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Rethinking life-support decisions

Harvard-led study IDs statin that may block pathway to some cancers

Cholesterol-lowering drug suppresses chronic inflammation that creates dangerous cascade

Tracy Hampton

MGH Communications

Statins, commonly used cholesterol-lowering drugs, may block a pathway that leads to the development of cancer from chronic inflammation, according to a new study led by investigators from Harvard-affiliated  Mass General Cancer Center .

The team’s experiments showed that environmental toxins, such as those caused by exposure to allergens and chemical irritants, create a cascade effect that stimulates inflammation in the skin and pancreas that, when chronic, can result in cancer. Their findings suggest that using statins to suppress this pathway may have a protective effect.

The findings are published in Nature Communications.

In mice, pitavastatin suppressed environmentally induced inflammation in the skin and the pancreas and prevented the development of inflammation-related pancreatic cancers. 

“Chronic inflammation is a major cause of cancer worldwide,” said senior author Shawn Demehri, a principal investigator at the Center for Cancer Immunology and Cutaneous Biology Research Center of Massachusetts General Hospital and an associate professor of dermatology at Harvard Medical School and the Bob and Rita Davis Family MGH Research Scholar 2023-2028 .

“We investigated the mechanism by which environmental toxins drive the initiation of cancer-prone chronic inflammation in the skin and pancreas. Furthermore, we examined safe and effective therapies to block this pathway in order to suppress chronic inflammation and its cancer aftermath,” Demehri said.

The study relied on cell lines, animal models, human tissue samples, and epidemiological data. The group’s cell-based experiments demonstrated that environmental toxins (such as exposure to allergens and chemical irritants) activate two connected signaling pathways called the TLR3/4 and TBK1-IRF3 pathways. This activation leads to the production of the interleukin-33 (IL-33) protein, which stimulates inflammation in the skin and pancreas that can contribute to the development of cancer.

When they screened a library of U.S. Food and Drug Administration-approved drugs, the researchers found that the statin pitavastatin effectively suppresses IL-33 expression by blocking the activation of the TBK1-IRF3 signaling pathway. In mice, pitavastatin suppressed environmentally induced inflammation in the skin and pancreas and prevented development of inflammation-related pancreatic cancers. 

In human pancreas tissue samples, IL-33 was overexpressed in samples from patients with chronic pancreatitis (inflammation) and pancreatic cancer compared with normal pancreatic tissue. Also, in analyses of electronic health records data on more than 200 million people across North America and Europe, use of pitavastatin was linked to a significantly reduced risk of chronic pancreatitis and pancreatic cancer.

The findings demonstrate that blocking IL-33 production with pitavastatin may be a safe and effective preventive strategy to suppress chronic inflammation and the subsequent development of certain cancers.

“Next, we aim to further examine the impact of statins in preventing cancer development in chronic inflammation in liver and gastrointestinal tract and to identify other novel, therapeutic approaches to suppress cancer-prone chronic inflammation” said Demehri.

Research support was provided by the Burroughs Wellcome Fund, the LEO Foundation, the Sidney Kimmel Foundation, and the National Institutes of Health.

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• Published: 31 May 2024

Author Correction: Research on the method of determining the block size for an open-pit mine integrating mining parameters and shovel-truck’s operation efficiency

• Weiqiang Guo   ORCID: orcid.org/0000-0003-0095-2637 1 ,
• Guangwei Liu   ORCID: orcid.org/0000-0002-1678-7472 1 ,
• Jiaming Li 1 ,
• Senlin Chai   ORCID: orcid.org/0000-0002-8464-9522 2 &
• Shupeng Guo 3  

Scientific Reports volume  14 , Article number:  12551 ( 2024 ) Cite this article

Metrics details

The Original Article was published on 02 May 2024

Correction to: Scientific Reports https://doi.org/10.1038/s41598-024-52815-9 , published online 02 May 2024

The original version of this Article contained an error in the Acknowledgements section, where the grant number for the National Natural Science Foundation of China was incorrect. Consequently,

“This research was supported by the National Natural Science Foundation of China (51974144), the Youth Fund of the National Natural Science Foundation of China (52204158), 'Jie Bang Gua Shuai' (Take the Lead) of the Key Scientific and Technological Project for Liaoning Province (2021JH1/10400011), Discipline Innovation Team of Liaoning Technical University (LNTU20TD-07), and School level scientific research project of Yancheng Institute of Technology (xjr2020039).”

