BUFFALO, NY—February 18, 2025 — A new #research paper was #published by Aging (Aging-US) on January 8, 2025, in Volume 17, Issue 1, titled “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.”

Researchers Kamendra Kumar, Bo-Hyun Moon, Santosh Kumar, Jerry Angdisen, Bhaskar V.S. Kallakury, Albert J. Fornace Jr., and Shubhankar Suman from Georgetown University Medical Center explored whether a drug called ABT-263 could help reduce the risk of gastrointestinal (GI) cancer caused by radiation exposure. Their findings suggest that ABT-263, a senolytic agent, helps eliminate harmful aging cells in the gut, reducing inflammation and lowering cancer risk in mice. These results could lead to potential treatments for people exposed to radiation, including cancer patients and astronauts.

Radiation exposure, whether from medical treatments, environmental sources, or space travel, can damage cells and increase the risk of GI cancer. One key factor in this process is cellular senescence, where damaged cells stop dividing but continue to release harmful molecules that promotes tumor growth. This study tested whether ABT-263, a drug designed to remove these aged cells, could lower cancer risk in a mouse model of GI cancer.

In this study, researchers exposed mice to radiation and found that it increased the number of damaged cells in their intestines, leading to more tumors. However, when the mice were given ABT-263, the number of harmful cells decreased, and they developed fewer tumors. The drug also reduced inflammation and blocked signals that promote cancer growth.

“Oral administration of ABT-263 in Apc1638N/+ mice resulted in a significant reduction in low-LET IR-induced intestinal tumor burden at 5 months post-exposure."

These findings highlight the potential of senolytic drugs like ABT-263 as a preventive treatment for radiation-induced cancers. This approach could be especially beneficial for cancer patients undergoing radiation therapy, astronauts exposed to cosmic radiation, and individuals at risk from environmental sources such as radon gas.

However, while ABT-263 showed promise, it also has known side effects, including reduced platelet counts, which can impact blood clotting. Future research will focus on optimizing senolytic treatments to ensure they are both safe and effective for human use. Scientists are also exploring alternative drugs and combination therapies that might offer the same benefits with fewer risks.

This study provides strong evidence that removing senescent cells could help prevent radiation-related GI cancer. With further research, senolytic drugs may become an important tool in protecting at-risk populations from the long-term effects of radiation exposure.

DOI - https://doi.org/10.18632/aging.206183

Corresponding author - Shubhankar Suman - ss2286@georgetown.edu

Video short - https://www.youtube.com/watch?v=M_WEht4vy4w

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The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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Aging (Aging-US)

Senolytic ABT-263 Reduces Radiation-Induced Gastrointestinal Cancer

BUFFALO, NY - March 17, 2025 – Impact Journals (Oncotarget’s publisher), is pleased to announce its participation as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2025. The meeting is scheduled for April 25-30, 2025, at the McCormick Place Convention Center in Chicago, Illinois.

The 2025 AACR Annual Meeting's central theme, "Unifying Cancer Science and Medicine: A Continuum of Innovation for Impact," highlights major breakthroughs and innovative developments transforming cancer research. Oncotarget aligns directly with this vision, being always committed to rapidly publishing and disseminating impactful research findings across diverse areas of cancer science and thus advancing cancer treatment and patient care.

Conference attendees are warmly invited to visit Booth 2815 to meet members of the Oncotarget, discover notable recent publications, and discuss collaborative opportunities. Oncotarget, assisted by its publisher Impact Journals, remains focused on accelerating the sharing of crucial oncology research, fostering innovation, and maintaining excellence in cancer research.

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Oncotarget

Oncotarget to Participate at the AACR Annual Meeting 2025

BUFFALO, NY — March 17, 2025 —  Impact Journals (Aging’s publisher) is pleased to announce its participation as an exhibitor at theAmerican Association for Cancer Research (AACR) Annual Meeting 2025. The meeting is scheduled for April 25-30, 2025, at the McCormick Place Convention Center in Chicago, Illinois.

