in the two possible sequences, recently provided data on greatly improved disease-free survival for postmenopausal patients with endocrine-responsive disease who received letrozole compared with those who received tamoxifen.

Neoadjuvant (Primary) Systemic Treatments of Breast Cancer

Systemic primary treatment is usually offered to patients with large primary tumors and aims to reduce tumor size for breast-conserving surgery. With such treatment, physicians can also induce regression of axillary node metastases and obtain knowledge on the responsiveness of the disease to treatment.

Endocrine therapies for patients with endocrineresponsive disease showed an improved outcome for aromatase inhibitors compared with that for tamoxifen.

Endocrine-unresponsive disease and high proliferation rates (e.g., Ki67 expressed in 20% of tumor cells) are important predictors of complete pathological response to six courses of primary chemotherapy. Disease-free survival is substantially longer for patients with endocrineresponsive disease than for patients who do not express steroid-hormone receptors, even though patients with endocrine-unresponsive disease are at least four times more likely to obtain a pathological complete remission after primary chemotherapy (Colleoni et al., 2004).

Anthracyclines and taxanes are usually used for patients with both operable and locally advanced disease (Nowak et al., 2004). Anthracycline-based primary chemotherapy has been reported to yield a large proportion of responses in small-sized tumors with a high proliferation index (Ki67) or grade, and with simultaneous overexpression of HER-2/neu and topoisomerase II, whereas mutation of p53 has been associated with a reduced response rate to chemotherapy. Chemotherapy regimens that do not contain anthracycline (that have vinorelbine, platinum, and fluorouracil) were also reported to be effective, especially for patients with endocrine-unresponsive disease, with or without inflammatory features.

Conclusions

Breast cancer is the most common type of tumor in women in most parts of the world. Although stabilized in Western countries, its incidence is increasing in other continents. Prevention of breast cancer is difficult because the causes are not well known. We know of many risk factors such as nulliparity, late age at first pregnancy, little or no breastfeeding, which, however, are linked to the historic development of human society. On the contrary, a great effort is needed to improve early detection of the tumor. Screening programs among the female population should therefore be implemented. The early discovery of a small breast carcinoma leads to a very high rate of curability and entails very mild types of treatment, with preservation of the body image. Treatments are improving, but a strict interdisciplinary approach is essential. It is conceivable that in all countries specialized centers or units for breast cancer management should be set up.

Bibliography:

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• Cho E, Spiegelman D, Hunter DJ, et al. (2003) Premenopausal fat intake and risk of breast cancer. Journal of the National Cancer Institute 95(14): 1079–1085.
• Colleoni M, Viale G, Zahrieh D, et al. (2004) Chemotherapy is more effective in patients with breast cancer not expressing steroid hormone receptors: A study of preoperative treatment. Clinical Cancer Research 10: 6622–6628.
• Coombes RC, Hall E, Gibson LJ, et al. (2004) Intergroup Exemestane Study. A randomized trial of exemestane after two to three years of tamoxifen therapy in postmenopausal women with primary breast cancer. New England Journal of Medicine 350: 1081–1092.
• Cuzick J, Powles T, Veronesi U, et al. (2003) Overview of main outcomes in breast cancer prevention trials. Lancet 361: 296–300.
• Ferlay J, Bray F, Pisani P, and Parkin DM (2004) Globocan 2002: Cancer Incidence, Mortality and Prevalence Worldwide. IARC CancerBase No. 5, version 2 0. Lyon, France: IARC Press.
• Fisher B, Costantino JP, Wickerham DL, et al. (1998) Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel project p-1study. Journal of the National Cancer Institute 90: 1371–1388.
• Hong WK and Sporn MB (1997) Recent advances in chemoprevention of cancer. Science 278: 1073–1077.
• Nowak AK, Wilcken NR, Stockler MR, Hamilton A, and Ghersi D (2004) Systematic review of taxane-containing versus non-taxane containing regimens for adjuvant and neoadjuvant treatment of early breast cancer. Lancet Oncology 5: 372–380.
• O’Shaughnessy JA, Ljung BM, Dooley WC, et al. (2002) Ductal lavage and the clinical management of women at high risk for breast carcinoma: A commentary. Cancer 94: 292–298.
• Tavassoli FA and Devilee P (eds.) (2003) World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of the Breast and Female Genital Tract. Lyon, France: IARC Press.
• Tripathy D, Slamon DJ, Cobleigh M, et al. (2004) Safety of treatment of metastatic breast cancer with trastuzumab beyond disease progression. Journal of Clinical Oncology 22: 1063–1070.
• Veronesi U, Paganelli G, Viale G, et al. (2003) A randomized comparison of sentinel-node biopsy with routine axillary dissection in breast cancer. New England Journal of Medicine 349: 546–553.
• Veronesi U, Boyle P, Goldhirsch A, Orecchia R, and Viale G (2005) Breast cancer. Lancet 365: 1727–1741.
• Veronesi U, Mariani L, Decensi A, et al. (2006) Fifteen-year results of a randomized phase III trial of fenritinide to prevent second breast cancer. Annals of Oncology 17: 1065–1071.

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Essay on Cancer for Students and Children

500+ words essay on cancer.

Cancer might just be one of the most feared and dreaded diseases. Globally, cancer is responsible for the death of nearly 9.5 million people in 2018. It is the second leading cause of death as per the world health organization. As per studies, in India, we see 1300 deaths due to cancer every day. These statistics are truly astonishing and scary. In the recent few decades, the number of cancer has been increasingly on the rise. So let us take a look at the meaning, causes, and types of cancer in this essay on cancer.

Cancer comes in many forms and types. Cancer is the collective name given to the disease where certain cells of the person’s body start dividing continuously, refusing to stop. These extra cells form when none are needed and they spread into the surrounding tissues and can even form malignant tumors. Cells may break away from such tumors and go and form tumors in other places of the patient’s body.

Types of Cancers

As we know, cancer can actually affect any part or organ of the human body. We all have come across various types of cancer – lung, blood, pancreas, stomach, skin, and so many others. Biologically, however, cancer can be divided into five types specifically – carcinoma, sarcoma, melanoma, lymphoma, leukemia.

