BUFFALO, NY – June 20, 2025 – A new #review was #published in Volume 16 of Oncotarget on June 10, 2025, titled “Beyond DNA damage response: Immunomodulatory attributes of CHEK2 in solid tumors.”

In this paper, led by first author Helen Qian and corresponding author Crismita Dmello from Northwestern University Feinberg School of Medicine, researchers compiled growing evidence that the CHEK2 gene, long known for its role in repairing DNA damage, may also influence how tumors respond to immunotherapy. Their analysis suggests that problems in CHEK2 function might make cancer cells more vulnerable to immune system attacks, highlighting a new opportunity to improve treatment outcomes in solid tumors.

Immune checkpoint inhibitors (ICIs) have transformed cancer treatment; however, they are effective in only a subset of patients. This review suggests that tumors with reduced CHEK2 activity may accumulate more mutations that produce signals the immune system can recognize. These signals, known as neoantigens, help immune cells identify and destroy cancer cells more effectively. The review connects this process not only to CHEK2’s established role in the DNA damage response but also to a newly proposed function in shaping the immune environment of tumors.

CHEK2 normally helps maintain genomic stability by enabling precise DNA repair. When this function is lost, cells rely on more error-prone repair methods, leading to additional mutations. These mutations can increase tumor mutational burden, which has been linked to better outcomes with immunotherapy. Beyond DNA repair, the review highlights a second mechanism: activation of the cGAS-STING pathway. This pathway detects fragments of damaged DNA and triggers inflammation that attracts immune cells to the tumor.

The authors highlight studies where CHEK2-deficient tumors responded better to PD-1 inhibitors, a common type of immune checkpoint inhibitor. In both lab models and early-stage clinical settings, CHEK2 loss was associated with increased infiltration of CD8+ T cells—immune cells essential for attacking cancer cells. In cancers such as glioblastoma and renal cell carcinoma, which are typically resistant to immunotherapy, reduced CHEK2 expression was linked with more favorable immune activity and higher expression of interferon-related genes.

The compiled evidence points to CHEK2 as a potential biomarker for identifying patients likely to respond to immunotherapy. In addition, combining CHEK2 inhibitors with existing immunotherapies may enhance anti-tumor effects, particularly in cancers with limited treatment options. The review notes that some clinical trials using the CHEK1/2 inhibitor prexasertib alongside immune checkpoint therapies have already shown promising early results.

“The initial results from this Phase I clinical trial support the immunomodulatory role of CHEK2 expression and even suggest CHEK2 potentiates immunosuppression.”

Although more research is needed to confirm these mechanisms and improve treatment approaches, this review underscores the expanding role of DNA repair genes like CHEK2—not only in maintaining genome integrity but also in helping the immune system fight cancer.

DOI - https://doi.org/10.18632/oncotarget.28740

Correspondence to - Crismita Dmello - stellacpak@outlook.com

Video short - https://www.youtube.com/watch?v=C26pEBc0itk

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Oncotarget

CHEK2 Identified as a Potential Target to Improve Immunotherapy in Solid Tumors

BUFFALO, NY — July 8, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on May 30, 2025, titled “Impact of waist-to-hip and waist-to-height ratios on physical performance: insights from the Longevity Check-up 8+ project.”

In this study, researchers led by first author Anna Maria Martone and corresponding author Elena Levati from the Fondazione Policlinico Universitario “Agostino Gemelli” IRCCS and Università Cattolica del Sacro Cuore found that adults with higher waist-to-hip and waist-to-height ratios tend to have poorer physical performance. These simple body shape measures emerged as important tools for assessing strength and mobility, which are essential for maintaining independence as people age.

The analysis included data from more than 10,000 Italian adults aged 18 to 98 years who participated in the Longevity Check-up 8+ project, a nationwide health initiative aimed at promoting healthy lifestyles and raising awareness of cardiovascular risks. Researchers measured participants’ waist-to-hip (WHR) and waist-to-height (WHtR) ratios and assessed their physical function using the five-repetition chair stand test, a standard evaluation of lower body strength and mobility.