“This research was supported by the National Natural Science Foundation of China (52374123), the Youth Fund of the National Natural Science Foundation of China (52204158), 'Jie Bang Gua Shuai' (Take the Lead) of the Key Scientific and Technological Project for Liaoning Province (2021JH1/10400011), Discipline Innovation Team of Liaoning Technical University (LNTU20TD-07), and School level scientific research project of Yancheng Institute of Technology (xjr2020039).”

The original Article has been corrected.

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Weiqiang Guo, Guangwei Liu & Jiaming Li

School of Economics & Management, Yancheng Institute of Technology, Yancheng, 224051, China

Senlin Chai

State Grid Energy Hami Coal and Electricity Co., Ltd., Dananhu No. 2 Mine, Hami, 839000, China

Shupeng Guo

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Correspondence to Guangwei Liu .

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Guo, W., Liu, G., Li, J. et al. Author Correction: Research on the method of determining the block size for an open-pit mine integrating mining parameters and shovel-truck’s operation efficiency. Sci Rep 14 , 12551 (2024). https://doi.org/10.1038/s41598-024-62919-x

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Circadian clock can be leveraged to enhance cancer immunotherapy

Optimizing individual time-of-day delivery offers new avenues for prevention and treatment.

A multidisciplinary research team at the University of California, Irvine has revealed that the circadian clock -- the biological pacemaker that governs daily rhythms in physiological processes, including immune functions -- can be leveraged to enhance the efficacy of checkpoint inhibitor cancer therapy. Checkpoint inhibitors block different proteins from binding to tumor cells, allowing the immune system's T cells to kill the tumor.

The study, published online today in the journal Nature Immunology , provides deeper insights into the intricate relationship among the circadian clock, immune regulation and tumor development and found that a therapeutic approach optimizing time-of-day delivery based on an individual's unique circadian patterns offers new avenues for prevention and treatment.

"Disruption of the internal biological pacemaker is an inherent aspect of modern society that may contribute to the rising incidence of many cancer types. We found that proper regulation of circadian rhythms is necessary to suppress inflammation and support peak immune function," said corresponding author Selma Masri, UC Irvine associate professor of biological chemistry. "Understanding precisely how circadian disruption promotes disease progression could lead to behavior modification to reduce cancer risk."

Team members used an advanced single-cell RNA sequencing technique in a genetic model of colorectal cancer and identified clock-dependent changes controlling the number of myeloid-derived cells that suppress T cell activation. They discovered that disruption of the internal clock in the epithelial cells lining the intestine alters secretion of cytokine proteins, leading to heightened inflammation, increased numbers of immunosuppressive myeloid cells and cancer progression. These findings were leveraged to demonstrate that providing immunotherapy at the time of day when these immunosuppressive myeloid cells are most abundant significantly enhanced the efficacy of immune checkpoint blockades in solid tumors.

"As we enhance our understanding of the fundamental mechanism of circadian regulation of immunity, we will be able to harness the power of the body's natural rhythms to fight cancer and develop more personalized and effective treatment strategies," said lead author Bridget Fortin, a UC Irvine doctoral student in the Department of Biological Chemistry.

While this study represents a significant step forward in defining circadian control of anti-tumor immunity, the team believes future research should focus on exploring additional factors and cell types influencing time-of-day response to checkpoint inhibitor therapy.

Other team members included UC Irvine School of Medicine graduate students and faculty from the departments of biological chemistry, physiology and biophysics, surgery, and medicine.

This work was supported by the National Cancer Institute, the V Foundation and Johnson & Johnson, among others.

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Materials provided by University of California - Irvine . Note: Content may be edited for style and length.