Among these, carcinomas are the most diagnosed type. These cancers originate in organs or glands such as lungs, stomach, pancreas, breast, etc. Leukemia is the cancer of the blood, and this does not form any tumors. Sarcomas start in the muscles, bones, tissues or other connective tissues of the body. Lymphomas are the cancer of the white blood cells, i.e. the lymphocytes. And finally, melanoma is when cancer arises in the pigment of the skin.

Get the huge list of more than 500 Essay Topics and Ideas

Causes of Cancer

In most cases, we can never attribute the cause of any cancer to one single factor. The main thing that causes cancer is a substance we know as carcinogens. But how these develop or enters a person’s body will depend on many factors. We can divide the main factors into the following types – biological factors, physical factors, and lifestyle-related factors.

Biological factors involve internal factors such as age, gender, genes, hereditary factors, blood type, skin type, etc. Physical factors refer to environmental exposure of any king to say X-rays, gamma rays, etc. Ad finally lifestyle-related factors refer to substances that introduced carcinogens into our body. These include tobacco, UV radiation, alcohol. smoke, etc. Next, in this essay on cancer lets learn about how we can treat cancer.

Treatment of Cancer

Early diagnosis and immediate medical care in cancer are of utmost importance. When diagnosed in the early stages, then the treatment becomes easier and has more chances of success. The three most common treatment plans are either surgery, radiation therapy or chemotherapy.

If there is a benign tumor, then surgery is performed to remove the mass from the body, hence removing cancer from the body. In radiation therapy, we use radiation (rays) to specially target and kill the cancer cells. Chemotherapy is similar, where we inject the patient with drugs that target and kill the cancer cells. All treatment plans, however, have various side-effects. And aftercare is one of the most important aspects of cancer treatment.

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The 15 Best Argumentative Essay Topics About Breast Cancer

What is argumentative essay.

Before beginning with the details one must be quite clarified with the type and formats of writing. If you are not aware of that then you can never come up with a nice essay even having a great knowledge about the topic. Each format of essay has its own beauty and one must know how to observe that beauty and come up with a great description. There are several formats of essays like compare and contrast, persuasive, definition, argumentative etc. All these have their own technique and quality of writing. You should not mix up.

The argumentative format of writing is the one where the author has to have a stern writing technique. Without a strong and persuasive approach one can never incept anything in the mind of the reader. The ways of persuasion should be extremely strong and you should have a biased opinion about what you think and that is the only right thing. You have to make people understand that.

15 best argumentative essay topics about breast cancer

• Breast cancer should be considered as the new epidemic for the modern era.
• Are women becoming too casual about the growing rates of breast cancer?
• Is the society becoming too casual about the approach to take strict action for curing breast cancer?
• Curing breast cancer might lead to loosing of breast- is that a taboo?
• There should be a convention on breast cancer in WHO every month to reduce the growing risk.
• The third world countries are the most affected in breast cancer diseases due to lack of knowledge about the disease.
• There should be classes of how to reduce the risk of breast cancer in the society.
• Detecting breast cancer with the help of machines like MRI increases the rate of Mastectomy- do you believe in the notion?
• There should be many local breast cancer hot spot s that people could go and have check-ups often.
• Breast cancer is due to the susceptibility of the genes BRCA1 and BRCA 2.
• Breast cancer is curable and is a form of malignant tumour- should this be the new notion of the era.
• Women are still ashamed of having breast cancer- How to avoid it?
• Representation of breast cancer in to the society should be done in a much simpler way so that everyone can understand.
• Educate people about men breast cancer.
• Breast cancer should be treated with extra care and what are the measures taken by government about it?

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• Open access
• Published: 16 May 2024

d -arabinose induces cell cycle arrest by promoting autophagy via p38 MAPK signaling pathway in breast cancer

• Zhenning Tang 1 ,
• Hanying Song 2 ,
• Shaojie Qin 1 ,
• Zengjian Tian 2 ,
• Chaolin Zhang 1 ,
• Yang Zhou 2 ,
• Ruizhi Cai 2 &
• Yongzhao Zhu 3  

Scientific Reports volume  14 , Article number:  11219 ( 2024 ) Cite this article

103 Accesses

Metrics details

• Breast cancer
• Medical research

Breast cancer patients often have a poor prognosis largely due to lack of effective targeted therapy. It is now well established that monosaccharide enhances growth retardation and chemotherapy sensitivity in tumor cells. We investigated whether d -arabinose has capability to restrict the proliferation of tumor cells and its mechanism. Here, we report that d -arabinose induced cytotoxicity is modulated by autophagy and p38 MAPK signaling pathway in breast cancer cell lines. The proliferation of cells was evaluated by CCK-8 and Colony formation assay. The distribution of cells in cell cycle phases was analyzed by flow cytometry. Cell cycle, autophagy and MAPK signaling related proteins were detected by western blotting. Mouse xenograft model was used to evaluate the efficacy of d -arabinose in vivo. The proliferation of cells was dramatically inhibited by d -arabinose exposure in a dose-dependent manner, which was relevant to cell cycle arrest, as demonstrated by G2/M cell cycle restriction and ectopic expression of cell cycle related proteins. Mechanistically, we further identified that d -arabinose is positively associated with autophagy and the activation of the p38 MAPK signaling in breast cancer. In contrast, 3-Ma or SB203580, the inhibitor of autophagy or p38 MAPK, reversed the efficacy of d -arabinose. Additionally, d -arabinose in vivo treatment could significantly inhibit xenograft growth of breast cancer cells. Our findings were the first to reveal that d -arabinose triggered cell cycle arrest by inducing autophagy through the activation of p38 MAPK signaling pathway in breast cancer cells.

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Introduction.

