BUFFALO, NY — June 17, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 1, 2025, titled “Oxytocin modulates insulin and GLP-1 secretion in pancreatic islets.”

In this study, scientists from Fukushima Medical University School of Medicine investigated how the hormone oxytocin (Oxt) influences insulin levels by acting on specific cells in the pancreas. The team led by first author Kasumi Hattori and corresponding authors Kenju Shimomura and Yuko Maejima discovered that oxytocin may indirectly increase insulin secretion by triggering another hormone, GLP-1, from within the pancreas. This finding could lead to new strategies for improving blood sugar control in people with diabetes.

Oxytocin is commonly known for its roles in childbirth and social bonding, but scientists have also been exploring its effects on metabolism. While previous studies offered mixed results about whether oxytocin raises or lowers blood sugar, this research brings new clarity. The study focused on oxytocin’s impact on insulin and a hormone called GLP-1, which helps regulate insulin production. Researchers tested this by using mice with and without oxytocin receptors and found that oxytocin’s ability to raise insulin levels depended on the presence of these receptors and high blood sugar conditions.

Researchers found that oxytocin stimulates the release of “intra-islet GLP-1,” a form of GLP-1 produced inside the pancreas rather than the intestine. In the pancreas, insulin is produced by beta cells, while alpha cells produce glucagon, a hormone that raises blood sugar. But recent research, including this study, has shown that alpha cells can also release GLP-1, which in turn helps beta cells secrete insulin. Oxytocin appears to increase this internal GLP-1 release, especially when blood sugar levels are high, thereby leading to insulin release in a natural and targeted way.

In this study researchers were also able to detect the difference between oxytocin’s effect on blood sugar and its effect on insulin. They observed that right after oxytocin was given, blood sugar levels rose in all mice—even in those that lacked oxytocin receptors. However, only the mice with working oxytocin receptors showed a later increase in insulin. This suggests that oxytocin may trigger insulin production through a separate, receptor-dependent pathway involving the hormone GLP-1.

"WT mice showed a significant increase in insulin levels at 15-min, while OxtR KO mice did not."

This indirect action—oxytocin triggering alpha cells to release GLP-1, which then acts on beta cells—may represent a novel mechanism for controlling insulin release. It also explains why oxytocin does not increase insulin in low-glucose conditions, making it a potentially safer option for regulating blood sugar.

As treatments for type 2 diabetes increasingly focus on GLP-1–based drugs, this study opens the door to using oxytocin or similar compounds to naturally enhance the body’s own insulin-producing system. With further research, this mechanism could help develop new therapies that better mimic the body’s natural glucose control, particularly beneficial for older adults with diabetes.

DOI - https://doi.org/10.18632/aging.206244

Corresponding authors - Kenju Shimomura - shimomur@fmu.ac.jp, and Yuko Maejima - maejimay@fmu.ac.jp

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New Hormonal Pathway Links Oxytocin to Insulin Secretion in the Pancreas

BUFFALO, NY - June 17, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 10, 2025, titled “Exceptional responders to immunotherapy in pancreatic cancer: A multi-institutional case series of a rare occurrence.”

The study, led by first author Kavin Sugumar and corresponding author Jordan M. Winter, from University Hospitals Seidman Cancer Center, reports on a rare group of pancreatic cancer (PC) patients who responded remarkably well to immunotherapy, a treatment typically considered ineffective for this cancer type. The analysis, which includes data from 14 patients across multiple U.S. institutions, identifies outcomes that could help refine treatment strategies for one of the most aggressive and deadly forms of cancer.

“Between 2020–21, 471 oncologists from 91 major cancer centers in the United States were contacted.”

Pancreatic cancer has among the lowest survival rates and few effective therapies. While immunotherapy has transformed the treatment landscape for several other cancers, it generally offers little benefit for pancreatic cancer. However, this study highlights a small but important group of patients who experienced significant and sustained responses to immune-based treatment without chemotherapy. Most had advanced or metastatic disease and had already progressed after standard treatments.

