A new research paper was published in Aging (Aging-US) Volume 14, Issue 23, entitled, “DNA methylation-based measures of biological aging and cognitive decline over 16-years: preliminary longitudinal findings in midlife.”

DNA methylation-based (DNAm) measures of biological aging associate with increased risk of morbidity and mortality, but their links with cognitive decline are less established. 

In this new study, researchers Rebecca G. Reed, Judith E. Carroll, Anna L. Marsland, and Stephen B. Manuck from University of Pittsburgh and University of California examined changes over a 16-year interval in epigenetic clocks (the traditional and principal components [PC]-based Horvath, Hannum, PhenoAge, GrimAge) and pace of aging measures (Dunedin PoAm, Dunedin PACE) in 48 midlife adults enrolled in the longitudinal arm of the Adult Health and Behavior project (56% Female, baseline AgeM = 44.7 years), selected for discrepant cognitive trajectories. 

“We hypothesized that overall, cognitive Decliners would be biologically older compared to cognitive Maintainers.”

Cognitive Decliners (N = 24) were selected based on declines in a composite score derived from neuropsychological tests and matched with participants who did not show any decline, Maintainers (N = 24). Multilevel models with repeated DNAm measures within person tested the main effects of time, group, and group by time interactions. DNAm measures significantly increased over time generally consistent with elapsed time between study visits. 

There were also group differences: overall, Cognitive Decliners had an older PC-GrimAge and faster pace of aging (Dunedin PoAm, Dunedin PACE) than Cognitive Maintainers. There were no significant group by time interactions, suggesting accelerated epigenetic aging in Decliners remained constant over time. Older PC-GrimAge and faster pace of aging may be particularly sensitive to cognitive decline in midlife.

“In conclusion, these preliminary results suggest PC-GrimAge and DNAm based pace of aging measures (Dunedin PoAm and PACE) associate with 16-year, neuropsychologically-validated cognitive decline in midlife. The results warrant a larger-scale study to better examine longitudinal associations between changes in DNAm measures and changes across multiple cognitive domains. Ultimately, establishing DNAm measures as biomarkers of cognitive function in midlife may offer pre-clinical markers of a molecular aging mechanism that can help identify individuals at increased risk for cognitive impairment and dementia in later life.”

DOI: https://doi.org/10.18632/aging.204376 

Corresponding Author: Rebecca G. Reed - rebecca.reed@pitt.edu 

Keywords: epigenetic age, aging biomarker, pace of aging, geroscience, cognitive aging

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About Aging-US:

Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Aging (Aging-US)

DNA Methylation-Based Measures of Biological Aging and Cognitive Decline Over 16 Years

BUFFALO, NY — July 30, 2025 — A new #research paper was #published in Aging (Aging-US) on July 23, 2025, titled “Second generation DNA methylation age predicts cognitive change in midlife: the moderating role of childhood socioeconomic status.”

In this study, led by Sophie A. Bell and Eric Turkheimer from the University of Virginia, researchers investigated how biological aging, measured through DNA methylation, is connected to changes in thinking skills during midlife and whether childhood socioeconomic status influences this relationship. 

Biological age provides a picture of how the body is aging that goes beyond simply counting years. In this study, researchers used both first- and second-generation DNA methylation clocks—tools that track chemical changes in DNA as markers of aging. GrimAge and PhenoAge, the second-generation clocks designed to reflect broader health and aging processes, were more accurate at predicting long-term changes in Intelligence Quotient (IQ) than the first-generation models that only estimated chronological age. The study analyzed 287 participants from the Louisville Twin Study, which is a long-term project that has followed twins from childhood into midlife.

“DNAmAge was estimated with five commonly used algorithms, or epigenetic clocks (Horvath, Horvath Skin and Blood, GrimAge, and PhenoAge).”

The results showed that twins with more rapid epigenetic aging had a larger drop in IQ scores. This pattern remained even after considering genetic background and early family environment, made possible by the twin-based design. Importantly, the relationship was strongest in twins who had grown up in families with lower socioeconomic status. This finding suggests that early-life disadvantage may make individuals more vulnerable to the effects of biological aging on brain health.