Breast cancer is among the top-ranked malignancies in women, with characteristics including high incidence, heterogeneity, morbidity, mortality, and recurrence rate, as well as poor prognosis, which severely threatens human health 1 . Although adjuvant chemotherapy, targeted therapy, immunotherapy, and non-selective chemotherapy remain the cornerstones of treatment for breast cancer, they confer few benefits for patients with advanced stage disease 2 , 3 , 4 . Therefore, there is an urgent requirement to find additional or alternative drugs to improve therapeutic outcomes for patients with breast cancer.

Recently, regulatory relationships between monosaccharides and cancer cells have been established 5 , 6 . And some studies have indicated that d -arabinose can inhibit the biological growth. For instance, d -arabinose can suppress the formation of biofilms originating from single or consortia bacteria on titanium discs by inhibiting the activity of the quorum sensing molecule, autoinducer 2 7 . Furthermore, Caenorhabditis elegans growth is markedly inhibited by d -arabinose in a concentration dependent manner 8 . More importantly, Tanaka-Okamoto and colleagues found elevated levels of d -arabinose-containing free-glycans in the urine of cancer patients, indicating that d -arabinose may play a pivotal role in cancer development. Nonetheless, the regulatory functions and mechanism of d -arabinose influence the characteristic of cancer cells remain need to be elucidated.

Autophagy is an evolutionarily conserved catabolic process that parcels cytoplasmic proteins and damaged or senescent organelles into vesicles, which eventually fuse with lysosomes to form autophagy lysosomes for further degradation 9 . An increasing body of evidence has established the complex regulatory relationship between autophagy and cell cycle arrest in various cancer types 10 , 11 . However, whether d -arabinose impaired growth by regulating cell cycle via induction of autophagy in breast cancer has not been studied.

In the present study, we demonstrated that breast cancer cell proliferation is sensitive to d -arabinose exposure, which induced cell cycle arrest. This phenomenon could be attributed to growth retardation mediated by induction of autophagy. Inhibition of autophagy counteracted the suppressive effect of d -arabinose on breast cancer cells. Furthermore, we found that activation of p38 signaling is responsible for the induction of autophagy by d -arabinose in breast cancer cells.

Materials and methods

Cell culture.

The MCF-7, MDA-MB-231 and MCF10A cell lines were purchased from Procell (Procell, Wuhan, China), and were originally obtained from American Type Culture Collection. All cell lines were cultured in special culture medium purchased from Procell. Special medium for MDA-MB-231 (Procell, CM-0150A): Leibovitz's L-15(PM151010) + 10% FBS (164210-50) + 1% P/S(PB180120). Special medium for MCF-7 (Procell, CM-0149): MEM (contain NEAA)(PM150410) + 10 μg/mL Insulin(PB180432) + 10% FBS(164210-50) + 1% P/S(PB180120). Special medium for MCF-10A(Procell, CM-0525): DMEM/F12(PM150312) + 5% HS(164215) + 20 ng/mL EGF + 0.5μg/mL Hydrocortisone + 10 μg/mL Insulin(PB180432) + 1% NEAA(PB180424) + 1% P/S(PB180120). Cells were maintained as monolayer cultures in a humidified atmosphere of 5% CO 2 at 37 °C. When cultured cells reached 90% confluence, they were passaged after detachment using Recombinant Trypsin EDTA Solution (Biological Industries, Israel). All cell lines used were confirmed to be free of mycoplasma, and used for experiments when they entered an exponential growth stage.

Assessment of cell viability and proliferation

MCF-7, MDA-MB-231 and MCF10A cells were seeded in triplicate in 96-well plates (1000 cells per well). After 24 h of adhesion culture, cells were treated with d -arabinose (Solarbio, SA8380) at different concentration. After 72 h incubation with different concentrations of d -arabinose, 10 μL CCK8 solution (AR1160, Boster, China) was added to each well and incubated for 1–4 h. Absorbance of each well was measured at 450nm using a microplate reader. The percentage of viable cells was determined for each well using the following equation: Percentage cell viability = (OD sample − OD blank)/(OD control − OD blank) × 100%.

Colony formation assay

MCF-7 and MDA-MB-231 cells were seeded in 6-well plates at 2000 cells per well. After incubation overnight, cells were treated with various concentration of d -arabinose for a further 2 weeks. Then, plates were washed three times with cold PBS, fixed with 4% paraformaldehyde at room temperature for 15min, and stained with 0.1% crystal violet for 20min. After washing with distilled water until the background became clear, images were photographed using a digital camera. Numbers of colonies in each well were quantified by microscopy.

Cell cycle analysis

Adherent breast cancer cells were exposed to 50 mM d -arabinose for 24 h. Cells were then suspended using 0.25% trypsin–EDTA and washed with ice-cold PBS. Then, control and treated group cells were fixed in chilled 75% ethyl alcohol for 1 h at 4 °C before being transferred to − 20 °C until they were required for analysis. After washing three times with PBS, cells were suspended in 0.1 mg/mL propidium iodide at 37 °C for 30 min in the dark. The distribution of cells in cell cycle phases was assessed by flow cytometry, and the number of cells at each event, namely, G0/G1, S, and G2/M phases, determined in control and d -arabinose-treated cells.

Western blot assays

Cells or tissue derived from tumor-bearing mice were washed three times with cold PBS and lysed in cold RIPA buffer supplemented with protease inhibitor cocktail (Thermo Fisher Scientific, USA). Lysates were centrifuged at 12,000× g at 4 °C for 5 min, and isolated protein samples mixed with loading buffer and boiled at 100 °C for 5 min. Total protein concentrations were measured using a bicinchoninic acid protein assay kit (Beyotime, Jiangsu, China). Equivalent amounts of protein samples were separated by SDS-PAGE and transferred to PVDF membranes (Millipore, Sigma, USA). After blocking with 5% skimmed milk, membranes were probed with the following antibodies: Cyclin B1 (1:1000,cat:383324, Zenbio), p21 (1:1000, cat:10355-1-AP, Proteintech), p27 (1:1000, cat:25614-1-AP, Proteintech), Atg5(1:1000, cat:10181-2-AP, Proteintech), LC3-I/II (1:500, cat:14600-1-AP, Proteintech), ERK1/2 (1:1000, cat:PTM-5850, Ptmbio), p-ERK1/2 (1:1000, cat:PTM-7155, Ptmbio), p38(1:1000, cat:WL00764, Wanleibio), p-p38 (1:1000, cat:WLP1576, Wanleibio), JNK (1:1000, cat:17572-1-AP, Proteintech), p-JNK (1:1000, cat:80024-1-RR, Proteintech), and β-Tubulin (1:1000, cat:K200059M, Solarbio). After incubation with corresponding horseradish peroxidase-conjugated secondary antibodies for 1 h at room temperature and extensive washes with TBST, immunoreactive proteins were visualized using enhanced chemiluminescence detection reagents (Sigma). Finally, images of the membranes were captured using a gel imaging system, analyzed with Image J 1.4.3 software (Bethesda, MD, USA), and normalized to β-Tubulin levels, followed by calculations of relative ratios to controls.