“Among 10690 participants (mean age 57.0 ± 14.8 y; 54% females), men exhibited higher WHR and WHtR and a higher prevalence of abnormal values (61% and 71%).”

The results showed that individuals with higher waist-to-hip and waist-to-height ratios took longer to complete the test, reflecting reduced physical function. Even after adjusting for lifestyle factors such as diet, exercise habits, and cardiovascular health, these ratios remained strongly linked to poorer performance. The waist-to-height ratio, in particular, proved to be a more effective predictor of physical ability across different age and gender groups.

These findings highlight how abdominal fat, already tied to serious health risks like heart disease and diabetes, may also impair mobility and independence as people age. Monitoring waist measurements could help identify individuals at risk of functional decline, offering a simple tool to support public health in aging populations.

The waist-to-height ratio is especially valuable because of its simplicity and practicality. Requiring only waist and height measurements, it can be easily used in clinical settings and community health programs to screen for potential mobility issues. Encouraging healthy waist sizes through balanced diets and regular exercise could help preserve physical performance and delay age-related decline. These findings may guide future prevention strategies. By identifying individuals at higher risk, healthcare professionals can implement targeted interventions to support long-term health and independence.

DOI - https://doi.org/10.18632/aging.206260

Corresponding author - Elena Levati - elena.levati01@icatt.it

Video short - https://www.youtube.com/watch?v=WqGlZ1qGZPI

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Keywords - aging, physical performance, body composition, waist-to-hip ratio, waist-to-height ratio, chair-stand test

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Aging (Aging-US)

Abdominal Fat Linked to Reduced Strength and Mobility in Adults

The James Sarcoma Program continues to grow, with the recent opening of the multidisciplinary Sarcoma Clinic, new and cutting-edge clinical trials and a project in Ecuador to train doctors to treat sarcoma patients. “The entire continuum of cancer care is improving and that’s why it’s important to have a multi-disciplinary team and clinic, so patients have access to all these advances,” said Joel Mayerson, MD, director of the James Sarcoma Program.
Mayerson described the recent advances made by the Sarcoma Program. A renowned sarcoma surgeon, in recent years Mayerson has been utilizing 3D printing to create replacement “bones” for sarcoma patients. “We can take scans and create [with the 3D printer] ‘bones’ the exact size of what we remove.”
In a new clinical trial “we’ve found that if we give immunotherapy concurrently with radiation therapy it helps the radiation works better,” Mayerson said, adding “we have the first proton radiation center in Ohio and that allows us to hone the beam to a smaller area and damages less tissue.”
Mayerson and the sarcoma team have been collaborating with the world-class veterinarians at Ohio State Veterinary Medical Center to create a probe that allows surgeons to see, in real time during surgery, the difference between normal tissue and tumorous tissue. Seeing the difference enables surgeons to remove less normal tissue, which leads to better function and quality of life for patients. “We used pilot data funded by Steps for Sarcoma to apply for and receive an Ohio State President’s Accelerator grant,” Mayerson said. Steps for Sarcoma is the annual fundraising walk; the next Steps will be held September 21.
After operating on a patient from Ecuador, Mayerson and the sarcoma team “were asked to help build the program there,” he said. An Ecuadorian surgeon spent a year at the James working with Mayerson and his team, additional physicians will be trained and “our sarcoma tumor board helps guide them in treating their sarcoma patients … This has been one of the most satisfying things I’ve done in my career, to know that we’re impacting patients a couple thousand miles away.”

Episode 192: The James Sarcoma Programs Continues to Grow and Lead, with Dr. Joel Mayerson

Dr. Amparo Santamaria describes a #research paper she co-authored that was #published in Volume 17, Issue 6 of Aging (Aging-US), titled “Enhancing oocyte activation in women with ovarian failure: clinical outcomes of the Stem Cell Regenera study using G-CSF mobilization of peripheral blood stem cells and intraovarian injection of stem cell factor-enriched platelet rich plasma in real-world-practice.”

