BUFFALO, NY- November 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 25, 2024, Volume 16, Issue 20, titled, ”Canonical ligand-dependent and non-canonical ligand-independent EphA2 signaling in the eye lens of wild-type, knockout, and aging mice.“

Researchers from the School of Optometry and Vision Science Program at Indiana University have uncovered important new insights into how the aging affects the eye lens and contributes to cataract formation, a condition impacting millions worldwide. This study focuses on the EphA2 protein, traditionally associated with cancer, which researchers have now identified as essential for maintaining the lens’s clarity and function as it ages.

Cataracts are the leading cause of blindness worldwide, primarily affecting older adults, yet the precise biological mechanisms behind their formation remain unclear. This research sheds light on the role of the EphA2 protein receptor in the eye lens, revealing that it operates through two distinct signaling pathways: a canonical (ligand-dependent) and a non-canonical (ligand-independent) pathway. By studying various groups of mice, including those lacking the EphA2 protein receptor and its ligand partner ephrin-A5, scientists observed how these signaling pathways change with age, affecting the organization and maturation of lens cells.

Researchers Jenna L. Horner, Michael P. Vu, Jackson T. Clark, Isaiah J. Innis, and Catherine Cheng observed that EphA2’s canonical signaling, which organizes lens cells, remains stable in aging lens tissue, particularly in epithelial cells. They found that the non-canonical signaling pathway—previously associated primarily with aggressive cancer cells—increases with age in normal lens cells. This increase suggests that non-canonical signaling plays a crucial role in helping lens fiber cells mature and maintain their structure over time.

“Here, we report that canonical ligand-mediated EphA2 activation is restricted to the lens epithelial cells and show the first evidence of physiological non-canonical EphA2 activity in a normal tissue.”

This understanding could lead to new therapies targeting EphA2 to delay or prevent cataracts.

In conclusion, this study represents a significant advance in understanding the cellular mechanisms behind lens aging and cataract development, potentially paving the way for new non-surgical cataract treatments.

DOI - https://doi.org/10.18632/aging.206144

Corresponding author - Catherine Cheng - ckcheng@iu.edu

Video short - https://www.youtube.com/watch?v=3ScKLgOxQvA

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Keywords - aging, fiber cells, epithelial cells, Y588, Y589, S897, phosphorylation, maturation, ephrin

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.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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Aging (Aging-US)

EphA2 Signaling in Eye Lens Aging: Wild-Type, Knockout, and Aging Mice

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

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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

*Content warning: this episode features references to suicidal thoughts.

In this episode, we chat with Steve in Fermanagh about living with young-onset Alzheimer’s disease.

After his diagnosis, Steve had to retire from his beloved job as a long-distance truck driver. But he's found new sources of joy, and the strength and confidence to advocate for other people living with dementia.  

You can visit alzheimers.org.uk/publications for our range of publications and factsheets designed to support and inform anyone affected by dementia.

For personalised information and advice, call our Dementia support line on 0333 150 3456, or for Welsh speakers call 03300 947 400.

‘I've found a different me’ – Dementia together podcast August 2025

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

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Oncotarget

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

BUFFALO, NY — August 19, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 7, 2025, titled “Epigenetic age and accelerated aging phenotypes: a tumor biomarker for predicting colorectal cancer.”

In this study led by Su Yon Jung from the University of California, Los Angeles, researchers found a strong association between accelerated epigenetic aging and an increased risk of colorectal cancer in postmenopausal women. The study also indicated that lifestyle factors influence this risk.

Colorectal cancer is one of the leading causes of cancer-related deaths worldwide, particularly in people over the age of 50. However, individuals do not all age at the same biological rate. Two people of the same chronological age can differ in their biological aging, which reflects the condition of their cells and tissues. This study focused on a specific measure of biological aging known as epigenetic aging, which is based on chemical changes to DNA.

The researchers used data from the Women’s Health Initiative Database for Genotypes and Phenotypes (WHI-dbGaP), which includes genetic and health information from postmenopausal white women aged 50 to 79. They applied three established “epigenetic clocks” to estimate epigenetic age from blood samples collected up to 17 years before a colorectal cancer diagnosis. These clocks measure how quickly a person is aging at the molecular level by tracking DNA methylation. Women with a higher epigenetic age than expected were significantly more likely to develop colorectal cancer

“[…]we examined biological aging status in PBLs via three well-established epigenetic clocks—Horvath’s, Hannum’s and Levine’s […].”