Lentivirus construction and infection

Lentiviruses expressing short hairpin RNA (shRNA) specific for Atg5 were designed and synthesized by Hanbio Tech (Shanghai, China). Target nucleotide sequences were as follows: Atg5-shRNA, 5′-CCTGAACAGAATCATCCTTAA-3′ (sh-Atg5); scrambled control-shRNA, 5′-CCTAAGGTTAAGTCGCCCTCG-3′ (sh-NC). A lentivirus multiplicity of infection (MOI) of 20 was used for infection of MCF-7 and MDA-MB-231 cells.

Autophagy flux analysis

Cells plated on coverslips in 24-well plates were infected with adenoviral vector expressing mRFP-GFP-LC3 (Hanbio Tech, Shanghai, China) at a MOI of 20 for 24 h. After d -arabinose treatment, cells were fixed with 4% ice-cold paraformaldehyde (Beyotime, Jiangsu, China) for 10 min, embedded in fluorescent mounting medium with DAPI (4,6-diamidino-2-phenylindole), and autophagic flux analyzed by assessing the number of GFP and mRFP puncta visible under confocal microscopy (TCS SP5, Leica Microsystems, Wetzlar, Germany).

Mouse xenograft model

Four-week-old BALB/c female nude mice were purchased from Charles River (Beijing, China). All animals were acclimated under standard laboratory conditions (ventilated room, 25 °C ± 1 °C, 60% ± 5% humidity, 12 h light/dark cycle) and had free access to standard water and food. All animal experiments conducted for this study were approved by the Laboratory Animal Ethics and Welfare Committee of the Laboratory Animal Center of Ningxia Medical University (IACU-NYLAC-2021-035). Mice were adapted to the breeding environment for three days before the experiment. A total of 2 × 10 6 MDA-MB-231 cells were suspended in 100 μL PBS with Matrigel and injected into the breast fat pads of nude mice, then tumor growth observed. And 10 nude mice with successful tumor formation were ultimately selected for subsequent experiments. When tumors were visible to the naked eye, tumor-bearing mice were randomly divided into two groups (control and experimental) of 5 mice each. An aqueous solution containing 50% (w/v) d -arabinose was administered to mice by gavage 200 μL/every day. Tumor volume was measured twice per week using vernier calipers, and the tumor volume calculated according to the formula: Volume = (Length × (Width)2)/2. Mouse activity, weight, food and water intake, and other basic indicators were observed. After 4 weeks, all mice were anesthetised with 4% isoflurane and sacrificed by cervical dislocation, the tumors were collected, weighed, and photographed. Then, tumor tissues were divided into two parts: one of which was stored in liquid nitrogen for total protein extraction and the other fixed in 4% paraformaldehyde for subsequent pathological examination. All methods were performed in accordance with the relevant guideline and regulations. The animal study is reported in accordance with ARRIVE guidelines.

Histopathology and Immunohistochemistry

Mouse tissue samples were fixed in paraformaldehyde and embedded in paraffin. Tumor specimens were stained with hematoxylin and eosin after cutting into 5 µm sections. For immunohistochemistry assays, slides were incubated with Ki67 after blocking with 5% BSA. The next day, samples were incubated with secondary antibodies at 37 °C for 1 h, followed by treatment with DAB chromogen. Images were visualized using an Olympus microscope (Olympus Corporation, Japan).

Statistical analysis

Results are presented as the mean ± standard error of the mean (SEM). Data normality was first tested with Kolmogorov Smirnov test. As the data was normal, using one-way analysis of variance with post hoc Bonferroni correction. The statistical significancy was set at 0.05. All data were analyzed using GraphPad Prism 8.0.1. (GraphPad, La Jolla, CA, USA).

Ethics approval

All procedures were approved by the Laboratory Animal Ethics and Welfare Committee of the Laboratory Animal Center of Ningxia Medical University (IACU-NYLAC-2021-035).

The study is reported in accordance with ARRIVE guidelines.

d -Arabinose inhibits breast cancer cell growth in vitro

Cancer cell growth can be restricted by treatment with natural products 12 , 13 . To evaluate the role of d -arabinose in regulating the growth of breast cancer cells or normal breast cells growth, MCF-10A, MCF-7 and MDA-MB-231 cell lines were grown in complete culture medium containing different concentrations of d -arabinose. MCF-7 and MDA-MB-231 cell proliferation was significantly and dose-dependently suppressed by d -arabinose treatment, however, MCF-10A exhibited more tolerance than MCF-7 and MDA-MB-231 in d -arabinose condition (Fig.  1 A). In addition, the suppressive efficacy of d -arabinose on breast cancer cells was further confirmed by the formation of adhesive cell colonies in treated cells (Fig.  1 B). These results indicate that d -arabinose can restrict breast cancer cell proliferation in vitro.

d -Arabinose suppresses breast cancer cell proliferation and colony formation in vitro. ( A ) MCF10A, MCF-7, and MDA-MB-231cells were seeded onto 96-well plates at 1.0 × 10 3 per well, treated with different concentrations of d -arabinose, after 72 h cell viability measured by CCK8 assay. ( B ) MCF-7 and MDA-MB-231 cells were seeded in 6-well plates at 1.0 × 10 3 cells per well and colony numbers counted under a dissection microscope after d -arabinose treatment for 2 weeks. Results are mean values ± SEM of three independent experiments; * P  < 0.05, ** P  < 0.01.

