BUFFALO, NY - November 12, 2025 – A new #research paper was #published in Oncotarget (Volume 16) on November 6, 2025, titled “LRIG1-3 in gliomas: LRIG1 protein expression decreased in higher grade gliomas.”

In this study by Marlene Happe, Saskia Kuhl, Lukas Görtz, Roland Goldbrunner and Marco Timmer, from the University of Cologne, researchers found that the LRIG1 protein, which may help suppress tumors, is present at lower levels in more aggressive gliomas, a type of brain tumor. The findings suggest that LRIG1 could serve as a useful marker for tumor severity and potentially as a target for future therapies.

Gliomas are the most common malignant brain tumors in adults and carry a poor prognosis, particularly in their most severe form, glioblastoma. This study investigated three related proteins: LRIG1, LRIG2, and LRIG3, which are involved in regulating cell growth signals. While LRIG1 and LRIG3 have shown tumor-suppressing effects in previous studies, LRIG2 is thought to support tumor growth. The researchers analyzed tumor samples from patients to understand how these proteins behave across different glioma grades and how they respond to chemotherapy.

The results showed that LRIG1 protein levels decline significantly as tumor grade increases. Low-grade gliomas displayed much higher LRIG1 expression than high-grade tumors. Among high-grade tumors, primary glioblastomas had the lowest levels of LRIG1. Interestingly, secondary glioblastomas, which typically develop from lower-grade tumors, had higher levels of LRIG1 than primary glioblastomas. This difference may contribute to their relatively better clinical outcomes. These results highlight LRIG1’s potential role in slowing tumor progression.

In contrast, LRIG2 showed a more complex pattern. While its gene expression was higher in lower-grade tumors, the actual protein levels were slightly elevated in higher-grade ones, which are more aggressive. This mismatch suggests that processes occurring after gene transcription may influence how much LRIG2 protein is produced. 

“However, our data on LRIG2 indicate that its role in glioma may be more complex than previously thought, warranting further investigation.”

Concerning LRIG3, it was found in higher amounts in glioma tissue compared to surrounding healthy tissue. Its expression was particularly high in low-grade tumors. However, chemotherapy did not consistently affect LRIG3 levels, and results varied depending on tumor type and treatment status.

Overall, the study suggests that members of the LRIG protein family, especially LRIG1, could serve as important biomarkers to distinguish between glioma types and grades. Although chemotherapy did not significantly change their expression in most cases, these proteins have high potential as diagnostic tools or therapeutic targets. Further research is needed to better understand their roles in glioma development and treatment response.

DOI - https://doi.org/10.18632/oncotarget.28775

Correspondence to - Marco Timmer - marco.timmer@uk-koeln.de

Abstract video - https://www.youtube.com/watch?v=ZHsKLBEyBbM

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Keywords - cancer, oncology, glioma, glioblastoma, LRIG1, LRIG2, LRIG3

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Oncotarget

Lower LRIG1 Expression Linked to Aggressive Gliomas

BUFFALO, NY — December 19, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 18, 2025, titled “Epigenetic age predicts depressive symptoms during the COVID-19 pandemic in the Canadian Longitudinal Study on Aging: importance of biological sex.”

This study, led by Cindy K. Barha of the University of Calgary and the University of British Columbia, along with Teresa Liu-Ambrose of the University of British Columbia, found that older women with a younger biological age measured years before the COVID-19 pandemic experienced a greater increase in depressive symptoms during the early lockdown period. These findings could help shape future mental health strategies, particularly for women with high emotional or caregiving demands.

Epigenetic age is a biological marker that reflects how the body is aging and may differ from a person’s actual age. Using long-term data from the Canadian Longitudinal Study on Aging (CLSA), the researchers investigated whether epigenetic age could predict changes in mental health during a major public health crisis. The study included over 600 adults, with an average baseline age of 63, and used two widely accepted epigenetic clocks, the DNAmAge and the Hannum Age, to estimate biological age. Depressive symptoms were tracked at four time points between 2012 and 2020, including during the height of the pandemic.