The study also explored the role of lifestyle in modifying this risk. Women who consumed more fruits and vegetables showed no increased risk, even if they were epigenetically older. In contrast, women with both lower fruit and vegetable intake and signs of accelerated aging were up to 20 times more likely to develop colorectal cancer. This suggests that a healthy diet may help reduce cancer risk associated with biological aging.

Another key finding involved women who had both ovaries removed before natural menopause. These women had a higher epigenetic age and, when combined with accelerated aging, a greater likelihood of developing colorectal cancer. This highlights the potential influence of hormonal and reproductive factors on aging and disease risk.

The researchers validated their findings across several independent datasets, supporting the potential of blood-based epigenetic aging markers as early indicators of colorectal cancer risk. These markers could help guide early detection and prevention strategies in aging populations. However, the authors emphasize the need for independent large-scale replication studies.

Overall, this study contributes to a better understanding of the association between epigenetic aging and cancer. It also supports the idea that modifiable lifestyle factors may reduce disease risk, even among those aging more rapidly at the cellular level.

DOI - https://doi.org/10.18632/aging.206276

Corresponding author - Su Yon Jung - sjung@sonnet.ucla.edu

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Epigenetic Aging Markers Predict Colorectal Cancer Risk in Postmenopausal Women

A new #study published as the #cover of Aging (Aging-US) Volume 17, Issue 7, explores how factors in young human blood may affect the biological age of human skin. Researchers from Beiersdorf AG, Research and Development Hamburg in Germany, used a microphysiological co-culture system—a lab-based model simulating human circulation—to test the effects of young versus old blood serum on skin cells. The findings suggest that bone marrow-derived cells play a key role in converting blood-borne signals into effects that support skin rejuvenation.

Understanding Skin Aging and Systemic Influence

As we age, the skin’s ability to regenerate declines, while its biological age increases. This contributes to visible signs of aging and a weakened barrier function. While cosmetic treatments can improve appearance, they rarely target the cellular processes underlying skin aging.

Animal studies have shown that exposure to young blood can promote tissue repair and rejuvenation, likely due to molecules circulating in the bloodstream. However, reproducing these effects in human skin has proven difficult. Applying young serum directly to skin tissue has not produced significant results, indicating that additional cellular interactions may be required.

Full blog - https://aging-us.org/2025/08/skin-rejuvenation-how-young-blood-and-bone-marrow-influence-it/

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

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

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Keywords - aging, skin rejuvenation, microphysiological systems, systemic factors, bone marrow model, human serum

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Skin Rejuvenation: How Young Blood and Bone Marrow Influence It

BUFFALO, NY – August 19, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 19, 2025, titled “The SCD1 inhibitor aramchol interacts with regorafenib to kill GI tumor cells in vitro and in vivo.”

In this study, led by first authors Laurence Booth and Michael R. Booth, along with corresponding author Paul Dent from Virginia Commonwealth University, researchers investigated how aramchol, a drug originally developed for liver disease, works with the cancer drug regorafenib in gastrointestinal (GI) tumor cells. They found that the combination is effective, especially in tumor cells with a specific genetic variant. The combined approach offers a potential new strategy for treating liver and colon cancers.

Gastrointestinal cancers, such as liver and colon cancer, are serious global health challenges. Regorafenib, already approved for cancer treatment, can have limited impact and frequently causes side effects. Aramchol, a drug developed to treat fatty liver disease, affects how cancer cells process fats and energy. In this study, researchers tested whether combining these two drugs could improve GI cancer treatment, both in cells and mouse models.

The results showed that the drug combination killed liver and colorectal cancer cells more effectively than either drug alone. In animal models, mice with human liver tumors had slower tumor growth, without showing signs of weight loss or other toxicity. 

The researchers also found that aramchol and regorafenib work together to block important survival pathways inside cancer cells. This combination was especially effective in cells with a genetic variant called ATG16L1 T300, which is more common in people of African ancestry. The treatment triggered stress responses in the cancer cells and disrupted key proteins required for survival. It also activated autophagy, a natural recycling process that clears out damaged parts, eventually leading to cancer cell death.