d -arabinose arrests the breast cancer cell cycle in the G2/M phase

To investigate the anti-cancer activity of d -arabinose, we assessed changes in the distribution of the breast cancer cell cycle and the expression of critical checkpoint regulators. Following d -arabinose stimulation, flow cytometry analysis showed that MCF-7 and MDA-MB-231 cells accumulated in the G2/M phase, with no influence on the number of cells in G1 phase (Fig.  2 A,B). Further, after treatment of MCF-7 and MDA-MB-231 cells with d -arabinose at 20, 50, and 100 mM, the expression of Cyclin B1, p21, and p27 were evaluated by western blot, revealing reduced expression of Cyclin B1 in d -arabinose-treated MCF-7 and MDA-MB-231 cells, while levels of p21 and p27 were elevated (Fig.  2 C, p < 0.01). These data indicate that d -arabinose inhibits BC cell growth by blocking cell cycle progression at the G2/M phase.

d -Arabinose induces breast cancer cell cycle arrest. ( A , B ) Breast cancer cells (MCF-7 and MDA-MB-231) were treated with d -arabinose (50 mM) for 24 h. Control and treated cells were harvested, stained with 0.05% propidium iodide, and subjected to flow cytometric analysis. ( C ) MCF-7 and MDA-MB-231 cells were stimulated with different doses of d -arabinose (0, 20, 50, and 100 mM) for 24 h, and the expression of Cyclin B1, p21, and p27 detected by western blot. Representative data from three separate experiments are shown. * # P  < 0.05, ** ## P  < 0.01.

d -Arabinose induces autophagy in breast cancer cells

In cancer cells, cell cycle phase of is closely regulated by autophagy in different contexts 14 , 15 . To assess whether autophagy is triggered by d -arabinose, autophagy activation of breast cancer cells cultured with d -arabinose was assessed at different time points. d -arabinose treatment resulted in prominent elevation of LC3-II in MDA-MB-231 and MCF-7 cells with the most significant augmentation observed at 8 h (Fig.  3 A, p < 0.01). Moreover, mRFP-GFP-LC3 adenovirus was applied and the formation of autophagosomes observed by fluorescence microscope. The results demonstrated that d -arabinose increased the number of cytoplasmic autophagosomes (Fig.  3 B). To further evaluate autophagic flux during d -arabinose treatment, the autophagy inhibitor, chloroquine (CQ), was used to arrest autophagy flux in MDA-MB-231 and MCF-7 cells. Following treatment with d -arabinose, the expression of Atg5 significantly increased. And after treatment with CQ, p62 and LC3-II induction was further enhanced in MDA-MB-231 and MCF-7 cells (Fig.  3 C, p < 0.01). Furthermore, we observed an increase in the number of cytoplasmic autophagosomes after treatment with d -arabinose using transmission electron microscopy (Fig.  3 D). These findings suggest that exposure of breast cancers to d -arabinose can indeed mediate autophagy.

Autophagy was induced by d -arabinose in breast cancer cells. ( A ) MDA-MB-231 and MCF-7 were stimulated with d -arabinose (50 mM) and LC3-II expression detected by western-blot at different time points. ( B ) After infection with mRFP-GFP-LC3 overexpression adenovirus, MCF-7 and MDA-MB-231 cells on slides were treated with d -arabinose (50 mM) for 8 h, then analyzed by confocal microscopy. LC3-II puncta-positive cells in five images from each group were counted. Scale bar = 50 μm ( C ) MCF-7 and MDA-MB-231 cells were treated with or without chloroquine (CQ) before exposure to d -arabinose (50 mM). Expression levels of Atg5, p62 and LC3-II were analyzed by western blot. ( D ) Transmit electron microscopy was used to observe autophagosomes in MDA-MB-231 and MCF-7 cells treated with or without d -arabinose (50 nM, 8 h). Autophagic vacuoles are indicated by red arrows. Scale bar = 1μm Representative data from three separate experiments are shown. AV autophagic vacuoles. * # P  < 0.05, ** ## P  < 0.01.

d -arabinose regulated cell cycle arrest via the autophagic pathway

To determine whether the effect of d -arabinose on cell cycle arrest was triggered by autophagy, lentivirus expressing shRNA specific for Atg5 (sh-Atg5) was used to inhibit MDA-MB-231 and MCF-7 cells autophagy, and the expression proteins associated with the cell cycle measured in presence or absence of d -arabinose. The control group comprised MDA-MB-231 and MCF-7 cells infected with lentivirus expressing scrambled shRNA (sh-NC). Atg5 knockdown significantly inhibited autophagy induced by exposure to d -arabinose, as illustrated by decreased Atg5 expression compared with sh-NC-treated controls (Fig.  4 A, p < 0.01). Further, the results indicate that Atg5 knockdown in MDA-MB-231 and MCF-7 cells treated with d -arabinose remarkably increased the expression of Cyclin B1, while it suppressed the expression of p21 and p27 compared with sh-NC treated cells (Fig.  4 B, p < 0.01). These findings provide solid evidence that cell cycle arrest in response to d -arabinose treatment is mediated by autophagy of breast cancer cells, while inhibition of autophagy counteracted the suppressive effect of d -arabinose.

Effects of autophagy induced by d -arabinose on cell cycle arrest in breast cancer cells. ( A ) MCF-7 and MDA-MB-231 cells were infected with control lentivirus (sh-NC) or lentivirus-expressing shRNA targeting Atg5 (sh-Atg5), and treated with or without d -arabinose (50 mM). Expression of Atg5 was analyzed by western blot. ( B ) Western blot analysis to measure the protein expression levels of Cyclin B1, p21, and p27 in sh-Atg5 lentivirus-infected MDA-MB-231 and MCF-7 cells after treatment with d -arabinose. Representative data from three separate experiments are shown. * # P  < 0.05, ** ## P  < 0.01.