This research adds knowledge to earlier work showing that childhood poverty can influence long-term health. It also highlights the value of second-generation epigenetic clocks as early indicators of brain aging. Unlike the first generation of clocks, these newer tools capture broader biological changes such as inflammation, disease risk, and behaviors like smoking.

Although smoking partly explained the results because it strongly influences DNA methylation, it did not fully account for the association between accelerated biological aging and cognitive decline. This suggests that both life experiences and lifestyle factors shape body and brain aging.

By combining decades of developmental data with a genetically informed twin design, the study provides new evidence that biological aging, especially when shaped by childhood adversity, is a key factor in midlife cognitive decline. These findings may inform early health strategies that consider both social and biological risks and support the use of second-generation methylation clocks to predict age-related cognitive changes.

DOI - https://doi.org/10.18632/aging.206284

Corresponding authors - Sophie A. Bell - bvf7pa@virginia.edu, and Eric Turkheimer - ent3c@virginia.edu

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Study in Twins Links Childhood Environment to Epigenetic Aging and Cognitive Decline

Prostate cancer is the second most diagnosed cancer among men worldwide and remains a leading cause of cancer-related death. While early forms of the disease can usually be treated successfully, advanced cases remain a major challenge. Scientists have now discovered a new potential way to slow the growth of advanced, treatment-resistant prostate cancer. These results were recently published in Volume 16 of Oncotarget by researchers from the University of Cincinnati College of Medicine.

Understanding Advanced Prostate Cancer

Early-stage prostate cancer can often be treated successfully. Most treatments work by lowering testosterone levels or blocking the hormone from activating the androgen receptor (AR), which drives cancer growth.

In some patients, however, the disease progresses to castration-resistant prostate cancer (CRPC). Even with drastic reductions in testosterone levels, the tumors continue to grow at this stage. CRPC is much more difficult to treat, and current therapies such as hormone blockers or chemotherapy typically extend life by only a few months.

One reason for this resistance is that cancer cells often switch to a different form of the androgen receptor called AR-V7. This variant remains permanently active, even without testosterone, making hormone-based drugs less effective. Because of this, new treatment strategies that work independently of hormone levels are needed.

The Study: Targeting a New Weakness in Prostate Cancer Cells

In the study titled “Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells,” researchers Shan Lu and Zhongyun Dong from the University of Cincinnati College of Medicine investigated a new way to block CRPC growth.

Full blog - https://www.oncotarget.org/2025/07/29/a-new-way-to-target-resistant-prostate-cancer-cells/

Paper DOI - https://doi.org/10.18632/oncotarget.28722

Correspondence to - Zhongyun Dong - dongzu@ucmail.uc.edu

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Keywords - cancer, PCNA, androgen receptor, PCNA inhibitors, AR splicing variants, CRPC

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Oncotarget

A New Way to Target Resistant Prostate Cancer Cells

BUFFALO, NY — August 1, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 7 of Aging (Aging-US) was #published on July 25, 2025, titled “Systemic factors in young human serum influence in vitro responses of human skin and bone marrow-derived blood cells in a microphysiological co-culture system.”

The study, led by first author Johanna Ritter and corresponding author Elke Grönniger from Beiersdorf AG, Research and Development Hamburg, shows that components in young human blood serum can help restore youthful properties to skin, but only when bone marrow cells are also present. This discovery highlights the role of bone marrow in supporting skin health and may allow for novel approaches aimed at slowing or reversing visible signs of aging.

The research explored how factors present in blood serum, already known to influence aging in animal studies, act on human cells. Using an advanced system that mimics human circulation, the researchers connected a 3D skin model with a 3D bone marrow model. They found that young human serum alone was not enough to rejuvenate skin. However, when bone marrow cells were present, these serum factors changed the activity of those cells, which then secreted proteins that rejuvenated skin tissue.

“Interestingly, we detected a significant increase in Ki67 positive cells in the dynamic skin model co-cultured with BM model and young serum compared to the model co-cultured with BM and old serum, indicating an improved regenerative capacity of the tissue.”

Detailed analysis indicated that young serum stimulated the bone marrow to produce a group of 55 proteins, with 7 of them demonstrating the ability to boost cell renewal, collagen production, and other features associated with youthful skin. These proteins included factors that improved energy production in cells and reduced signs of cellular aging. Without the interaction between skin and bone marrow cells, these rejuvenating effects did not occur.