Journal Reference :

• Bridget M. Fortin, Shannon M. Pfeiffer, Jacob Insua-Rodríguez, Hamad Alshetaiwi, Alexander Moshensky, Wei A. Song, Alisa L. Mahieu, Sung Kook Chun, Amber N. Lewis, Alex Hsu, Isam Adam, Oliver S. Eng, Nicholas R. Pannunzio, Marcus M. Seldin, Ivan Marazzi, Francesco Marangoni, Devon A. Lawson, Kai Kessenbrock, Selma Masri. Circadian control of tumor immunosuppression affects efficacy of immune checkpoint blockade . Nature Immunology , 2024; DOI: 10.1038/s41590-024-01859-0

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A deeper look at anti-pd-1/pd-l1 checkpoint inhibitors for cancer.

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Interaction between checkpoint protein PD-1 on T cells (blue) and PD-L1, its partner receptor on ... [+] cancer cells (red), blocked by therapeutic antibodies.

In a previous story, I described pembrolizumab, a PD-1 targeting checkpoint inhibitor, in some detail. Since its launch, several companies have introduced antibodies targeting the same receptor. This article summarizes some of these recent advances and how they work.

Fight Cancer with Checkpoint Inhibitors

When many cancers advance, spread and reoccur, checkpoint inhibitors can help keep difficult tumors at bay. These antibody-based immunotherapies can restore the body’s ability to recognize and eliminate cancer cells—an approach that often pairs well with other treatment options, including surgery, chemotherapy and radiation.

The antibodies are delivered intravenously. Once in the blood, these antibodies block molecules called checkpoint proteins on immune T cells. This blocking interaction restores the immune system’s ability to recognize and kill cancer cells.

While not all inhibitors are crafted alike, around half of the inhibitors currently on the market share the same immune target: a protein known as PD-1 found on white blood T cells. This strategy demonstrates clinical efficiency for many cancers, including melanoma, lung, and head and neck cancers.

What Immune Checkpoints Do

Immune checkpoints lie at the center of this mechanism. This naturally occurring system helps the immune system maintain self-tolerance—the body’s ability to recognize self against aberrant proteins that arise from cancer or infections —and minimize immune response damage to healthy tissues.

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One key immune checkpoint is known as PD-1, or Programmed Cell Death Protein-1. This receptor is found on the surface of T cells and other immune cells. These proteins protect the body from overly strong immune responses and autoimmunity. When PD-1 binds to its partner receptors on other cells, PD-L1 or PD-L2, it sends a signal to the T cell to paralyze its normal immune function.

Block PD-1 Checkpoints, Shrink Tumors

The immune system is equipped to suppress tumors on a small scale. Cancer cells overcome this anti-tumor activity by producing molecules to inhibit immune cell killing. By over-expressing PD-L1 checkpoint proteins, cancer cells can turn off T cells that would otherwise attack the tumor.

Enter anti-PD-1 checkpoint inhibitors. These therapies bind antibodies to PD-1 proteins, preventing the PD-1 protein from binding to its ligands, PD-L1 or PD-L2. The resulting T cell is freed of its restraints and can sustain its activity in the tumor microenvironment. In a previous story, I described pembrolizumab, a PD-1 targeting checkpoint inhibitor, in some detail. Since its launch, several companies have introduced antibodies targeting the same receptor. This article summarizes what they are and how they work.

Checkpoint inhibitors boost anticancer activity by targeting immune checkpoint proteins. The ... [+] antibodies here block two different checkpoint proteins: PD-1 on T cells (highlighted in yellow) and its corresponding ligand, PD-L1 on tumor cells (highlighted in orange).

Anti-PD-1 Checkpoint Inhibitors

Checkpoint inhibitors use antibodies to bind to and prevent checkpoint protein interactions. Currently, there are six federally approved checkpoint inhibitors that block PD-1 checkpoint receptors. Each inhibitor benefits a distinct array of cancers. For example, pembrolizumab , sold by Merck & Co., is indicated to treat over 18 different types of cancers. In comparison, BeiGene’s tislelizumab only gained FDA approval to treat patients with a certain type of esophageal cancer.

These drugs can be administered alone as a monotherapy or with other cancer treatments, including inhibitors targeting different checkpoint proteins and chemotherapy. The characteristics of the cancer at hand will dictate how each inhibitor is used.

Table 1: List of all anti-PD-1 checkpoint inhibitors approved in the United States as of May 2024.