This 2025 AACR Annual Meeting theme, “Unifying Cancer Science and Medicine: A Continuum of Innovation for Impact,” highlights significant advancements and groundbreaking discoveries in cancer research. Aging closely aligns with this mission, dedicated to disseminating impactful scientific research at the intersection of oncology and gerontology.

Visit Booth 2815 to meet directly with members of the Aging team, explore the latest research publications, and discuss opportunities for collaboration and manuscript submissions. Aging, supported by its publisher Impact Journals, remains dedicated to promoting innovation, collaboration, and advancing scientific knowledge in aging-related cancer research.

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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Aging (Aging-US) to Participate at the AACR Annual Meeting 2025

BUFFALO, NY — March 18, 2025 — A new #research paper was #published by Aging (Aging-US) on March 7, 2025, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors.”

Led by first author Cong Wang and corresponding author Xiao-Ou Shu from Vanderbilt University, this study examines how breast cancer and its treatments contribute to accelerated aging in survivors. Their study revealed that breast cancer patients show signs of faster biological aging compared to cancer-free individuals, with long-term effects lasting up to ten years post-diagnosis. This finding raises concerns about the potential lasting impact of cancer therapies on aging and overall health.

Breast cancer is one of the most common cancers in women worldwide, with improved treatments leading to longer survival rates. However, emerging evidence suggests that these treatments may also accelerate aging. The study used Phenotypic Age Acceleration (PAA), a biological marker that estimates a person’s aging rate based on blood tests. Researchers compared data from 1,264 breast cancer patients and 429 cancer-free controls. The results indicated that breast cancer survivors had significantly higher PAA at diagnosis and continued to show signs of accelerated aging up to ten years later.

“This is the first large study with 10 years of follow-up to evaluate PAA among BC survivors.”

The study found that tumor severity played a role in aging acceleration. Women with advanced-stage (Stage III/IV) or high-grade tumors showed the highest levels of aging acceleration. Additionally, treatments such as chemotherapy and endocrine therapy were linked to increased biological aging. One year after diagnosis, chemotherapy was associated with the most significant rise in PAA, while endocrine therapy had long-term effects, increasing aging markers even ten years after treatment.

Interestingly, not all cancer treatments had the same effect. Surgery and radiation therapy were associated with lower aging acceleration over time. These findings suggest that systemic therapies, which affect the whole body, may contribute more to aging-related changes than localized treatments.

The findings highlight the need for ongoing monitoring of breast cancer survivors beyond their initial recovery. Understanding how cancer treatments influence aging can help improve post-treatment care and potentially lead to strategies that reduce these effects. Further research is needed to explore whether lifestyle changes, medications, or other interventions could slow down aging in cancer survivors.

As the number of breast cancer survivors continues to grow, addressing the long-term health consequences of cancer treatment is crucial. This study provides valuable insights into how different factors contribute to accelerated aging, helping to shape future research and healthcare approaches for breast cancer survivors.

DOI - https://doi.org/10.18632/aging.206218

Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org

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

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Breast Cancer Treatments Linked to Accelerated Aging in Survivors

BUFFALO, NY - March 18, 2025 – A new precision oncology paper was #published in Oncotarget, Volume 16, on March 12, 2025, titled “Worldwide Innovative Network (WIN) Consortium in Personalized Cancer Medicine: Bringing next-generation precision oncology to patients."

Led by Oncotarget Editor-in-Chief Dr. Wafik S. El-Deiry and a global team of researchers, this special publication highlights the groundbreaking work of the Worldwide Innovative Network (WIN) Consortium, a global collaboration dedicated to transforming cancer care through personalized medicine. By leveraging artificial intelligence (AI), molecular profiling, and innovative clinical trials, WIN is helping clinicians tailor treatments to each patient’s unique cancer profile—moving beyond the traditional one-size-fits-all approach.