This finding explains why earlier experiments in mice, where young and old animals shared a blood supply, showed rejuvenation across organs. It suggests that bone marrow-derived cells are critical messengers that transform signals from blood into effects on other tissues, including the skin.

While these results are preclinical and not from human trials, they offer a starting point for new strategies in regenerative medicine and skin care. By identifying specific proteins that may carry rejuvenating signals, the study points to a new way to address age-related changes. Researchers emphasize that further studies will be needed to confirm these effects in humans and to test how these proteins can be safely and effectively applied in future therapies.

Overall, this research is an important step in understanding how young blood serum factors influence human tissue and could guide the development of novel methods to maintain healthier skin as people age.

DOI - https://doi.org/10.18632/aging.206288

Corresponding author - Elke Grönniger - elke.groenniger@beiersdorf.com

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Young Human Blood Serum Factors Show Potential to Rejuvenate Skin Through Bone Marrow

BUFFALO, NY — August 11, 2025 — Aging (Aging-US) is proud to support a milestone event for the global senescence and aging research community.

This coming September 16-19, 2025, Rome, Italy will host two back-to-back events that will define the next chapter of senescence science and translation:

-10th Annual International Cell Senescence Association (ICSA) Conference
-Senotherapeutics Summit – organized with the Phaedon Institute

This combined program could not come at a more important time. The field is entering a transformative phase:

-Multiple clinical trials on senolytics and senomorphics are now reporting results, offering the first real-world evidence of their therapeutic potential.

-Exciting new discoveries in senescence mechanisms, biomarkers, and tissue-specific roles are reshaping our understanding of when and how to target these cells.

For the first time, the leading fundamental science meeting on cellular senescence will be directly connected with a global summit dedicated to the clinical and commercial development of senotherapeutics. This unique integration will allow participants to seamlessly move from bench to bedside discussions, exploring both the latest research and its translation into therapies that could transform how we approach aging and age-related diseases.

Highlights include:

-Keynotes from pioneers driving both discovery science and translational innovation

-Sessions on mechanisms, biomarkers, and emerging targets

-Industry and regulatory panels on clinical trial design, safety, and approval pathways

-Case studies from ongoing and completed human trials

-Networking with leaders from academia, biotech and pharma

Celebrate a decade of ICSA and help chart the path for the next generation of senescence science and therapeutics.

Registration is still open: https://icsa2025rome.com/

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Aging-US Supports Landmark Senescence and Aging Research Events in Rome

Aging (Aging-US) Supports Landmark Senescence and Aging Research Events in Rome

BUFFALO, NY – August 11, 2025 – A new #researchpaper was #published in Volume 16 of Oncotarget on July 25, 2025, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.”

In this study, researchers led by first author Aiden Deacon and corresponding author Justin Hwang from the University of Minnesota-Twin Cities investigated a group of genes known as the R-spondin family (RSPO1/2/3/4) in advanced prostate cancer (PC). The RSPO gene family regulates Wnt signaling, a pathway involved in cancer progression.

Prostate cancer is the most common cancer among men in the United States and becomes especially dangerous when it spreads beyond the prostate. Most patients are treated with hormone therapies that target the androgen receptor; however, many tumors eventually become resistant.

The research team analyzed thousands of tumor samples and found that RSPO2 alterations were more common than changes in other R-spondin genes or even some well-known cancer-related genes like CTNNB1 and APC. RSPO2 amplification occurred in over 20% of metastatic prostate cancer. Patients with these alterations showed signs of more aggressive disease, including higher mutation rates and greater tumor complexity.

Using laboratory models, the team discovered that RSPO2 increases cancer cell growth and triggers a biological process called epithelial-mesenchymal transition (EMT). EMT is known to promote tumor spread and resistance to standard treatments. Unlike other genes in the same pathway, RSPO2 also appeared to reduce the activity of androgen receptor genes, suggesting it drives a type of prostate cancer that no longer relies on hormones for growth.

“In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1.”

Importantly, RSPO2 showed structural differences from other R-spondin proteins, which may allow researchers to design drugs that specifically block its activity. Current therapies targeting the Wnt pathway are limited, and there are no approved drugs that inhibit RSPO2. However, this study highlights RSPO2 as a promising therapeutic target, especially for patients who do not respond to existing hormone-based treatments.