DOI - https://doi.org/10.18632/aging.206274

Corresponding author -Amparo Santamaria - Amparo.santamaria@ivirma.com

Video interview - https://www.youtube.com/watch?v=oRFJNwnXZWI

Abstract

The study assesses the effectiveness and safety of the Stem Cell Regenera Treatment for oocyte activation in women with ovarian failure, including conditions such as Poor Ovarian Response (POR), Diminished Ovarian Reserve (DOR), and Premature Ovarian Insufficiency (POI). This retrospective observational study was conducted from January 2023 to December 2024 at the IVIRMA Alicante Clinics in Spain.

Women diagnosed with ovarian failure participated in the study, which involved mobilizing Hematopoietic Stem Cells from bone marrow into peripheral blood using granulocyte colony- stimulating factor (G-CSF). This was followed by an intraovarian injection of Stem Cell Factor- enriched Platelet Rich Plasma (SCFE-PRP).

The primary outcome measures were the rate of oocyte activation, leukocytes and stem cell count, and pregnancy rates. Oocyte activation was defined as an increase in total Antral Follicle Count of three or more follicles after treatment and/or at least a 20% rise in Anti-Müllerian Hormone levels. Safety was assessed based on adverse effects. Pregnancy rates were evaluated for both spontaneous gestation and following in vitro fertilization (IVF) treatment.

A total of 145 women participated: the overall activation rate was 68.28%, with 7.07% achieving spontaneous gestation and 14.14% achieving pregnancy following IVF. Mobilization of CD34+ cells was successful in all participants, with an average collection of 32.96 CD34+ cells/μl. No severe adverse effects were observed. The study concluded that the Stem Cell Regenera Treatment is effective and safe for oocyte activation in women with ovarian failure in real-world practice.

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Keywords - aging, Stem Cell Regenera, oocyte activation, ovarian regeneration, G-CSF, SCFE-PRP, ovarian failure

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Behind the Study: Enhancing Oocyte Activation in Women with Ovarian Failure

BUFFALO, NY – July 14, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 25, 2025, titled “Hypoxia induced lipid droplet accumulation promotes resistance to ferroptosis in prostate cancer.”

In this study, researchers led by Shailender S. Chauhan and Noel A. Warfel from the University of Arizona discovered that prostate cancer cells survive treatment by storing fats in tiny cellular compartments when oxygen levels are low. This process makes the cancer cells less vulnerable to a type of cell death known as ferroptosis. The findings provide new insight into why prostate tumors often resist therapies and suggest potential strategies to improve treatment outcomes.

This study focused on ferroptosis, a form of programmed cell death that relies on iron and lipid oxidation to destroy cancer cells. Researchers tested prostate cancer cells under normal and low oxygen conditions and found that hypoxia, or reduced oxygen levels, allowed cancer cells to build up lipid droplets (LD). These structures act as storage units for fats, shielding cancer cells from oxidative damage and preventing ferroptosis from occurring.

The researchers found that this adaptation of prostate cancer cells made them less sensitive to ferroptosis-inducing drugs like Erastin and RSL3, even when these drugs were combined for a stronger effect. The team also reported that hypoxia caused significant changes in lipid metabolism, decreasing the availability of specific fatty acids that normally promote ferroptosis. 

“Transcriptomic analysis revealed that hypoxia significantly reduced the expression of genes related to incorporating polyunsaturated fatty acids into phospholipids (ACSL4, LPCAT3), and parallel lipidomic analysis demonstrated that hypoxia significantly decreased the levels of the ferroptosis-prone lipid class, phosphatidylethanolamine (PE) and increased production of neutral lipid species, cholesteryl ester (ChE (22:5)) and triglycerides (TG(48:1), TG:(50:4), and TG(58:4)).”