Among the 14 patients, 82% had partial tumor shrinkage, and nearly one-third had a notable decrease in tumor markers. The median progression-free survival was 12 months, and most patients were still alive at follow-up, with survival rates of 80% at one year and 70% at two years. These outcomes contrast sharply with standard therapies, which often provide only a few months of benefit for similar patients.

Interestingly, while some patients had high microsatellite instability (MSI-high)—a known marker for immunotherapy success—more than half did not, suggesting other biological mechanisms may be involved. This result highlights the need for new biomarkers to be discovered to predict treatment response in future studies.

This case series is the largest focused exclusively on exceptional immunotherapy responders in pancreatic cancer. By excluding patients who received chemotherapy, the study isolates the effects of immune-based drugs, including PD-1 inhibitors such as pembrolizumab and nivolumab, CTLA-4 inhibitors like ipilimumab, and agents targeting macrophages.

While the sample size is small, the findings challenge the assumption that immunotherapy is ineffective for nearly all pancreatic cancer patients. The study suggests that, under certain biological conditions, this treatment can be remarkably successful. Further research is needed to understand the underlying mechanisms.

This work supports the need to reconsider how clinical trials are designed for pancreatic cancer and who is eligible for immunotherapy. Broader criteria and more personalized molecular profiling could help uncover hidden opportunities for treatment in this highly lethal cancer.

DOI - https://doi.org/10.18632/oncotarget.28739

Correspondence to - Jordan M. Winter - jordan.winter@UHHospitals.org

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

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Oncotarget

Rare Pancreatic Cancer Patients Show Strong Response to Immunotherapy

BUFFALO, NY — June 18, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 12, 2025, titled “Frailty transitions in electronic health records: who first? what first?”

The study, led by Fabienne Hershkowitz Sikron from Meuhedet HMO, analyzed how frailty develops over time in older adults using electronic health record data from nearly 120,000 individuals aged 65 and above. Researchers found that frailty worsened in over 13% of participants within a year, particularly among women, adults aged 85 or older, and people with chronic illnesses, while nearly 3% showed signs of improvement. The findings highlight early indicators of decline that could help guide preventive care and improve outcomes for aging populations.

Frailty is a condition marked by increased vulnerability to health complications and tends to change gradually. The study used the Meuhedet Electronic Frailty Index (MEFI) to track yearly transitions in frailty among older adults in Israel. While many people remained in the same frailty category, a significant proportion experienced deterioration in just one year, and a smaller group improved.

“Worsening frailty is defined as a higher frailty level one year later in 2024 compared to 2023. A new frailty deficit is defined as a deficit appearing in 2024 that was not present in 2023.”

Those most at risk of worsening included adults over 85, women, individuals from lower socio-economic backgrounds, and members of the Arab sector. Additional predictors of decline included recent hospitalizations, multiple chronic diseases, and signs of cognitive or mobility issues. Importantly, the first signs of worsening were often not new chronic conditions but more manageable health deficits such as sleep disturbances, muscle weakness, hearing loss, and memory decline. Those who improved were more likely to be younger, male, from higher socio-economic backgrounds, and have fewer chronic conditions and hospitalizations.

The study also found that common chronic illnesses like diabetes and hypertension were often already present and did not usually signal the beginning of frailty progression. Instead, declines in overall function and quality of life were more frequently the first new issues to appear. This suggests that early intervention on modifiable health deficits could delay or prevent further decline.

This work is one of the first large-scale, real-world studies to identify both who is most likely to worsen first and what health problems typically appear first. The authors emphasize the importance of using routinely collected electronic medical data to monitor frailty and tailor care. By doing so, health providers can implement timely strategies to reduce disease burden and support aging individuals in maintaining independence.

These findings support the creation of proactive health programs focused on maintaining physical strength, cognitive function, and sensory abilities. Preventing frailty progression can reduce hospitalizations, ease disease burden, and help older adults maintain independence and a higher quality of life.