Adverse Effects

Although successful in treating several cancers, anti-PD-1 therapies can trigger several adverse effects . Most reactions occur as a consequence of unleashing immune activity, resulting in a variety of issues. Most notably, the inhibitors can stoke inflammation throughout the body, such as on the skin or in the lungs, colon or liver. These inhibitors can also tamper with hormone levels in the thyroid and adrenal glands.

The skin can turn itchy or red with a rash. Issues with lung inflammation, or pneumonitis , often cause coughing, shortness of breath, and fever. Patients with colitis typically experience frequent diarrhea, abdominal pain, nausea, vomiting, fatigue or decreased appetite. Liver and kidney dysfunction can similarly cause nausea, fatigue or loss of appetite. Patients also commonly report feeling pain in the joints, back, and/or muscles.

Though these adverse events can range from mild to life-threatening, checkpoint inhibitors are generally considered more tolerable than chemotherapy and radiation. Clinicians monitor each patient to prevent these reactions from becoming life-threatening and are often successful.

Targeting Partner Receptors PD-L1 & PD-L2

Originally, checkpoint inhibitors could only target T cells to interfere with the PD-1 immune checkpoint axis. Now, it is possible to interrupt PD-1 interactions by targeting PD-1’s partner receptors on other cells.

PD-1 possesses two known binding partners: PD-L1 and PD-L2 . These proteins are often over-expressed on tumor cells. Though there are federally approved checkpoint inhibitors for the former, the clinical potential for the latter is still under investigation.

Three anti-PD-L1 inhibitors are available for use: atezolizumab (Tecentriq), durvalumab (Imfinzi), and avelumab (Bavencio). They emerged a few years after the FDA approved the first anti-PD-1 inhibitor.

Interestingly, though these inhibitors target the other side of the PD-1 axis, they do not treat exactly the same diseases as their anti-PD-1 counterparts. Certain cancers, such as a kind of soft tissue tumor called alveolar soft part sarcoma and small cell lung cancer , have only shown improvement under anti-PD-L1 inhibitors. For other cancers, including non-small cell lung cancer, hepatocellular carcinoma, and melanoma, either type of inhibitor could elicit clinical benefit. The decision between which inhibitor to choose will depend on several factors, such as the available efficacy data for the disease and the patient’s previous treatment history.

Potential Future Research

The full potential for anti-PD-1 checkpoint inhibitors remains untapped. Investigational inhibitors will continue gaining approval and expanding this inhibitor mechanism's applicability. However, an important caveat exists. Although these drugs can help suppress difficult-to-treat tumors, their effect is not consistent across different cancer types; some tumors respond better than others. As a result, improving drug safety profiles and overall clinical benefit are major research focuses for the field.

Clinical trials administering anti-PD-1 inhibitors alongside other known cancer treatments, such as chemotherapy, are pivotal in understanding how best to deliver this therapy. While combining distinctly-targeting inhibitors is possible, an anti-PD-1 and anti-PD-L1 inhibitor regime has yet to be approved. With more investigation, anti-PD-L1 and anti-PD-L2-targeting therapies could one day join this pool, as well.

Checkpoint inhibitors represent one of the most significant advances in cancer treatment over the past twenty years. While they are not the answer to all cancers, their impact is profound, especially when used in combination with other treatments such as therapy, chemotherapy, and emerging cell-based therapies such as CAR T Therapy. This is just the beginning; as research continues and new checkpoints are discovered, the potential of these therapies will only grow, offering greater hope for cancer patients.

This article joins a growing series on mono cancer treatments, including novel immunotherapies such as CAR T therapy and checkpoint inhibitors . Find more at www.williamhaseltine.com .

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Four takeaways from UCLA Chancellor Gene Block's testimony on campus antisemitism, protests

U CLA Chancellor Gene Block found himself in the nation's culture wars hot seat Thursday, interrogated by members of Congress about his handling of complaints of campus antisemitism, amid student protests over the Israel-Hamas war.

For Republican Congress members, the hearing organized by the GOP-led House Committee on Education and the Workforce was a chance to present UCLA as exhibit A in how not to deal with protests.