This research highlights the importance of the tumor microenvironment, particularly oxygen levels, in shaping how cancer cells respond to therapy. By altering their metabolism and storing lipids, prostate tumors may evade treatments designed to trigger ferroptosis. These findings underscore the need to develop new strategies targeting LD dynamics or lipid metabolism to overcome this resistance.

Understanding how prostate cancer (Pca) adapts to survive in hypoxic conditions offers a potential avenue for improving therapies. For example, preventing lipid accumulation in cancer cells or releasing stored fats may restore their sensitivity to ferroptosis and improve the effectiveness of current therapies. This approach could have broader implications for treating other solid tumors that share similar metabolic features.

DOI - https://doi.org/10.18632/oncotarget.28750

Correspondence to - Noel A. Warfel - warfelna@arizona.edu, and Shailender S. Chauhan - shailenderc@arizona.edu

Video short - https://www.youtube.com/watch?v=xFypDT4ALmc

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Keywords - cancer, hypoxia, lipid droplets, ferroptosis, resistance, prostate

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Prostate Cancer Cells Survive Treatment by Storing Fat in Low Oxygen Conditions

Hannah has news, and you have new friends! Tune in to meet guest hosts Whitney and Misty as they join Brandon in interviewing Hannah for our season finale. Why is Gregory of Nyssa’s take on salvation so different from what Hannah heard in church growing up? Are there risks in the regular ways we talk about Christian salvation? How did feminist theology help her untangle all of this? How much can we know or talk about God? And why is wonder, an antidote to certainty, so important? Listen to find out.

56: Wonder and Salvation with Hannah Black

Scientists have uncovered a promising new strategy to weaken cancer cells’ natural defense mechanisms, potentially making chemotherapy more effective. In a study published in Volume 16 of Oncotarget, researchers identified the protein PRDX1 as a key player in helping tumors resist treatment. By targeting this protein, they propose a novel way to combat aggressive, treatment-resistant cancers.

Understanding Why Some Cancers Resist Treatment

Chemotherapy works by damaging the DNA of cancer cells, forcing them to self-destruct. However, many cancers develop robust repair systems that fix this damage, allowing the tumor to survive and grow. A central component of this repair machinery is a protein called ATM, which acts like a first responder in the cell, detecting DNA damage and coordinating its repair.

In ovarian cancer and other aggressive tumors, high levels of ATM have been associated with poor survival rates and resistance to chemotherapy.

The Study: How PRDX1 Protects Cancer Cells

The study, titled “PRDX1 protects ATM from arsenite-induced proteotoxicity and maintains its stability during DNA damage signaling,” was led by first author Reem Ali and corresponding author Dindial Ramotar from Hamad Bin Khalifa University in Qatar, in collaboration with researchers from the University of Nottingham in the UK. 

Full blog - https://www.oncotarget.org/2025/07/14/prdx1-identified-as-key-to-chemotherapy-resistance-in-cancer-cells/

Paper DOI - https://doi.org/10.18632/oncotarget.28720

Correspondence to - Dindial Ramotar - dramotar@hbku.edu.qa

Video short - https://www.youtube.com/watch?v=suOhF7mPlNQ

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Keywords - cancer, redox signaling, homologous recombination, protein interaction, cell cycle, protein modification

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PRDX1 Identified as Key to Chemotherapy Resistance in Cancer Cells

Futurist and Berkeley Divinity at Yale alum Rachel Hatch (‘08) joins Brandon and Hannah for a conversation about how to look for signals of change within our own parishes and communities as we make thoughtful choices for the future. In this episode, Rachel encourages leaders to cultivate a practice of imagining possibilities and taking steps toward hope-filled futures, while still addressing the urgencies of the present.

57: Forecasting the Future with Rachel Hatch

BUFFALO, NY — July 15, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 5, 2025, titled “Senescence caused by telomerase inactivation in myeloid, mesenchymal, and endothelial cells has distinct effects on cancer progression.”