“Aramchol interacted with the multi-kinase inhibitors sorafenib, regorafenib or lenvatinib, to kill GI tumor cells, with regorafenib exhibiting the greatest effect.”

Aramchol is currently in clinical trials for fatty liver disease and has a well-established safety profile, while regorafenib is already FDA-approved for cancer treatment. Together, their combination could advance fast into clinical testing for patients with GI cancers. However, researchers note that additional studies are needed to support the launch of early-phase clinical trials.

Altogether, this study may offer a more effective and less toxic alternative to current treatments for GI cancers. It also highlights the role of genetic variants in shaping treatment response, suggesting that future therapies could be more precisely tailored to each patient’s unique genetic profile.

DOI - https://doi.org/10.18632/oncotarget.28762

Correspondence to - Paul Dent - paul.dent@vcuhealth.org

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Keywords - cancer, macroautophagy, flux; ER stress, aramchol, regorafenib

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Aramchol Boosts Regorafenib Effectiveness in Gastrointestinal Tumors

BUFFALO, NY — August 21, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 17, 2025, titled “The influence of cancer on a forensic age estimation tool.”

In this study by Charlotte Sutter, Daniel Helbling, Cordula Haas and Jacqueline Neubauer from the Zurich Institute of Forensic Medicine, University of Zurich and Onkozentrum Zurich, the researchers investigated how cancer might affect the accuracy of forensic tools used to estimate a person’s age from blood samples.

DNA methylation is a natural chemical modification of DNA that changes with age. Forensic scientists can use these changes to predict someone’s age from biological traces, such as blood found at a crime scene. However, medical conditions like cancer can alter these patterns and potentially reduce the accuracy of such predictions. This study investigated whether various cancer types influence the DNA markers used in age estimation.

“Our study is among the first to show whether it might be necessary to account for the influence of cancer on forensic age estimation tools in order to enhance estimation accuracy as much as possible.”

The researchers applied the VISAGE enhanced age estimation tool, a widely used DNA methylation-based method, to blood samples from 100 cancer patients and 102 healthy individuals. Age predictions in the control group were generally accurate, with small average errors. Patients with solid tumors, including breast and lung cancers, showed only slightly less accurate results. In contrast, individuals with blood cancers, particularly chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML), sometimes had large errors, with ages overestimated by as much as 50 years. 

Despite these few extreme cases, the study found that cancer does not typically have a strong impact on the accuracy of this forensic tool. Most cancer patients, even those undergoing treatment, had DNA methylation patterns similar to those of healthy individuals. The researchers found no consistent differences based on cancer type, stage, or treatment, except in isolated cases involving aggressive forms of cancer.

The findings support the continued use of current forensic age estimation methods. While aggressive cancers may occasionally affect prediction accuracy, such cases are rare. The researchers suggest noting these conditions as a possible factor in unusually large errors, without requiring changes to standard practice.

This study provides valuable information about how health conditions, such as cancer, may influence DNA-based age estimation. It strengthens confidence in the reliability of forensic age prediction tools, even when applied to individuals with a medical history of cancer.

DOI - https://doi.org/10.18632/aging.206281

Corresponding author - Cordula Haas - cordula.haas@irm.uzh.ch

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Keywords - aging, forensic age, estimation age prediction, cancer, DNA methylation, age acceleration

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Impact of Cancer on Forensic DNA Methylation Age Estimation

BUFFALO, NY — August 26, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 21, 2025, titled “Association of DNA methylation age acceleration with digital clock drawing test performance: the Framingham Heart Study.”

In this study, led by first author Zexu Li from the Department of Anatomy and Neurobiology at Boston University Chobanian and Avedisian School of Medicine, and corresponding author Chunyu Liu from Boston University Chobanian and Avedisian School of Medicine and Boston University School of Public Health, researchers found that individuals with signs of faster biological aging had lower scores on a digital cognitive test taken seven years later. The findings suggest that the rate at which a person ages at the molecular level may be associated with how well their brain functions as they grow older.

Using data from the Framingham Heart Study, the researchers examined the relationship between biological aging and cognitive health. They used DNA methylation (DNAm) patterns—chemical changes that occur in the DNA with aging, known as epigenetic aging—to estimate biological age acceleration, and used the digital Clock Drawing Test (dCDT) to assess cognitive performance. The dCDT is a computerized version of a traditional pen-and-paper test that evaluates memory, thinking speed, and motor control. It provides an overall score and measures performance in specific areas such as spatial reasoning and movement.