“The mean participant chronological age at study entry was 63±10 years (46% female).”

The analysis showed that in women, a younger biological age predicted a greater rise in depression during the early phase of the COVID-19 pandemic. This was not observed in men or in individuals with older biological ages.

The study challenges the common belief that a younger biological age always signals better mental or physical resilience. The researchers suggest that women with younger biological profiles may have been more socially or professionally active before the pandemic. When lockdowns disrupted daily routines and social connections, these individuals may have experienced more emotional distress.

Additional factors, such as reduced physical activity, loss of routine, and decreased social interaction, known to affect both mental health and biological aging, may have had a stronger emotional effect on this group. The findings highlight the importance of considering biological sex when studying how aging affects mental well-being during stressful events.

Although the study has some limitations, including the time gap between biological age measurement and the pandemic, it gives valuable insights into how biological and social factors interact during periods of crisis. Future research could use epigenetic clocks to better identify individuals at greater risk of mental health challenges during large-scale public health emergencies.

Overall, this study adds to the growing field of social epigenetics and suggests that biological age may support more targeted public health planning, especially for older adults.

DOI - https://doi.org/10.18632/aging.206337

Corresponding author - Teresa Liu-Ambrose - teresa.ambrose@ubc.ca

Abstract video - https://www.youtube.com/watch?v=DVm78jKsdkY

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Aging-US

Younger Biological Age May Increase Depression Risk in Older Women During COVID-19

BUFFALO, NY — December 23, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 25, 2025, titled “A natural language processing–driven map of the aging research landscape.”

In this study, Jose Perez-Maletzki from Universidad Europea de Valencia and Universitat de València, together with Jorge Sanz-Ros from Stanford University School of Medicine, used artificial intelligence (AI) to analyze a century of global aging research, revealing shifts in focus and highlighting underexplored areas.

The team analyzed over 460,000 scientific abstracts published between 1925 and 2023 to identify key themes, trends, and research gaps in the study of aging. Their goal was to provide a comprehensive, unbiased view of how the field has evolved and where future research could have the greatest impact.

The study found that aging research has moved from basic cellular studies and animal models to a growing focus on clinical topics, particularly age-related diseases such as Alzheimer’s and dementia. Using natural language processing and machine learning, the researchers grouped publications into thematic clusters and tracked how interest in each topic changed over time.

“By integrating Latent Dirichlet Allocation (LDA), term frequency-inverse document frequency (TF-IDF) analysis, dimensionality reduction and clustering, we delineate a comprehensive thematic landscape of aging research.”

One key finding was the growing separation between basic biological studies and clinical research. While both areas have grown significantly, they often progress independently with limited overlap. Clinical studies tend to focus on geriatrics, healthcare, and neurodegenerative diseases, while basic science emphasizes cellular mechanisms such as oxidative stress, telomere shortening, mitochondrial dysfunction, and senescence. The authors note that this lack of integration limits the translation of laboratory discoveries into medical applications.

The study also showed that some emerging topics, such as autophagy, RNA biology, and nutrient sensing, are expanding rapidly but remain separated from clinical applications. In contrast, long-established links, such as those between cancer and aging, remain strong. The analysis also highlighted that potentially important associations, such as those between mitochondrial dysfunction and senescence or epigenetics and autophagy, are rarely studied and may be new research opportunities.

This AI-driven analysis offers a new way to guide future research by identifying how different areas of aging science are interconnected or isolated. It also highlights how research priorities may be shaped by policy or funding trends, as seen in the heavy focus on Alzheimer’s disease. 

As the global population continues to age, understanding how biological processes relate to clinical outcomes is critical. This study not only offers a historical map of aging science but also serves as a tool to support more connected, interdisciplinary, and effective future research.