Inhibition of autophagy interrupts cell cycle arrest by p38 MAPK pathway

Next, we investigated the mechanisms underlying cell cycle arrest via autophagy following d -arabinose treatment of breast cancer cells. The MAPK signaling pathway contributes to regulation of autophagy induced by various stress conditions, resulting in modulation of cellular functions 16 , 17 . As expected, we observed that levels of phosphorylated p38 (p-p38) were significantly increased on exposure of both MDA-MB-231 and MCF-7 cells to different concentrations of d -arabinose; however, the trend in changes to phosphorylated JNK (p-JNK) and ERK1/2 (p-ERK1/2) expression was not consistent between MDA-MB-231 and MCF-7 cells (Fig.  5 A, p < 0.01). Furthermore, the p38 MAPK inhibitor, SB203580, suppressed autophagy mediated by d -arabinose by down-regulating LC3-II expression, which enhanced the expression levels of Cyclin B1, but reduced those of p21 and p27 (Fig.  5 B, p < 0.01). Together, these results demonstrated that d -arabinose induced autophagy lead to cell cycle arrest through activation of the p38 MAPK signaling pathway in breast cancer cells.

d -Arabinose induces cell cycle arrest via autophagy-dependent p38 MAPK signaling in breast cancer cells. ( A ) Breast cancer cells (MCF-7 and MDA-MB-231) were conditioned with or without various concentration of d -arabinose (0, 20, 50, and 100 mM), total cell proteins harvested, and expression levels of JNK, ERK1/2, p38, and their phosphorylated forms measured by western blot. ( B ) MDA-MB-231 and MCF-7 cells were treated with the p38 MAPK inhibitor, SB203580 (10 μM), for 2 h prior to d -arabinose (50 mM, 24 h) treatment, and expression levels of p-p38, Atg5, LC3-II, Cyclin B1, p21, and p27 assessed by western blot. Representative data from three separate experiments are shown. * # P  < 0.05, ** ## P  < 0.01.

d -arabinose represses breast tumor growth in vivo

In order to explore the function of d -arabinose in tumor formation, a tumor xenograft model was generated by subcutaneous injection of MDA-MB-231 cells into the fat pads of female BALB/c nude mice. One week after cell injection, tumors were treated with d -arabinose (2.5 g/kg/day) via gavage for a further 20 days. The results showed that d -arabinose reduced tumor size (Fig.  6 A, p < 0.01), without prominently influencing mouse weight (Fig.  6 B). Hematoxylin–eosin staining revealed that tumors had a loose structure, with increased inflammatory cell infiltration in tumor tissues treated with d -arabinose (Fig.  6 C). Further, Ki-67 expression was lower in tumors from d -arabinose treated mice than in those from controls (Fig.  6 C, p < 0.01). Subsequently, we examined the expression of p-p38, Atg5 and LC3-II in the extracted animal samples and found elevated levels of both proteins(Fig.  6 D, p < 0.01). Together, these results suggested that d -arabinose can induce autophagy by activating the p38 signaling pathway in vivo, ultimately inhibiting the progression of breast cancer.

d -Arabinose remarkably decreases the growth of breast cancer xenograft tumors. Nude mice were inoculated with 2 × 10 6 human MDA-MB-231 cells each. One week after cell injection, mice in the treatment group were administered 2.5 g/kg d -arabinose by gavage every day for 4 weeks; control mice received the same volume of solvent. ( A ) Images of tumor masses from each group. Changes in tumor volume and weight after d -arabinose treatment were quantified in each group. ( B ) Nude mice body weight during d -arabinose treatment. ( C ) Tumor tissue sections stained with hematoxylin–eosin and for Ki67 by immunohistochemistry. ( D ) Western blot was performed to detect the expression of p-p38, Atg5 and LC3 in animal samples. All data are presented as mean ± SD. * P  < 0.05, ** P  < 0.01, NS not significant.

Treatment of breast cancer remains challenging, due to poor responses, drug resistance, and intolerance in a significant proportion of patients. Hence, there is an urgent need to explore new drugs or therapeutic targets to achieve improvements in clinical efficacy 18 , 19 , 20 . Recently, monosaccharides derived from natural products have been the subject of increasing attention for use in prevention and treatment for various types of cancer 21 . d -arabinose is unlike other monosaccharides, as humans cannot derive it naturally from food. Although d -arabinose contributes to the regulation of various biological activities, such as metabolism and cell proliferation, there was previously no direct evidence suggesting that d -arabinose has anti-cancer effects by inhibiting tumor cell growth 22 , 23 . In present study, we found that d -arabinose could significantly restrict the proliferation of breast cancer cells in vivo and in vitro. Similar inhibitory efficacy of d -arabinose has previously been observed in another eukaryote, Caenorhabditis elegans 8 . More importantly, normal breast cells present more resistance than cancer cells under d -arabinose stimulation, imply that d -arabinose is adapt to clinical application. Collectively, these results represent the first demonstration that d -arabinose has significant anti-cancer activity against breast cancer cells. In clinical applications, d -arabinose is expected to exhibit efficacy and safety, even in combination with chemotherapeutic drugs, due to its compatibility with human physiology.

Aberrant cell cycle progression is an important feature in limiting the proliferation of tumor cells, and therapy targeting cell cycle progression is considered a promising anti-cancer strategy 24 , 25 . The regulatory relationships among cyclins, cyclin-dependent kinases (CDKs), CDK inhibitors (CKIs), and the eukaryotic cell division cycle are established 26 . The Cdc2-cyclin B complex, also known as M-phase promoting factor, is responsible for cell cycle phase transition and mitotic entry, and inhibition of its activity arrests the cell cycle at G2 phase 27 . p21 and p27 belong to the Cip/Kip family of cyclin-dependent kinase CKIs, which inhibit the CDK-cyclin activity and restrain cell cycle progression 28 . In this study, flow cytometry analysis indicated that d -arabinose arrests breast cancer cells at G2/M phase. Further, we assessed the expression of proteins associated with G2/M phase, and confirmed that d -arabinose can elevate the expression of p21 and p27, and down-regulated that of Cyclin B1. High expression of Cyclin B1 and low levels of p21/p27 are frequently detected in various types of cancer and associated with cancer development and poor prognosis 29 , 30 , 31 . Together, these results illustrate that d -arabinose has a pivotal role in modulation of cell cycle progression by regulating the activity of Cyclin B1, p21, and p27 in breast cancer cells.