DOI - https://doi.org/10.18632/aging.206247

Corresponding author - Fabienne Hershkowitz Sikron - fabian_hershkowitz@meuhedet.co.il

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Early Signs of Frailty Detected Through Health Records in Aging Adults

Dr. Josh Mitteldorf summarizes his #research perspective #published in Volume 17, Issue 5 of Aging (Aging-US), titled “Methylation clocks for evaluation of anti-aging interventions.”

DOI - https://doi.org/10.18632/aging.206245

Corresponding author - Josh Mitteldorf - aging.advice@gmail.com

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Abstract

Methylation clocks have found their way into the community of aging research as a way to test anti-aging interventions without having to wait for mortality statistics. But methylation is a primary means of epigenetic control, and presumably has evolved under strong selection. Hence, if methylation patterns change consistently at late ages it must mean one of two things. Either (1) the body is evolved to destroy itself (with inflammation, autoimmunity, etc.), and the observed methylation changes are a means to this end; or (2) the body detects accumulated damage, and is ramping up repair mechanisms in a campaign to rescue itself. My thesis herein is that both Type 1 and Type 2 changes are occurring, but that only Type 1 changes are useful in constructing methylation clocks to evaluate anti-aging interventions. This is because a therapy that sets back Type 1 changes to an earlier age state has stopped the body from destroying itself; but a therapy that sets back Type 2 changes has stopped the body from repairing itself. Thus, a major challenge before the community of epigenetic clock developers is to distinguish Type 2 from Type 1. The existence of Type 1 epigenetic changes is in conflict with conventional Darwinian thinking, and this has prompted some researchers to explore the possibility that Type 1 changes might be a form of stochastic epigenetic drift. I argue herein that what seems like directed epigenetic change really is directed epigenetic change. Of five recent articles on “stochastic methylation clocks,” only one (from the Conboy lab) is based on truly stochastic changes. Using the Conboy methodology and a methylation database, I construct a measure of true methylation drift, and show that its correlation with age is too low to be useful.

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Keywords - aging, methylation, stochastic, entropy, programmed aging, aging clock, epigenetic clock

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Behind the Study: Using Methylation Clocks to Evaluate Anti-Aging Interventions

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

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

BUFFALO, NY — June 24, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 20, 2025, titled “Short-term moderate caloric restriction in the rhesus macaque attenuates markers of ovarian aging in select populations.”

In this study, led by first author Emma S. Gargus and corresponding author Francesca E. Duncan from Feinberg School of Medicine at Northwestern University, researchers explored how dietary changes impact ovarian aging in female rhesus macaques. They found that a three-year moderate reduction in caloric intake preserved a youthful distribution of ovarian follicles and reduced age-related tissue stiffness. These findings are relevant to women’s health as they suggest that caloric restriction (CR) may help delay the decline in reproductive function associated with aging.

Ovarian aging, which leads to reduced fertility and hormone production, is one of the earliest signs of aging in women. This study investigated whether a 30% reduction in caloric intake could protect the ovaries from age-related damage in nonhuman primates (NHP), whose reproductive biology closely mirrors that of humans. Ovaries were collected from young (10–13 years) and old (19–26 years) rhesus macaques who were either on a diet of moderate caloric restriction or a control diet for three years.

“To test the effect of CR on follicle number, follicles were analyzed in histological sections from animals across experimental cohorts: Young Control, Young CR, Old Control, Old CR (n = 4–8/group).”

Although total follicle numbers still declined with age, caloric restriction helped maintain the types of follicles most associated with reproductive potential. In older monkeys who were still cycling, even if irregularly, caloric restriction preserved more primordial follicles, the key indicators of ovarian reserve, than in those on a normal diet.

The benefits of caloric restriction were also seen in the structure of ovarian tissue. Normally, aging leads to fibrosis, a stiffening of the ovarian environment caused by increased collagen and decreased hyaluronic acid. This study showed that caloric restriction reduced this fibrotic process, suggesting a more supportive environment for maintaining reproductive health.