In this study, first author Joseph Rupert, along with corresponding author Mikhail G. Kolonin and colleagues from The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, McGovern Medical School, at The University of Texas Health Sciences Center at Houston, investigated how aging-related changes in different cell types affect cancer progression. By turning off telomerase in specific cell populations in mice, the researchers discovered that cell aging, or senescence, can slow primary tumor growth but also trigger unexpected effects. This work sheds light on the complex relationship between aging cells and cancer and may help guide future anti-cancer strategies.

The team used genetically modified mice to deactivate telomerase, the enzyme that maintains chromosome ends, specifically in immune, connective tissue, and blood vessel cells. This caused these cells to enter a state of senescence, where they stop dividing and release inflammatory signals. The researchers then implanted breast, prostate, and pancreatic cancer cells into the mice and tracked how tumors developed. They found that when telomerase was inactivated in immune cells or connective tissue cells, tumors grew more slowly. However, these tumors showed signs of increased tissue damage and potential aggressiveness.

Interestingly, when telomerase was turned off in endothelial cells, which cover blood vessels, tumors shrank and became poorly supplied with blood, leading to oxygen deprivation. In the case of pancreatic cancer cells, this low-oxygen environment made them more likely to spread to the liver, highlighting a potential risk of targeting these cells.

“[…] this study shows that senescence and metabolic dysfunction resulting from telomerase inactivation in distinct cells in the tumor microenvironment have different effects on tumor growth and metastasizing of carcinomas.”

This research provides important insights into how aging cells within the tumor microenvironment (TME) influence cancer behavior. While senescence in certain cell types can help suppress tumor growth, it may also create conditions that favor cancer metastasis. These findings highlight the need to consider cell type-specific effects when developing therapies that target senescent cells. By mapping how different cell populations contribute to cancer progression in aging tissues, this study opens the door for more precise approaches to prevent both tumor growth and spread.

DOI - https://doi.org/10.18632/aging.206268

Corresponding author - Mikhail G. Kolonin - mikhail.g.kolonin@uth.tmc.edu

Video short - https://www.youtube.com/watch?v=py8wFKj7enE

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Keywords - aging, senescence, telomerase, myeloid, mesenchymal, endothelial

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How Telomerase Inactivation in Aging Cells Influences Cancer Growth and Metastasis

BUFFALO, NY - July 16, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 9, 2025, titled “A novel anti-human CD25 mAb with preferential reactivity to activated T regulatory cells depletes them from the tumor microenvironment.”

In this study, researchers from the National Institute of Allergy and Infectious Diseases, led by first author Maja Buszko and corresponding author Ethan M. Shevach, discovered a new monoclonal antibody that selectively targets a subset of immune cells called regulatory T cells (Tregs). These cells, while normally important for preventing autoimmunity, also can block the body’s ability to fight cancer by suppressing anti-tumor immune responses. This discovery could lead to novel cancer therapies that strengthen the immune system’s capacity to attack tumors.

The researchers identified an anti-CD25 monoclonal antibody with several atypical properties and named it 2B010.  To evaluate its effects, they used humanized mice, laboratory mice that are engineered to carry human immune cells, to closely mimic how human immune systems respond to cancer. The treatment of these mouse models with 2B010 significantly decreased the number of Tregs in tumors and boosted the activity of CD8+ T cells, which are essential for killing cancer cells. Importantly, 2B010 worked without disrupting other key immune functions. Unlike traditional Anti-CD25 antibodies, it did not interfere with interleukin-2 (IL-2) signaling, which is essential for the growth and activity of effector T cells that fight cancer. 

“2B010 also had no effect on IL-2 induced STAT5 phosphorylation or CD4+ T cell proliferation in vitro while both were blocked by Clone D1 further supporting the view that 2B010 does not recognize the IL-2 binding site.”