Autophagy is a ubiquitous, highly conserved, self-protective mechanism through which damaged organelles, misfolded proteins, and invading pathogens are sequestered within vesicles and delivered to lysosomes for degradation or recycling, thus maintaining intracellular environmental homeostatic stability in eukaryotic cells 32 . The role of autophagy in d -arabinose regulated cell cycle arrest has not been reported previously; therefore, this is the first study to assess whether autophagy can be attributed to cell cycle arrest mediated by d -arabinose in breast cancer cells. LC3-II, derived from cleaved LC3-I, is a pivotal element of autophagy, which represents the progress of autophagy and the number of autophagosomes, in certain contexts 33 . In this study, our results indicate that levels of LC3-II increased in a time-dependent manner following d -arabinose exposure. Further, autophagosome formation was confirmed, based on the number of puncta in the cytoplasm. Furthermore, we assessed autophagy flux using autophagy inhibitors. As a late autophagy inhibitor CQ blocks the fusion of autophagosomes and lysosomes, leading to accumulation of large numbers of autophagosomes and augmented levels of LC3-II and p62 34 . Our data show that CQ treatment dramatically increased LC3-II and p62 levels induced by d -arabinose compared with the control group. These results clarify that d -arabinose can induce breast cancer cell autophagy. In addition, there is ample evidence demonstrating that various cell cycle regulators contribute to modulation of autophagic processes. For example, constitutive expression and accumulation of p21 and p27 arrest the cell cycle at G0/S phase by inducing autophagy in non-small cell lung cancer and head and neck squamous cancer cells 35 , 36 . The results of the present study show that autophagy initiated by d -arabinose is accompanied by down-regulation of Cyclin B1 and up-regulation of p21 and p27, suggesting that d -arabinose may modulate autophagy via cell cycle regulators in breast cancer cells. Intriguingly, a previous study clarified that autophagy plays a pivotal role in regulating cell cycle arrest of proximal epithelial cells, and that enhanced expression of Atg5 could suppress renal fibrosis by rescuing G2/M arrest 37 . In contrast, Qiang Ma et al. found that autophagy deficiency induced by dihydroartemisinin blocked cell cycle arrest at the G2/M phase in esophageal cancer cells 15 . Nevertheless, whether or not autophagy contributes to cell cycle progression of breast cancer cells treated with d -arabinose as an upstream regulator has yet to be confirmed. In this study, inhibition of autophagy by specific downregulation of Atg5 using a lentivirus expressing a targeted shRNA, interrupted breast cancer cell cycle arrest in response to d -arabinose treatment, observed as increased expression of Cyclin B1, as well as reduced levels of p21 and p27 and enhanced cell proliferation potential. These results suggest that autophagy contributes to modulation of cell cycle regulators, and determines the cell cycle progression of breast cancer cells treated with d -arabinose. Collectively, our data reveal that d -arabinose can induce cell cycle arrest at the G2/M phase in an autophagy-dependent manner, indicating that enhancement of autophagy may strengthen its anti-breast cancer efficacy.

JNK, ERK1/2, and p38 MAPK are members of the MAPK signaling pathway, which plays a pivotal role in regulation of cell growth, differentiation, senescence, and stress responses under various extracellular stimuli, via modulating the activity of downstream transcription factors 38 , 39 . MAPK family members are established as involved in regulation of autophagy and cell cycle arrest 40 , 41 . To explore the mechanism by which d -arabinose regulates autophagy and the cell cycle, we investigated MAPK signaling pathway protein expression levels in breast cancer cells. We found that d -arabinose treatment significantly increased the expression of p-p38 MAPK in both breast cancer cell lines tested (MCF-7 and MDA-MB-231). Previous studies also confirmed that the p38 MAPK pathway can influence the cell cycle to control breast cancer cell proliferation 42 , 43 . Intriguingly, p-JNK and p-ERK1/2 did not exhibit the same expression tendencies in MCF-7 and MDA-MB-231 cells. This phenomenon may be attributable to differences in molecular classification between these two cell lines: MCF-7 is derived from luminal A type breast cancer, where MDA-MB-231 is a triple-negative breast cancer cell line. Furthermore, we observed that the p38 MAPK inhibitor, SB203580, synergistically reversed the expression of autophagy and cell cycle arrest associated proteins, suggesting that p38 MAPK signaling contributes to d -arabinose-mediated autophagy and cell cycle arrest in breast cancer cells.

Conclusions

In summary, the results of the present study demonstrate that d -arabinose has potent anti-tumor efficacy against breast cancer, which may be attributable to induction of cell cycle arrest at G2/M phase and autophagy. Moreover, we found that the anti-tumor potential of d -arabinose is closely associated with p38 signaling pathway activation, regulating the cell cycle and autophagy processes in breast cancer cells. These results provide solid evidence supporting the potential of d -arabinose as a novel breast cancer treatment.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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This work was supported by grants from the Ningxia Natural Science Foundation Project (2020AAC03418, 2023AAC02072), Project of Ningxia Medical University (XZ20200020), and the Key Project of Research and Development of Ningxia Hui Autonomous Region of China (2021BEG03060).

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Department of Oncology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, People’s Republic of China

Zhenning Tang, Shaojie Qin & Chaolin Zhang

School of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, People’s Republic of China

Hanying Song, Zengjian Tian, Yang Zhou & Ruizhi Cai

Institute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, 750004, People’s Republic of China

Yongzhao Zhu

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Z.T. contributed the original draft preparation. H.S. provides the conceptualization. S.Q., Z.T., C.Z. and R.C. contributed to the interpretation of the data. Y.Z. reviewed and edited the article.Z.T. provided the methodology. Z.T. and Y.Z. provided funding for the project. H.S. supervised work and wrote manuscripts. All the authors have contributed to the paper and have reviewed the manuscript and agree with its contents.