Among 1,789 participants, higher levels of epigenetic age acceleration were associated with significantly lower cognitive scores, particularly those over age 65. Of all the epigenetic aging markers examined, the DunedinPACE measure showed the strongest association with reduced brain function in both younger and older adults. Other measures, such as Horvath and PhenoAge, were associated with lower scores only in older adults. Key areas affected included motor skills and spatial reasoning.

The researchers also studied blood-based protein markers used in an aging measure called GrimAge. Two proteins, PAI1 and ADM, were closely associated with lower cognitive scores, especially in older individuals. These results suggest that declines in brain and motor functions may reflect broader aging-related changes throughout the body.

“Digital cognitive measures displayed stronger associations with most DNAm aging metrics among older compared to younger participants, likely to reflect the cumulative and nonlinear age influences on both brain health and DNAm.”

This study supports the idea that epigenetic age may be a more accurate predictor of cognitive decline than chronological age. The dCDT, which is easy to use, automated, and more precise than traditional tools, may help detect early signs of brain aging. When combined with DNAm measures, it could become a valuable part of regular health screenings.

Overall, the findings provide strong evidence that faster biological aging is associated with cognitive decline. This research may lead to better ways of identifying and monitoring brain health in aging populations.

DOI - https://doi.org/10.18632/aging.206285

Corresponding author - Chunyu Liu - liuc@bu.edu

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Faster Biological Aging Linked to Cognitive Decline in Older Adults

Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality. While the development of targeted therapies has improved outcomes for many patients with EGFR-mutated NSCLC, those with rare EGFR variants often face limited treatment options, especially when the disease involves the central nervous system (CNS).

A recent research paper, titled “Durable complete response in leptomeningeal disease of EGFR mutated non-small cell lung cancer to amivantamab, an EGFR-MET receptor bispecific antibody, after progressing on osimertinib” published in Volume 16 of Oncotarget, describes a patient with NSCLC harboring two uncommon EGFR mutations—G719A and A289V—who experienced a prolonged and clinically significant response to amivantamab monotherapy, after prior treatments had failed.

Full blog - https://www.oncotarget.org/2025/08/26/amivantamab-monotherapy-in-rare-egfr-mutated-advanced-nsclc/

Paper DOI - https://doi.org/10.18632/oncotarget.28730

Correspondence to - Young Kwang Chae - young.chae@northwestern.edu

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Keywords - cancer, amivantamab, monotherapy, rare EGFR mutation, NSCLC, leptomeningeal disease

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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Amivantamab Monotherapy in Rare EGFR-Mutated Advanced NSCLC

Aiden Deacon from the University of Minnesota-Twin Cities, Minneapolis, discusses a research paper he co-authored that was published in Volume 16 of Oncotarget, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.”

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

Correspondence to - Justin Hwang - jhwang@umn.edu

Video interview - https://www.youtube.com/watch?v=OXKhWWU1gnY

Abstract

This study investigates the R-spondin family of genes (RSPO1/2/3/4), a group of secreted proteins that act as Wnt regulators, and their subsequent role in advanced prostate cancer (PC). When evaluating transcriptomic data from primary and metastatic PC patients, we found that alterations in RSPO2 were more prevalent than in other RSPO family members or Wnt-regulating genes APC and CTNNB1. Further, we found that RSPO2 alterations in PCs were significantly associated with worse disease-free survival. Through our in silico modeling, RSPO2 exhibited strong positive associations with genes regulating epithelial-mesenchymal transition (EMT) and double-negative prostate cancer (DNPC), but had negative correlations with androgen receptor (AR) and AR-associated genes. Furthermore, 3D modeling of RSPO2 revealed structural differences between itself and other RSPOs. In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1. Conversely, this was not observed when CTNNB1 was overexpressed in the same models. These findings highlight that, in PC, RSPO2 functions as a unique member of the R-spondin family by promoting genes and signaling pathways associated with aggressive PC, and RSPO2 amplifications are associated with poor outcomes in PC patients.

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

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Oncotarget author interview: Aiden Deacon

Behind the Study: R-spondin Family Roles in Metastatic Prostate Cancer

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

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