DOI - https://doi.org/10.18632/aging.206340

Corresponding author - Jorge Sanz-Ros - jsanzros@stanford.edu

Abstract video - https://www.youtube.com/watch?v=O4dJUGQ2ZcU

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AI Tracks Nearly 100 Years of Aging Research, Revealing Key Trends and Gaps

In this lively conversation, Brandon, Misty, and Whitney talk with The Most Rev'd Sean Rowe, presiding bishop and primate of The Episcopal Church. In this role, he serves as the church’s chief pastor and CEO. Known for his expertise in organizational learning and adaptive change, Rowe is committed to strengthening support for local ministry and mission. This episode offers a wide-ranging conversation, touching upon everything from the role of seminary in spiritual formation, to leadership in a church that is still becoming, to our willingness to engage with God’s imagination. 


Hosts: Brandon Nappi, Whitney Kimball Coe, Misty Krasawski 

Guest: Sean Rowe 

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77: Being Grounded in the Love of God with Sean Rowe

BUFFALO, NY — December 30, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 26, 2025, titled “Epigenetic aging signatures and age prediction in human skeletal muscle.”

In this study, first author Soo-Bin Yang and corresponding author Hwan Young Lee from Seoul National University College of Medicine investigated how DNA methylation patterns in skeletal muscle change with age. Their findings offer a new and highly accurate method for estimating a person’s age, with potential applications in forensic science and aging research.

Skeletal muscle is essential for movement, energy balance, and physical strength, functions that become more important to monitor as people age. This study improves our understanding of how muscle tissue changes over time at the molecular level. Unlike previous research, which mainly analyzed living individuals of European descent, this study used postmortem samples from an Asian population.

“We analyzed DNA methylation profiles from 103 pectoralis major muscle samples from autopsies of South Korean individuals (18–85 years) using the Infinium EPIC array.”

The researchers analyzed DNA from over 100 pectoralis major muscle samples taken from individuals aged 18 to 85. They identified 20 DNA methylation sites, called CpGs, that were strongly associated with age. These CpGs were found in genes involved in muscle function, stress response, metabolism, and age-related diseases. Using these markers, the team built two machine learning models to predict age: one using Next-Generation Sequencing (NGS) and another using Single Base Extension (SBE). Both models were highly accurate, with average prediction errors between 3.8 and 5.5 years.

The new “epigenetic clocks” outperformed existing age-prediction models designed for other tissue types. However, when applied to cardiac and uterine muscle, these models showed much lower accuracy, reinforcing the need for tissue-specific approaches in molecular age estimation.

Beyond predicting age, the study also provides insight into how DNA methylation may affect muscle aging. Several of the identified CpGs were located in regions that regulate gene expression, being associated with a reduction of it in older muscle samples. Some of the affected genes are associated with sarcopenia, an age-related loss of muscle mass and strength.

Overall, this study introduces two reliable and cost-effective methods to estimate age from skeletal muscle, even when the DNA is partially degraded, making it especially useful in forensic settings. It also offers a path forward for developing future therapies that may slow age-related muscle decline and highlights how skeletal muscle aging can differ depending on population, tissue type, and anatomical location.

DOI - https://doi.org/10.18632/aging.206341

Corresponding author - Hwan Young Lee - hylee192@snu.ac.kr

Abstract video - https://www.youtube.com/watch?v=1i6Ua0cceMU

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Keywords - aging, skeletal muscle, age, DNA methylation, next generation sequencing, single base extension

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Skeletal Muscle Epigenetic Clocks Developed Using Postmortem Tissue from an Asian Population

BUFFALO, NY — January 5, 2026 — A new #research paper featured as the #cover of Volume 17, Issue 12 of Aging-US was #published on December 22, 2025, titled “A combination of differential expression and network connectivity analyses identifies a common set of RNA splicing and processing genes altered with age across human tissues.”