This finding is especially significant because high levels of Tregs in tumors are associated with poor outcomes in many cancers. By specifically removing these cells, 2B010 may help overcome one of the main barriers to current immunotherapy approaches. Its ability to preserve IL-2 signaling could also make it safer and more effective when used alone or in combination with existing therapies such as immune checkpoint inhibitors.

While the 2B010 antibody showed strong effects in reducing Tregs and boosting immune cell activity, the study did not observe changes in tumor size in these models. Researchers suggest this may be due to limitations in the preclinical systems used, such as the lack of tumor-specific T cells in humanized mice. Nevertheless, these findings demonstrate that 2B010 has a unique mechanism of action that could complement other cancer immunotherapies in future clinical trials.

In conclusion, the development of 2B010 is a promising step toward selectively disrupting the immune suppressive environment in tumors. As researchers continue to refine and test this antibody, it could become a powerful tool for enhancing the effectiveness of cancer treatments and improving outcomes for patients.

DOI - https://doi.org/10.18632/oncotarget.28752

Correspondence to - Ethan M. Shevach - eshevach@Niaid.NIH.gov

Video short - https://www.youtube.com/watch?v=2NJcGsI7WXA

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Keywords - cancer, Treg, CD25, TME, mAb, GVHD

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New Antibody Selectively Targets Immune Cells That Suppress Anti-Tumor Responses

BUFFALO, NY — July 17, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 9, 2025, titled “Developing a quantitative estimate of muscle age acceleration by a novel phenotypic clock: cross-sectional study in healthy, middle-aged and older adults.”

In this study, led by first authors Lucia Ventura, Antonella Cano and Marco Morrone, along with corresponding author Franca Deriu from the University of Sassari, researchers introduce a new method to predict how muscles age, offering an early warning system for sarcopenia, the condition of age-related muscle loss. The study demonstrates how a simple, low-cost approach can identify middle-aged and older adults at higher risk for declining muscle health, allowing timely preventive strategies.

The researchers developed a tool called Muscle Age Acceleration (MAA), which measures how quickly an individual’s muscles are aging compared to their actual age. By analyzing physical performance tests and body composition in 215 healthy participants aged 50 to 90 years, the researchers found that about 25% of individuals experience accelerated muscle aging. These individuals had a higher probability of developing sarcopenia, despite appearing healthy and not yet having received a diagnosis of the condition.

Sarcopenia reduces muscle strength and physical performance, being a growing concern for older adults. It contributes to frailty, falls, and an increased risk of disability. Despite greater awareness, this condition often goes undetected until significant muscle loss occurs. This new muscular clock offers an opportunity to detect subtle changes in muscle health before they progress to more severe stages.

By using common tests such as handgrip strength, walking speed, and mobility assessments, the MAA tool can classify individuals as having accelerated, normal, or decelerated muscle aging. Those with accelerated muscle aging also showed small changes in blood markers, suggesting early and hidden inflammation linked to muscle decline. This finding indicates that MAA may act as both a predictor of muscle-related aging and an indicator of overall health risks.

“According to MAA, three trajectories were identified: accelerated agers displayed higher risk for sarcopenia (19%), as compared to normal (9%; p < 0.0001) and decelerated (2%; p < 0.0001), paralleled by significant subclinical alterations of haemato-chemical markers in accelerated agers.”

If validated in future studies, this innovative approach could transform how clinicians and caregivers screen for early signs of sarcopenia. Its simplicity makes it suitable for use in clinics and community settings, helping older adults maintain independence and quality of life as they age.

In summary, these findings highlight the importance of monitoring muscle health and physical performance in older adults. By detecting early signs of muscle aging with tools like MAA, interventions such as exercise and dietary changes can be introduced earlier, potentially delaying or preventing sarcopenia and its complications.

DOI - https://doi.org/10.18632/aging.206269

Corresponding author - Franca Deriu - deriuf@uniss.it

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New Aging Clock Predicts Early Risk of Muscle Loss in Older Adults

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

CHEK2 Identified as a Potential Target to Improve Immunotherapy in Solid Tumors

Oncotarget Podcast

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