While the diet did not stop the overall loss of follicles with age, it improved the proportion of younger, more viable follicles in aging ovaries. The timing of the dietary intervention also appeared to matter. Positive effects were more noticeable in older animals with irregular cycles than in those who had completely stopped cycling. This indicates that starting caloric restriction at a certain point in the reproductive lifespan may yield the best results.

This research is an important step to identifying lifestyle-based strategies that can extend reproductive longevity. Although further studies are needed to test these findings in humans, the work supports the potential of moderate dietary changes to delay ovarian aging and help preserve fertility later in life.

DOI - https://doi.org/10.18632/aging.206253

Corresponding author - Francesca E. Duncan - f-duncan@northwestern.edu

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Moderate Caloric Restriction May Slow Ovarian Aging in Primates

BUFFALO, NY – June 24, 2025 – A new precision #oncology paper was #published in Volume 16 of Oncotarget on June 17, 2025, titled “Case Report WIN-MTB-2023001 WIN International Molecular Tumor Board A 62-year-old male with metastatic colorectal cancer with 5 prior lines of treatment.”

In this report, led by Alberto Hernando-Calvo from Vall d’Hebron University Hospital and Vall d’Hebron Institute of Oncology; Razelle Kurzrock from WIN Consortium and Medical College of Wisconsin; Oncotarget Editor-in-Chief Wafik S. El-Deiry from WIN Consortium and Legorreta Cancer Center at Brown University; and corresponding author Shai Magidi, also from WIN Consortium, along with colleagues, describe the case of a 62-year-old man with metastatic colorectal cancer who underwent multiple lines of therapy. After analysis, the WIN International Molecular Tumor Board proposed different personalized treatment plans based on the tumor’s unique genetic mutations. This case highlights the growing role of precision oncology in guiding therapies for patients with treatment-resistant cancers.

Colorectal cancer is one of the deadliest cancers worldwide, and managing advanced cases remains a significant challenge. This patient had already received five prior treatment regimens, including chemotherapy and targeted therapies. Although some treatments were initially beneficial, the cancer eventually developed resistance. Molecular analysis revealed key mutations in genes such as BRAF, MET, APC, TP53, and NRAS, which are often linked to aggressive tumor behavior and reduced treatment effectiveness.

With limited standard options left, the patient’s case was presented and reviewed by the WIN International Molecular Tumor Board, a global panel of cancer experts. The team analyzed the clinical history and genetic profile to design new treatment approaches. These involved off-label drug combinations tailored to the specific mutations found in the tumor. For example, one approach combined trametinib, a drug that blocks cancer cell growth signals, with amivantamab, an antibody that attacks cancer-related proteins MET and EGFR, and regorafenib, which helps cut off blood supply to tumors and may counteract effects from APC and TP53 mutations.

“Another option was trametinib at 1 mg daily, cetuximab (EGFR antibody), 250 mg/m² IV every two-weeks, and cabozantinib (MET and VEGFR inhibitor), 40 mg po daily.”

This case reflects a shift in cancer care from standardized protocols to precision approaches, where therapy is selected based on a tumor’s molecular features. Such strategies aim to delay resistance and slow disease progression more effectively. The WIN International Molecular Tumor Board also discussed practical challenges, including access to medications, combining off-label drugs, and the difficulties of enrolling patients in clinical trials after multiple prior treatments.

Although the ultimate treatment decision remained with the patient’s physician, this report shows how international collaboration and precision oncology can expand options for patients facing limited alternatives. It also emphasizes the value of repeat genetic analysis during disease progression to monitor new mutations in the tumor that may impact treatment.

While the patient ultimately died from cancer progression, this case serves as a model for how molecular analysis and expert input can be used to guide treatment even in complex and metastatic colorectal cancer. As personalized cancer strategies continue to evolve, they may offer potential pathways for patients who have exhausted standard treatment options.