This research adds critical knowledge about how aggressive prostate cancers develop and persist despite therapy. The identification of RSPO2 as a key driver of disease progression opens new possibilities for treatment strategies aimed at improving outcomes for patients with advanced prostate cancer.

DOI - https://doi.org/10.18632/oncotarget.28758

Correspondence to - Justin Hwang - jhwang@umn.edu

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Keywords - cancer, RSPO2, prostate cancer, Wnt signaling, genomics, therapeutics

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New Gene Linked to Aggressive, Treatment-Resistant Prostate Cancer

Lung cancer, particularly non-small cell lung cancer (NSCLC), is the deadliest cancer worldwide. Cigarette smoking is one of the main causes, but not every smoker develops the disease. This suggests that other biological factors help determine who develops cancer.

Researchers from the Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Indianapolis, and from the Richard L. Roudebush Veterans Affairs Medical Center have now found that cigarette smoke, combined with a weakened DNA repair system, can trigger the early stages of lung cancer, particularly NSCLC. This work, led by first author Nawar Al Nasralla and corresponding author Catherine R. Sears, was recently published in Volume 16 of Oncotarget.

Full blog - https://www.oncotarget.org/2025/08/11/cigarette-smoke-and-weak-dna-repair-a-double-hit-behind-lung-cancer-risk/

Paper DOI - https://doi.org/10.18632/oncotarget.28724

Correspondence to - Catherine R. Sears - crufatto@iu.edu

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Keywords - cancer, DNA repair, DNA damage, lung adenocarcinoma, squamous cell carcinoma, Xeroderma Pigmentosum Group C (XPC)

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Cigarette Smoke and Weak DNA Repair: A Double Hit Behind Lung Cancer Risk

BUFFALO, NY — August 12, 2025 — A new #research perspective was #published in Aging (Aging-US) on July 8, 2025, titled “Exercise as a geroprotector: focusing on epigenetic aging.”

In this perspective, led by Takuji Kawamura from Tohoku University, researchers reviewed existing evidence from scientific studies showing that regular exercise, physical activity, and fitness may influence epigenetic aging and potentially reverse it, offering a promising way to extend healthspan and improve long-term health.

Epigenetic aging refers to changes in the body’s DNA that reflect how quickly a person is aging at the molecular level. It is measured using epigenetic clocks, which analyze patterns of DNA methylation, a chemical modification that can affect gene activity. Unlike chronological age, which simply counts the number of years lived, epigenetic aging presents a more accurate picture of how well the body’s cells and tissues are functioning. This process is influenced by various factors, including lifestyle, and has become a powerful tool for studying aging.

This perspective highlights that while general physical activity, such as walking or doing household tasks, offers health benefits, structured exercise routines that are planned, repetitive, and goal-directed appear to have stronger effects on slowing epigenetic aging. Physical fitness, especially high cardiorespiratory capacity, is also closely associated with slower epigenetic aging.

The authors also discuss key findings from both human and animal studies. In mice, structured endurance and resistance training reduced age-related molecular changes in muscle tissue. In humans, multi-week exercise interventions demonstrated reductions in biological age markers in blood and skeletal muscle. One study found that sedentary middle-aged women reduced their epigenetic age by two years after just eight weeks of combined aerobic and strength training. Another study showed that older men with higher oxygen uptake levels, a key measure of cardiovascular fitness, had significantly slower epigenetic aging.

“These findings suggest that maintaining physical fitness delays epigenetic aging in multiple organs and supports the notion that exercise as a geroprotector confers benefits to various organs.”

The research also examines which organs benefit most from exercise. While skeletal muscle has been a central focus, new evidence shows that regular physical training may also slow aging in the heart, liver, fat tissue, and even the gut. In addition, Olympic athletes were found to have slower epigenetic aging than non-athletes, suggesting that long-term, intensive physical activity may have lasting anti-aging effects.

The authors call for further research to understand why some individuals respond more strongly to exercise than others and how different types of training influence aging in various organs. They also point out the importance of developing personalized exercise programs to maximize anti-aging benefits. Overall, the findings support the growing recognition that maintaining physical fitness is not only essential for daily health but may also serve as one of the most effective tools for slowing the body’s internal aging process.