The WIN Consortium is a fast-moving, non-profit organization bringing together nearly 40 academic, industry, and research institutions, along with patient advocacy groups, across 18 countries and five continents. Founded in 2010 in France by Dr. John Mendelsohn (MD Anderson Cancer Center) and Dr. Thomas Tursz (Gustave Roussy), WIN has been led by different renowned experts. Currently under Dr. El-Deiry’s leadership, WIN continues to break barriers in cancer research, ensuring cutting-edge treatments reach patients worldwide.

“The WIN global consortium is ready to take up the challenge by bringing the best possible Precision Oncology trial to patients.”

One of WIN’s most significant contributions is the development of N-of-1 clinical trials, a revolutionary approach that personalizes cancer treatment based on a patient’s specific tumor characteristics. Unlike traditional trials that test drugs on large groups, N-of-1 trials focus on finding the best therapy for an individual patient using AI-driven algorithms, genomic analysis, and real-world data. WIN’s WINTHER trial was one of the first to use both DNA and RNA analysis to match patients with the most effective therapies, while the WINGPO trial builds on this approach by integrating AI and liquid biopsies to refine treatment selection. These innovations are helping clinicians make more precise treatment decisions and improving outcomes for cancer patients.

While advancing research, the WIN Consortium is also addressing major challenges in precision oncology, including drug accessibility, regulatory barriers, and disparities in global healthcare. By working closely with governments, pharmaceutical companies, and advocacy organizations, WIN is aiming to ensure that life-saving treatments are accessible to all patients, regardless of location or financial status.

WIN’s mission is clear: to accelerate the future of precision oncology by delivering the latest scientific advancements into real-world cancer care. As the field continues to evolve, WIN remains at the forefront, developing next-generation trials and leveraging AI-driven insights to improve patient outcomes. Through global collaboration and groundbreaking research, the WIN Consortium is shaping a future where every cancer patient receives the most effective, personalized treatment possible.

DOI - https://doi.org/10.18632/oncotarget.28703

Correspondence to - Wafik S. El-Deiry - wafik@brown.edu

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

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com.

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WIN Consortium Leading the Future of Precision Cancer Medicine

BUFFALO, NY — March 19, 2025 — A new #research paper was #published in Aging (Aging-US) on February 27, 2025, in Volume 17, Issue 2, titled “Age, sex, and mitochondrial-haplotype influence gut microbiome composition and metabolites in a genetically diverse rat model.”

The research team, led by first author Hoang Van M. Nguyen and corresponding author Archana Unnikrishnan from the University of Oklahoma Health Sciences, studied how aging affects gut bacteria in a special group of rats generated to have genetic diversity similar to humans. Their research found that both biological sex and mitochondrial DNA—the small set of genes inherited only from mothers—play a key role in how gut bacteria change over time.

The gut microbiome, a collection of bacteria in the intestines, affects digestion, metabolism, and even brain function. As people age, these bacteria shift, and some of these changes are linked to diseases like Alzheimer’s, Parkinson’s, and metabolic disorders. However, most studies have looked at either men or women without comparing differences between sexes, and few have explored how mitochondrial DNA might influence these changes.

To better understand these factors, researchers analyzed fecal samples from the genetically diverse rats to assess gut bacteria composition and metabolic byproducts. The results showed that aging affects gut bacteria differently in males and females. More bacterial species changed with age in female rats than in males, and only a few changes were consistent across both sexes. These findings suggest that men and women may experience aging differently at the microbial level, which could impact nutrition and disease risk.

“Five microbial species changed significantly with age in male rats compared to nine microbial species in female rats. Only three of these microbes changed with age in both male and female rats.”

Another key discovery was that mitochondrial DNA influences how gut bacteria evolve with age. These effects were different in males and females, suggesting a deeper connection between mitochondrial function and gut health, with potential implications for personalized medicine and aging research.

In addition to studying bacteria, the researchers analyzed metabolic compounds such as short-chain fatty acids and bile acids, which help with digestion. They found that aging altered these compounds based on both sex and mitochondrial DNA. For example, older female rats had higher levels of short-chain fatty acids in their feces, possibly due to differences in nutrient absorption.