In this study by Caio M.P.F. Batalha from the University of São Paulo, André Fujita from the University of São Paulo and Kyushu University, and Nadja C. de Souza-Pinto also from the University of São Paulo, researchers investigated how gene activity changes with age across multiple human tissues. They found that many tissues share common aging-related alterations in genes involved in RNA splicing and RNA processing. These findings are important because RNA processing is essential for accurate protein production, and disruptions in this process are linked to aging and disease.

Aging affects all tissues, yet identifying molecular changes that are shared across the body has remained challenging. To address this, researchers moved beyond traditional approaches that focus exclusively on changes in gene expression levels. They also analyzed how genes alter their patterns of interaction within regulatory networks, capturing age-related changes that are not evident from expression data alone.

“Gene expression data (in TPM – transcripts per million) were obtained from the Genotype-Tissue Expression (GTEx) project.”

Using RNA sequencing data from nearly one thousand human donors aged 20 to 70, the research team analyzed eight tissues, including blood, brain, heart, skin, and muscle. The results showed that many aging-related changes become evident only when gene network behavior is considered. When gene expression and network connectivity were analyzed together, a consistent group of genes emerged across tissues, most of which were linked to RNA splicing and RNA processing, key steps in the production of functional proteins.

The study also revealed that these RNA-related genes are highly interconnected at the protein level. Many of them form known protein complexes, including components of the spliceosome, which plays a central role in RNA maturation. With age, the interactions among these genes tend to reorganize in similar ways across tissues, pointing to a shared biological response rather than independent, tissue-specific effects.

In addition to RNA processing, the researchers observed age-related changes in pathways involved in managing damaged RNAs and proteins, including protein degradation, autophagy, and DNA damage response mechanisms. These pathways support cellular quality control and help limit the accumulation of molecular errors that increase with age.

Overall, this study identifies RNA splicing and RNA processing as central, conserved features of human aging across tissues. It also demonstrates that network-based approaches provide a more complete view of the aging transcriptome, offering new insights into age-related biological changes and potential directions for aging research.

DOI - https://doi.org/10.18632/aging.206347

Corresponding author - Nadja C. de Souza-Pinto - nadja@iq.usp.br

Abstract video - https://www.youtube.com/watch?v=A1slKwaSd6g

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RNA Splicing and Processing Emerge as Central Features of Human Aging Across Tissues

 

The Reverend Dr. John F. Ross is the Executive Director of The Saint John’s Bible Heritage Program at Saint John’s University in Collegeville, Minnesota, where he shepherds global engagement with the Saint John’s Bible—the first handwritten illuminated Bible in over 500 years. In this episode of The Leader’s Way, Brandon Nappi asks John to tell the story of how this artistic and beautiful Bible came to be, from the early inspirations of renowned calligrapher Donald Jackson to the Bible's commissioning by a Benedictine monastery and its subsequent travels across the world. 

 
Explore more of the history and images from The Saint John’s Bible project here: https://saintjohnsbible.org/ 

 
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Guest: John Ross 


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78: Saint John's Bible with John Ross

Mohammed Rezwan, founder of Bangladesh’s pioneering floating school movement and a 2025 Yale World Fellow, joins the ILC’s Yale Leads podcast. 

Mohammed Rezwan

BUFFALO, NY — January 7, 2026 — A new #meetingreport was #published in Volume 17, Issue 12 of Aging-US on December 23, 2025, titled “Cellular senescence meets infection: highlights from the 10th annual International Cell Senescence Association (ICSA) conference, Rome 2025.”

Led by Stefanie Deinhardt-Emmer from Jena University Hospital and Marco De Andrea from the University of Piemonte Orientale and the University of Turin, the report summarizes key discussions from the 10th International Cell Senescence Association conference held in Rome in September 2025. It focuses on how infections can trigger cellular senescence, a state in which cells stop dividing and release inflammatory signals. This link is important since it connects infectious diseases with aging, chronic inflammation, and lasting tissue damage.