DOI - https://doi.org/10.18632/oncotarget.28744

Correspondence to - Shai Magidi - shai.magidi@winconsortium.org

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WIN International Molecular Tumor Board Recommends Tailored Treatment for Advanced Colorectal Cancer

BUFFALO, NY — June 25, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 28, 2025, titled “Investigating telomere length in progeroid syndromes: implications for aging disorders.”

In this study, led by first author Luma Srour and corresponding authors Yosra Bejaoui and Nady El Hajj, from Hamad Bin Khalifa University, Qatar Foundation, researchers investigated whether shortened telomeres, a marker of cellular aging, are present across various rare genetic disorders that mimic early aging, known as progeroid syndromes. The study found that telomere shortening, also called telomere attrition, is not a shared characteristic of all these disorders. This finding is important because it challenges the belief that telomere loss is a common thread in premature aging and could help refine how these syndromes are studied and treated.

Progeroid syndromes are rare conditions that cause individuals to display symptoms of aging far earlier than expected. While some of these syndromes share signs of typical aging, others arise from very different genetic alterations. Researchers focused on comparing telomere length in individuals with several of these syndromes to better understand how aging develops at the cellular level. Telomeres are protective ends of chromosomes that shorten as cells divide, acting as a biological clock linked to aging and disease.

Using DNA methylation data from blood samples, the team analyzed telomere length in patients with six progeroid syndromes: Werner Syndrome, Hutchinson-Gilford Progeria Syndrome, Berardinelli-Seip Congenital Lipodystrophy type 2, Dyskeratosis Congenita, Cerebroretinal Microangiopathy with Calcifications and Cysts, and Wiedemann-Rautenstrauch Syndrome. They found significant telomere shortening only in classical Werner Syndrome, Berardinelli-Seip Congenital Lipodystrophy type 2, and Dyskeratosis Congenita. Other syndromes, including the widely studied Hutchinson-Gilford Progeria Syndrome, did not show this pattern.

“To investigate whether progeroid syndromes have telomere attrition, we calculated telomere length using the DNAmAge web-based calculator.”

The findings suggest that telomere shortening cannot be used as a universal marker for all forms of premature aging. In fact, some syndromes linked to DNA repair problems showed telomere damage, while others with different genetic mutations did not. These results indicate that the underlying biology of each syndrome is crucial in determining whether telomere shortening plays a role. Researchers also compared telomere lengths in people with genetic variants known to protect against age-related diseases. Those with protective genes had longer telomeres than people with progeroid syndromes.

This study challenges assumptions about aging in rare disorders and highlights the need for more personalized approaches in aging research. By identifying which syndromes involve telomere attrition, it opens new avenues for treating or delaying aging-related symptoms. Future research may explore other biological factors behind premature aging and how genetic differences influence the aging process.

DOI - https://doi.org/10.18632/aging.206255

Corresponding authors - Yosra Bejaoui - yob4003@qatar-med.cornell.edu, and Nady El Hajj - nelhajj@hbku.edu.qa

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New Research Finds Telomere Shortening Not Consistent Across Premature Aging Disorders

Recent discoveries in #aging research reveal a powerful insight: the biological changes that lead to chronic #diseases begin far earlier than most people realize—often in midlife, well before symptoms appear. This early phase offers a valuable opportunity for prevention. As highlighted in a recent editorial by Marco Demaria, Editor-in-Chief of Aging and a researcher at the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen, and the University of Groningen (RUG), the aging process itself – not just the diseases it produces – can and should be a primary focus of healthcare. 

The Problem with Traditional Medicine

While modern healthcare has extended lifespan and improved treatment for many diseases, it tends to be insufficient in addressing the complex needs of aging populations. Older individuals frequently experience multiple chronic conditions simultaneously, such as cardiovascular disease, diabetes, cancer, and neurodegenerative disorders. This state of multimorbidity complicates care, increases the use of multiple medications, and reduces quality of life. The dominant traditional healthcare system, which typically begins only after symptoms appear, is costly and insufficient for addressing the interconnected nature of these conditions.