This study highlights new factors that shape the gut microbiome in aging populations. Understanding how biological sex and mitochondrial DNA influence these changes could lead to targeted approaches for maintaining gut health and preventing age-related diseases. These findings reinforce the importance of personalized health strategies that consider both genetic and biological differences.

DOI - https://doi.org/10.18632/aging.206211

Corresponding author - Archana Unnikrishnan - archana-unnikrishnan@ouhsc.edu

Video short - https://www.youtube.com/watch?v=RtsqRi2_uAI

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The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

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Influence of Age, Sex, and Mitochondrial Haplotype on Gut Microbiome in Rats

Could the air we breathe, the food we eat, or the chemicals in our everyday environment be accelerating our aging process? A recent study published in Aging suggests that exposure to certain environmental chemicals may be linked to faster biological aging through changes in DNA. These findings could have major implications for public health and longevity.

Understanding How Scientists Measure Aging at the DNA Level
Aging is not just about wrinkles and gray hair—it happens at the molecular level too. Scientists use epigenetic clocks to measure biological aging, which can differ from a person’s actual chronological age. These clocks track DNA methylation, a type of chemical modification that can change over time due to environmental factors like diet, pollution, and chemical exposure. Until now, there has been little research into how widespread environmental chemicals impact these aging markers. 

The Study: Investigating the Impact of Environmental Pollutants on Aging
A research team led by first author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, conducted an exposome-wide association study to examine how different environmental pollutants affect epigenetic aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they analyzed blood and urine samples from 2,346 adults aged 50 to 84. The study measured 64 environmental chemicals, including heavy metals, pesticides, plastics, and tobacco-related compounds, to identify potential links to accelerated aging. The study titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey,” was published in Aging on February 11, 2025.

Full blog - https://aging-us.org/2025/03/how-environmental-chemicals-may-accelerate-biological-aging/

Paper DOI - https://doi.org/10.18632/aging.206201

Corresponding author - Andres Cardenas - andresca@stanford.edu

Video short - https://www.youtube.com/watch?v=WcL-K399a7M

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Keywords - aging, epigenetic aging, environmental exposures, exposome, epigenetics

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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How Environmental Chemicals May Accelerate Biological Aging

BUFFALO, NY - March 21, 2025 – A new #editorial was #published in Oncotarget, Volume 16, on March 13, 2025, titled “No disease left behind."

In this editorial, Dr. Muzamil Arshad from the University of Chicago Medical Center and colleagues highlight a growing concern in cancer care: radiotherapy may leave behind microscopic cancer even when scan images suggest the tumor is gone. The authors argue that this “residual disease” is more common than expected and is linked to worse long-term outcomes. Their perspective calls for a rethinking of how treatment success is judged and how cancer is followed up after therapy.

Radiotherapy, especially a form known as stereotactic ablative radiotherapy (SABR), is widely used to treat cancers in the lung, liver, prostate, and other organs.  SABR delivers high-dose radiation with outstanding precision and often shows excellent results on scans. However, the authors highlight that relying only on imaging may not provide a complete picture. Months or even years later, follow-up biopsies frequently reveal cancer cells that scan imaging tests were unable to identify.

“Residual cancer is identified on histology in 40% of lung, 57–69% of renal cell, 7.7–47.6% of prostate and 0–86.7% of hepatocellular carcinoma.”

This gap between what scans show and what tissue analysis finds can have serious consequences. Studies across several cancer types have shown that patients with residual disease—even if small—are more likely to experience cancer recurrence and shorter survival. This pattern holds true for rectal, cervical, prostate, and liver cancers, among others. In some cases, not  destroying the tumor completely may allow it to spread to distant organs.

The authors point out that a complete response on scan imaging does not necessarily indicate the complete disappearance of the tumor. This mismatch can mislead both clinicians and patients into thinking treatment was more successful than it truly was. The editorial encourages more regular use of biopsy-based tests and new strategies to increase the true effectiveness—or “ablative power”—of SABR.

They also discuss promising approaches to improve outcomes, including increasing radiation doses and combining radiotherapy with other therapies, such as immune checkpoint inhibitors. While some trials have shown better tumor control with these combinations, results have not been consistent, and more research is needed to refine these strategies.