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Tang, Z., Song, H., Qin, S. et al. d -arabinose induces cell cycle arrest by promoting autophagy via p38 MAPK signaling pathway in breast cancer. Sci Rep 14 , 11219 (2024). https://doi.org/10.1038/s41598-024-61309-7

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DOI : https://doi.org/10.1038/s41598-024-61309-7

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Preserving breast tissue outside of body will aid cancer research – study

Experts say they have paved the way for the development of new drugs to treat and prevent breast cancer.

Researchers say they have managed to keep breast cancer tissue viable for at least a week outside of the human body, paving the way for enhanced cancer treatments.

A new study, funded by the Prevent Breast Cancer charity, found breast tissue could be preserved in a special gel solution, enabling scientists to examine it in great detail.

Experts found the preserved breast tissue maintained its structure, cell types and ability to respond to a series of drugs in the same way as normal breast tissue.

The study, published in the Journal of Mammary Gland Biology and Neoplasia, could boost the development of new drugs to treat and prevent breast cancer, without the need for testing on animals.

Lester Barr, consultant breast surgeon and founder of Prevent Breast Cancer, said: “Breast cancer mortality is decreasing in the UK thanks to improved screening and treatment options, but incidences continue to rise and breast cancer is the most commonly diagnosed cancer in the UK.

“It’s therefore really important that we develop new prevention and risk-reduction options for women, especially for those with a high risk due to their family history or genetics.

“This breakthrough means that researchers will be able to test new drugs in the lab with far greater accuracy, which should mean fewer drugs failing at clinical trials and ultimately better results for women affected by this terrible disease.

“It’s a hugely exciting development in animal-free research which puts us in a really strong place to find new drugs to prevent breast cancer.”

Researcher Hannah Harrison, from the University of Manchester, said: “There are various risk-reducing options for women at high risk of developing breast cancer – for example, those with a significant family history or who have mutations in the BRCA genes.

“However, not all drugs work for all women. This new approach means that we can start to determine which drugs will work for which women by measuring their impact on living tissue.

“Ultimately, this means that women can take the most effective drug for their particular genetic make up.

“By testing different hydrogel formulas we were able to find a solution that preserves human breast tissue for at least a week and often even longer.

“This is a real game-changer for breast cancer research in many ways.

“We can better test drugs for both the prevention and treatment of cancer, and can examine how factors like breast density – which we know is a risk factor for breast cancer – react to particular hormones or chemicals to see if this has an impact on cancer development.”

Scientists used the gel solution VitroGel to preserve the tissue.

In their work, they said the identification of new drugs has been previously “hampered by a lack of good pre-clinical models”.

What has been available until now cannot “fully recapitulate the complexities of the human tissue, lacking human extracellular matrix, stroma, and immune cells, all of which are known to influence therapy response”, they said.

It comes as Prime Minister Rishi Sunak hailed a new artificial intelligence (AI)-powered medical trial which “promises to improve the accuracy and speed” of breast cancer diagnosis.

A partnership between the NHS and South Korean firm Lunit uses the Korean company’s image-reading AI technology to help human radiologists in the process of analysing and assessing mammograms.

Writing for the i alongside South Korean President Yoon Suk Yeol, Mr Sunak said the trial was an example of how AI can be used to “transform the world for the better”.

The leaders said: “We all know how vital early detection is – so just imagine what improvements here could mean for millions of women and their families.”

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Home — Essay Samples — Nursing & Health — Breast Cancer — Treatment and Diagnosis of Breast Cancer

Treatment and Diagnosis of Breast Cancer

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Published: Dec 18, 2018

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Breast cancer: treatment options, adjuvant therapy, diagnosis of breast cancer, breast cancer treatment options.

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Journal of Materials Chemistry B

Radioactive hybrid semiconducting polymer nanoparticles for imaging-guided tri-modal therapy of breast cancer.

Due to the rapid progression and aggressive metastasis of breast cancer, its diagnosis and treatments remain a great challenge. The simultaneous inhibitions of tumor growth and metastasis are necessary for breast cancer to obtain ideal therapeutic outcomes. We herein report the development of radioactive hybrid semiconducting polymer nanoparticles (SPNH) for imaging-guided tri-modal therapy of breast cancer. Two semiconducting polymers are used to form SPNH with a diameter of around 60 nm via nano-coprecipitation and they are also labeled with iodine-131 (131I) to enhance the imaging functions. The formed SPNH show good radiolabeling stability, excellent photodynamic and photothermal effect under 808 nm laser irradiation to produce singlet oxygen (1O2) and heat. Moreover, SPNH can generate 1O2 with ultrasound irradiation via their sonodynamic property. After tail intravenous injection, SPNH can effectively accumulate into subcutaneous 4T1 tumors of living mice as verified via fluorescence and single photon emission computed tomography (SPECT) imaging. With the irradiation of tumors using 808 nm laser and US, SPNH mediate photodynamic therapy (PDT), photothermal therapy (PTT) and sonodynamic therapy (SDT) to kill tumor cells. Such a tri-modal therapy leads to an improved efficacy in inhibiting tumor growths and suppressing tumor metastasis compared to the sole SDT and combinational PDT-PTT. This study thus demonstrates the applications of SPNH to diagnose tumors and combine different therapies for effective breast cancer treatment.

• This article is part of the themed collections: Journal of Materials Chemistry B HOT Papers and Journal of Materials Chemistry B Emerging Investigators 2024

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J. Gu, D. Cheng, H. Li, T. Yu, Z. Zhang, Y. Liu, X. Wang, X. Lu and J. Li, J. Mater. Chem. B , 2024, Accepted Manuscript , DOI: 10.1039/D4TB00834K

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