A New Model for Healthcare: Insights from the Editorial

In his recent editorial, “Rethinking healthcare through aging biology,” published in Aging Volume 17, Issue 5, Dr. Demaria outlines a shift from disease-specific treatment to targeting the biological mechanisms of aging itself, a more integrated and forward-looking approach. He presents three evolving healthcare models.

Full blog - https://aging-us.org/2025/06/a-new-vision-for-healthcare-addressing-aging-before-disease-begins/

Paper DOI - https://doi.org/10.18632/aging.206262

Corresponding author - Marco Demaria - m.demaria@umcg.nl

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Keywords - aging, healthcare, senolytics, epigenetics, medical education

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A New Vision for Healthcare: Addressing Aging Before Disease Begins

BUFFALO, NY – June 27, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 17, 2025, titled “Molecular landscape of HER2-mutated non-small cell lung cancer in Northeastern Brazil: Clinical, histopathological, and genomic insights.”

In this study, researchers led by first authors Cleto Dantas Nogueira from the Federal University of Ceará and Argos Pathology Laboratory and Samuel Frota from Argos Pathology Laboratory, along with corresponding author Fabio Tavora from the previously mentioned institutions and Messejana Heart and Lung Hospital, investigated how HER2 gene mutations appear in cases of non-small cell lung cancer (NSCLC) in Northeastern Brazil. The team found that HER2 mutations showed significant genetic diversity and were often associated with other cancer-related genetic changes. These findings revealed diagnostic and treatment challenges in a population that is rarely studied, emphasizing the need for expanded access to molecular testing and targeted therapies.

HER2 mutations are a known factor in several cancers, including breast and gastric cancers. In lung cancer—particularly NSCLC—these mutations are less common but remain clinically significant. Most existing research on HER2-mutated lung cancer focuses on high-income countries, leaving important gaps in knowledge about underrepresented regions such as Latin America. This study helps fill that gap by analyzing 13 patients with HER2-mutated NSCLC using clinical, pathological, and genomic data.

The patients ranged in age from 34 to 82 years, and more than half were women. About half had never smoked. Their tumors often displayed complex genetic profiles, including additional mutations in genes such as TP53, KRAS, and STK11. The most common HER2 mutation identified was an insertion in exon 20, a known hotspot for activating mutations.

“Trastuzumab deruxtecan (T-DXd) is the first HER2-targeted agent to show clinical efficacy in HER2-mutant non-small cell lung cancer (HER2m NSCLC).”

Treatment strategies among the patients varied. Only one individual received HER2-targeted therapy. Most were treated with surgery, chemotherapy, immunotherapy, or a combination of these approaches. Outcomes also differed, with some patients surviving for years and others dying within months of diagnosis. These findings reinforce the need for early diagnosis and improved access to advanced treatments, particularly in low-resource settings.

The study emphasizes the value of comprehensive molecular profiling in NSCLC. Because HER2 mutations often occur alongside other genetic alterations, full genomic analysis is crucial for guiding treatment decisions. Yet, such testing is not always available. The researchers propose a tiered diagnostic approach, beginning with basic screening and expanding to more advanced tests when necessary, to enhance patient care.

This study provides valuable insights into the molecular characteristics of HER2-mutated NSCLC in a Brazilian population, highlighting the complexity and clinical relevance of these alterations. Larger studies are needed to clarify the prevalence and prognostic significance of HER2 mutations, as well as their impact on treatment response and survival. This knowledge is essential for advancing effective HER2-targeted therapies. The findings also support broader implementation of international clinical guidelines in Latin America and highlight the critical need to include underrepresented populations in cancer research.

DOI - https://doi.org/10.18632/oncotarget.28737

Correspondence to - Fabio Tavora - stellacpak@outlook.com

Video short - https://www.youtube.com/watch?v=hr5R9iDBFFI

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

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HER2-Mutated NSCLC in Brazil Shows Diverse Genetic Patterns and Treatment Gaps

Cancer and aging are two sides of age-related tumorigenesis.

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.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

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