In summary, this editorial encourages the cancer care community to look beyond the scan images. Residual cancer may remain even when imaging looks clear, and recognizing this hidden threat is key to improving long-term outcomes. The goal is not just to shrink tumors on screen but to fully eliminate the disease.

DOI - https://doi.org/10.18632/oncotarget.28700

Correspondence to - Muzamil Arshad - muzamil.arshad@uchicagomedicine.org

Video short - https://www.youtube.com/watch?v=XC0XNjJjC2o

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About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Clear Scans Can Be Misleading: Residual Cancer Linked to Worse Outcomes

In this installment of the Longevity & Aging Series, Dr. Julia Sidorova from the Department of Laboratory Medicine and Pathology at the University of Washington (Seattle, WA) joined host Dr. Evgeniy Galimov to discuss her co-authored research paper from Volume 16, Issue 20 of Aging (Aging-US), titled “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.”

DOI - https://doi.org/10.18632/aging.206132

Corresponding Author - Julia M. Sidorova - julias@uw.edu

Video interview - https://www.youtube.com/watch?v=3yn8O-JA6GE

Abstract

Werner syndrome of premature aging is caused by mutations in the WRN RECQ helicase/exonuclease, which functions in DNA replication, repair, transcription, and telomere maintenance. How the loss of WRN accelerates aging is not understood in full. Here we show that WRN is necessary for optimal constitutive heterochromatin levels in proliferating human fibroblasts. Locally, WRN deficiency derepresses SATII pericentromeric satellite repeats but does not reduce replication fork progression on SATII repeats. Globally, WRN loss reduces a subset of protein-protein interactions responsible for the organization of constitutive heterochromatin in the nucleus, namely, the interactions involving Lamin B1 and Lamin B receptor, LBR. Both the mRNA level and subcellular distribution of LBR are affected by WRN deficiency, and unlike the former, the latter phenotype does not require WRN catalytic activities. The phenotypes of heterochromatin disruption seen in WRN-deficient proliferating fibroblasts are also observed in WRN-proficient fibroblasts undergoing replicative or oncogene-induced senescence. WRN interacts with histone deacetylase 2, HDAC2; WRN/HDAC2 association is mediated by heterochromatin protein alpha, HP1α, and WRN complexes with HP1α and HDAC2 are downregulated in senescing cells. The data suggest that the effect of WRN loss on heterochromatin is separable from senescence program, but mimics at least some of the heterochromatin changes associated with it.

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Keywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeats

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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Longevity & Aging Series (S3, E2): Dr. Julia Sidorova

BUFFALO, NY — March 25, 2025 — A new #research paper was #published in Aging (Aging-US) on January 31, 2025, in Volume 17, Issue 2, titled “Cysteinyl leukotriene receptor 1 modulates retinal immune cells, vascularity and proteolytic activity in aged mice.”

The study, led by first author and corresponding author Andreas Koller from the University Hospital of the Paracelsus Medical University, found that blocking an inflammatory receptor called CysLTR1 in the retinas of aging mice improved retinal health. These findings suggest a new approach to slowing age-related vision loss and protecting eye health in older adults.

Age-related vision problems are a growing concern worldwide, and inflammation plays a key role in damaging the retina over time. The retina is the part of the eye that captures light and sends visual signals to the brain, making it vital for clear eyesight. In this study, scientists focused on the CysLTR1 receptor, which is known to promote inflammation and is found in high amounts in the retina. They explored whether blocking this receptor could reduce the harmful effects of aging in the eye.

To achieve this, researchers treated aged mice with montelukast (MTK), a drug commonly used for asthma, which specifically blocks CysLTR1. The oral treatment lasted eight weeks and results were compared with both untreated aged mice and healthy young mice. After treatment, the older mice showed major improvements in retinal health.