DOI - https://doi.org/10.18632/aging.206278

Corresponding author - Takuji Kawamura - takuji.kawamura.b8@tohoku.ac.jp

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Exercise May Slow Epigenetic Aging

BUFFALO, NY - August 13, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 29, 2025, titled “PCAIs stimulate MAPK, PI3K/AKT pathways and ROS-Mediated apoptosis in aromatase inhibitor-resistant breast cancer cells while disrupting actin filaments and focal adhesion.”

In this study, led by first author Jassy Mary S. Lazarte and corresponding author Nazarius S. Lamango from Florida A&M University College of Pharmacy and Pharmaceutical Sciences, researchers investigated a new class of compounds called polyisoprenylated cysteinyl amide inhibitors (PCAIs) as a potential treatment for aromatase inhibitor (AI) therapy resistant breast cancer. Aromatase inhibitors are a common treatment for estrogen receptor-positive (ER+) breast cancer, but many patients eventually develop resistance, leaving fewer therapeutic options.

The study focused on a PCAI compound called NSL-YHJ-2-27, which was tested in long-term letrozole-treated breast cancer cells (LTLT-Ca), an experimental model of AI therapy resistance. NSL-YHJ-2-27 activated two major signaling pathways, MAPK and PI3K/AKT. Although these pathways typically support cancer cell survival, their overstimulation by PCAIs led to increased oxidative stress, damaging the cells and inducing cell death by apoptosis. The compound also reduced levels of RAC1 and CDC42, proteins involved in maintaining cell shape and movement. These alterations resulted in cytoskeletal disruption and reduced structural integrity, making the cancer cells more vulnerable and less capable of spreading. Importantly, the effects of NSL-YHJ-2-27 persisted after the compound was removed, suggesting long-term control over AI resistant cancer cells may be possible.

“PCAIs inhibited cell proliferation and colony formation by 95% and 74%, respectively, increased active caspase 7 and BAX 1.5-fold and 56%, respectively. NSL-YHJ-2-27 (10 μM) induced LTLT-Ca spheroid degeneration by 61%.”

As a new class of targeted molecules, PCAIs represent an innovative approach distinct from traditional endocrine therapies. Their ability to affect multiple cellular mechanisms simultaneously makes them promising candidates for future drug development.

Overall, this study presents a promising new approach for treating AI therapy-resistant breast cancer. By targeting cellular pathways that support survival and mobility, PCAIs like NSL-YHJ-2-27 could provide a novel strategy to manage advanced or resistant forms of the disease. Further research, including in vivo studies and clinical trials, will be essential to confirm these findings and evaluate their therapeutic potential.

DOI - https://doi.org/10.18632/oncotarget.28759

Correspondence to - Nazarius S. Lamango - nazarius.lamango@famu.edu

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Keywords - cancer, PCAIs, ROS, MAPK, PI3K/AKT, LTLT-Ca cells

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New Compound Disrupts Survival Pathways in Aromatase Inhibitor-Resistant Breast Cancer Cells

BUFFALO, NY — August 14, 2025 — A new #research paper was #published in Volume 17, Issue 7, of Aging (Aging-US) on July 3, 2025, titled “Frailty associates with respiratory exacerbations and mortality in the COPDGene cohort.”

In this study, led by first author Eleanor Kate Phillips from Brigham and Women’s Hospital and corresponding author Dawn L. DeMeo from Brigham and Women’s Hospital and Harvard Medical School, researchers investigated how frailty impacts lung health and survival in individuals with a history of cigarette smoking. They found that frailty raises the risk of lung attacks and death, even in smokers with preserved lung function. This result shows why all current and former smokers should be checked for frailty.

Frailty is a condition that makes the body more vulnerable to illness, especially in older adults. This study focused on more than 2,600 adults with a history of heavy smoking, many of whom showed no signs of lung damage on standard tests. At the second follow-up visit, participants were categorized as robust, prefrail, or frail and followed for about three years. Researchers tracked how often they experienced respiratory attacks, such as episodes of severe coughing or breathlessness, and whether they survived during that period.

“COPDGene is a cohort study of individuals aged 45–80 with a minimum 10 pack-year smoking history.”