Almost as soon as activists set up a Palestinian solidarity encampment April 25 in the heart of campus, Jewish students and faculty complained that demonstrators established checkpoints restricting access to many students, at times singling out students they identified as Zionists. But other Jewish students helped set up the camp, arguing it was not antisemitic, but anti-Zionist.

After a violent mob of pro-Israeli counterprotesters attacked the encampment on April 30, it was dismantled May 2, with law enforcement arresting more than 200 people.

But Thursday’s interrogation was not a forum for a constructive discussion on how universities can navigate the balance between maintaining free speech and protecting students from discrimination.

Instead, Republicans — and some Democrats — took it as an opportunity to score political points.

“Over the course of years, decades even, universities gradually nurtured a campus culture of radicalism, in which antisemitism grew and became tolerated by administrators,” Virginia Foxx, the commitee chair, said in her opening remarks.

The Republican from North Carolina assailed Block for allowing UCLA’s protests to spiral out of control.

“For days, you stood by as Jews were assaulted and illegal checkpoints blocked access to campus in broad daylight," Foxx said. "Your actions were too little, too late.”

Here are some key takeaways from the hearing.

Block said he was late in shutting down the encampment

In his opening testimony, Block conceded that UCLA made errors in judgment. The encampment, he said, "disrupted normal access to some classes" and "impeded our educational mission."

“With the benefit of hindsight," he said, "we should have been prepared to immediately remove the encampment if and when the safety of our community was put at risk."

He was vague about what he would do differently

Block did not specify what UCLA should have done to prevent discrimination or violence as protests ramped up. And he did not explain why the university did not take action as students reported discrimination from protesters and outside agitators gathered on campus.

“Why did you fail to immediately clear these checkpoints?” Foxx asked.

Block said he instructed staff to make sure all students could freely pass without obstruction and then sent out a campuswide memo April 30, declaring that the encampment was "unlawful."

Striking a mild, noncombative approach throughout, Block did not say what campus discipline had been — or would be — meted out to students who violated UCLA rules.

Rep. Ilhan Omar (D-Minn.) criticized UCLA leaders for standing by for hours as a “mob of agitators” gathered near the encampment.

“This happened in front of your eyes on your campus, and it was live streamed for the whole world to see,” Omar said. “How did you fail these students at many critical points where you could have intervened?”

Block said he rejected the premise of the question.

“How can you reject the premise?” Omar said. “Are these pictures lying? Are any of these people in jail?”

Block said the Los Angeles Police Department was working to identify the attackers.

“It's been over a month,” Omar said, cutting him off.

UCLA protesters who blocked students’ passage have yet to be disciplined

Rep. Kevin Kiley, a California Republican, asked Block whether physically obstructing students from entering campus based on their race, ethnicity or religion is an expellable offense.

‘There is a disciplinary process,” Block said. “It could be.”

Kiley played a viral video showing UCLA protesters blocking a student, Eli Tsives, from passing a checkpoint.

“Were those students who formed blockade?” Kiley said. “Were they disciplined?"

Block said he didn’t know, repeating that he sent out a memo April 30 instructing the campus community that blocking students' passage was intolerable.

“I’m going to take that as a no,” Kiley said. “There’s been no consequence whatsoever?”

“I did not say that,” Block said. “This is being investigated, and we’ll see what happens with the disciplinary process.”

Block said campus antisemitism is a problem

Block, who is Jewish and has family members who died in the Holocaust, said UCLA has a problem with antisemitism.

“I am fully aware that many of our Jewish students have had to confront rhetoric and images on campus that any reasonable person would find repugnant,” Block said in his opening statement. “Trust me, I understand their pain."

Asked by Kathy E. Manning, a Democrat from North Carolina, about emails dating to 2014 that show alumni had alerted the chancellor of growing antisemitism, Block said the university had tried to respond with training.

About 90% of students, he said, had taken an online training course that includes discussion of antisemitism.

Manning asked whether students and staff need additional training.

“I think we need to do more," Block said.

But the chancellor also rebutted the Republican narrative that UCLA was awash in antisemitism.

"I don’t believe we are a hotbed of antisemitism," Block said. "I think we’ve had incidents of it that are disturbing we’re trying to address."

This story originally appeared in Los Angeles Times .

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