One key finding was a reduction in immune cells called microglia, which tend to increase with age and contribute to chronic inflammation in the retina. With CysLTR1 blocked, the number of these immune cells dropped significantly, suggesting reduced retinal inflammation. Lower inflammation is linked to a lower risk of age-related eye diseases like macular degeneration.

“The reduction in immune cells caused by Cysltr1 suppression may dampen neuroinflammation, a known promoter of tissue aging.”

Another important result was the restoration of blood vessel function. The tiny blood vessels in the retina had narrowed in aging mice, reducing blood flow and oxygen supply to the eye. MTK treatment increased the diameter of these vessels, improving circulation and possibly helping the retina work more efficiently.

The study also indicated that blocking CysLTR1 helped boost the retina’s natural ability to clear out waste proteins. As we age, this cleaning process slows down, allowing harmful material to build up in the eye. After treatment, the aged mice had stronger proteasome activity—the system responsible for breaking down cellular waste—and fewer signs of waste accumulation.

Importantly, the treatment did not harm retinal nerve cells, which are essential for vision. This evidence indicates that the therapy was not only effective but also safe.

While more research is needed to confirm these results in humans, this study highlights the potential of repurposing MTK to protect against age-related vision decline. Because it is already an approved drug, testing it for age-related eye diseases like macular degeneration or diabetic retinopathy could move forward more quickly. Blocking inflammation and supporting the eye’s natural cleaning systems may be a promising new way to preserve healthy vision in aging populations.

DOI - https://doi.org/10.18632/aging.206193

Corresponding author - Andreas Koller - a.koller@salk.at

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

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Montelukast Improves Retinal Health in Aging Mice

BUFFALO, NY - March 25, 2025 – A new #review was #published in Oncotarget, Volume 16, on March 13, 2025, titled “Signaling pathway dysregulation in breast cancer."

In this review article, Dinara Ryspayeva and colleagues from Brown University provide a detailed look at how breast cancer cells change the way they communicate and grow—helping tumors survive, spread, and resist treatment. The review highlights how certain gene mutations and disrupted signaling pathways influence therapy response across different types of breast cancer. It also outlines current treatment strategies and clinical trials, offering insights that could improve care for patients with aggressive or hard-to-treat cancers.

Breast cancer is the most common cancer in women and a major cause of cancer-related deaths worldwide. While many patients respond to treatment at first, some cancers return or stop responding. The review explores how signaling disruptions inside tumor cells are often behind these setbacks.

The authors discuss several major pathways involved in breast cancer, including PI3K/Akt/mTOR, RAS/RAF/MEK/ERK, HER2, Wnt/β-catenin, Notch, NF-κB, and the DNA damage response (DDR). These pathways help control cell growth, division, DNA repair, and survival. When altered by mutations or other changes, they can promote tumor progression and resistance to treatment.

One of the most disrupted pathways is PI3K/Akt/mTOR. It plays a central role in cell growth, but in many breast cancers—especially hormone receptor-positive and HER2-positive types—it becomes overactive due to gene mutations, or the loss of a tumor-suppressing protein called PTEN.

“Up to 25–40% of BC cases exhibit variations that hyperactivate the PI3K/Akt/mTOR pathway, underscoring its critical role in oncogenesis.”

Another key pathway, RAS/RAF/MEK/ERK, can also promote tumor growth. Even without mutations, it may become active when primary pathways are blocked, particularly in HER2-positive and triple-negative breast cancers.

The review also highlights several new and emerging treatments aimed at blocking down these signaling pathways. Some drugs are already approved, while others are in clinical trials. The authors suggest that combining different treatments may help stop multiple pathways at once, making it harder for cancer cells to adapt. Matching treatments to each tumor’s unique genetic changes could also improve patient outcomes.

This comprehensive review gives researchers and clinicians a clearer understanding of how breast cancer resists treatment and where future therapies should focus. A better understanding of these disrupted signaling systems could lead to more personalized and effective treatments for patients facing aggressive or recurring disease.

DOI - https://doi.org/10.18632/oncotarget.28701

Correspondence to - Dinara Ryspayeva - dinara_ryspayeva@brown.edu

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

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About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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