The results showed that people who were frail had a three- to five-fold higher chance of developing serious or frequent respiratory attacks compared to those who were robust. These risks were not limited to people with chronic lung disease. In fact, many frail participants with normal lung function still faced a significantly higher chance of lung attacks and death. Even those in the “prefrail” stage, a milder form of frailty, were more likely to experience health complications.

The research team also found that frailty was associated with an accelerated pace of biological aging, measured using a DNA-based test called DunedinPACE. This supports the idea that frailty may reflect deeper biological changes in the body that go beyond what traditional lung function tests can detect. These findings challenge the idea that standard lung tests can rule out future respiratory complications in people with a history of smoking. 

Altogether, the study shows that simple frailty checks could help identify early health problems, allowing for timely interventions that may prevent hospitalizations and potentially save lives. The study suggests that frailty screening may be a valuable tool in public health efforts to reduce respiratory disease and improve outcomes for aging adults.

DOI - https://doi.org/10.18632/aging.206275

Corresponding author - Dawn L. DeMeo - redld@channing.harvard.edu

Video short - https://www.youtube.com/watch?v=G1XQhQN6PQ8

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Keywords - aging, frailty, cigarette smoking, respiratory exacerbations, COPD, epigenetic aging

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Frailty Linked to Higher Risk of Respiratory Complications and Death in Smokers

BUFFALO, NY – August 15, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 13, 2025, titled “Clinical and analytical validation of MI Cancer Seek®, a companion diagnostic whole exome and whole transcriptome sequencing-based comprehensive molecular profiling assay.”

In this study, first authors Valeriy Domenyuk and Kasey Benson, along with corresponding author David Spetzler from Caris Life Sciences in Irving, Texas, introduce MI Cancer Seek, an FDA-approved test designed to deliver comprehensive tumor profiling. MI Cancer Seek demonstrated strong concordance with other FDA-approved companion diagnostics and serves as a powerful tool to guide treatment decisions in both adult and pediatric cancer patients.

Cancer remains one of the most complex and diverse diseases to treat. With many targeted therapies currently FDA-approved, selecting the right one for a specific patient requires detailed genetic insights. MI Cancer Seek addresses this need by analyzing both DNA and RNA from a single tumor sample. The tool identifies key biomarkers linked to FDA-approved treatments for several major cancers, including breast, lung, colon, melanoma, and endometrial cancers.

One of the most significant strengths of MI Cancer Seek is its ability to deliver accurate and reliable results from minimal tissue input (50 ng). Even when analyzing formalin-fixed paraffin-embedded samples, which are widely used but often degraded, the test maintained high levels of accuracy. It successfully detected important genetic alterations such as PIK3CA, EGFR, BRAF, and KRAS/NRAS mutations and measured tumor mutational burden (TMB) and microsatellite instability (MSI), both of which are key indicators for immunotherapy response.

In clinical comparisons, the test achieved over 97% agreement with other FDA-approved diagnostic tools, confirming its reliability in detecting critical biomarkers. Notably, it showed near-perfect accuracy in identifying MSI status in colorectal and endometrial cancers. The researchers also demonstrated that the test maintains precision across different lab conditions and varying DNA input levels, confirming its robustness for routine clinical use.

Beyond its role as a companion diagnostic, MI Cancer Seek incorporates additional features developed under its predecessor, MI Tumor Seek Hybrid. These include detection of homologous recombination deficiency, structural variants, and cancer-related viruses. It also includes advanced tools such as the Genomic Probability Score for identifying the tissue of origin in cancers of unknown primary, as well as a gene signature to guide first-line chemotherapy in colorectal cancer.

“One limitation to be considered is the low PPA for ERBB2 CNA detection.”

By offering deeper genetic insights from a single, small sample, MI Cancer Seek has the potential to streamline diagnostics, reduce testing costs, and connect patients to effective therapies more quickly. As precision medicine continues to expand, this assay stands out as a comprehensive and efficient solution for meeting the evolving needs of modern oncology.

DOI - https://doi.org/10.18632/oncotarget.28761

Correspondence to - David Spetzler - dspetzler@carisls.com

Video short - https://www.youtube.com/watch?v=D4hd2FxCYY8

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FDA-Approved MI Cancer Seek Test Enhances Tumor Profiling for Precision Oncology

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease.

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