Although cellular senescence is best known for its role in aging and cancer, the meeting highlighted its emerging importance in infection biology. Researchers described how viruses and bacteria can induce senescence in infected cells and spread its effects to nearby tissues. This process, known as infection-driven senescence (IDS), can help limit pathogen replication but may also prolong inflammation and slow recovery, particularly in older adults and during chronic infections.

Several sessions focused on respiratory viruses like influenza and SARS-CoV-2. Researchers showed that these viruses can promote senescence in lung cells, contributing to persistent inflammation and reduced healing. Experimental models suggested that decreasing the amount of senescent cells improved lung repair, even after the virus was cleared, offering insight into why some patients experience long-lasting respiratory symptoms.

Chronic viral infections were another major theme. Human cytomegalovirus and HIV were shown to drive senescence in immune and vascular cells. In people with HIV, viral proteins were associated with biological changes resembling accelerated aging, despite effective antiviral therapy. These findings help explain why age-related conditions occur earlier and more frequently in this population.

In the meeting, it was also demonstrated that senescence is not limited to viral infections. Researchers reported that the bacterium Mycobacterium abscessus induces senescence in immune cells during chronic infection. These senescent cells increased inflammation and susceptibility to further infection. Removing them reduced bacterial levels in experimental models, suggesting new directions for treating persistent bacterial disease.

“Mechanistically, IDS integrates DNA damage responses, inflammatory signaling, and metabolic stress, with consistent activation of p16INK4a, p21, and NF-κB pathways.”

Across the conference, speakers discussed therapies that either remove senescent cells or reduce their harmful inflammatory signals. These approaches, known as senolytic and senomorphic strategies, showed promise in preclinical studies as potential tools to limit infection-related tissue damage and chronic inflammation.

Overall, the meeting report presents infection-driven senescence as a unifying concept linking infection, immunity, and aging. The discussions at ICSA 2025 highlight a growing field with important implications for understanding chronic disease and the long-term health effects of infections.

DOI: https://doi.org/10.18632/aging.206349

Abstract video: https://www.youtube.com/watch?v=gOHEBJs7DIc

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International Experts Connect Infections and Aging Through Cellular Senescence

BUFFALO, NY – January 8, 2026 – A new #review was #published in Oncotarget (Volume 17) on January 3, 2026, titled “COVID vaccination and post-infection cancer signals: Evaluating patterns and potential biological mechanisms.”

Led by Charlotte Kuperwasser from Tufts University School of Medicine and Oncotarget Editor-in-Chief Wafik S. El-Deiry from The Warren Alpert Medical School of Brown University, the review examines published reports describing cancers that appeared after COVID-19 vaccination or SARS-CoV-2 infection. The authors analyze patterns across case reports, small patient series, and large population studies, and explain why these observations are relevant for cancer research and long-term public health monitoring.

Cancer remains a major global health concern, and understanding factors that may influence its behavior is important. The review covers reports published between January 2020 and October 2025 that describe cancer diagnoses, recurrence, or unusually rapid disease progression following vaccination or infection. In total, 69 publications were reviewed. Sixty-six article reports, representing more than 300 patients across multiple countries and cancer types; 2 retrospective investigations; and one longitudinal study spanning the pre-pandemic through post-pandemic periods.

The review explores how immune responses triggered by infection or vaccination could, in some individuals, influence existing cancer cells or previously dormant disease. Many article reports involved blood cancers such as lymphomas and leukemias and solid tumors, including breast, lung, pancreatic, brain, and skin cancers. Some cases described rapid disease progression or cancers appearing near vaccine injection sites or nearby lymph nodes. These observations are described as hypothesis-generating rather than evidence of risk.

In addition to individual case reports, the review examines findings from large population studies in South Korea, Italy, and the United States military. These studies assessed cancer trends over time in vaccinated populations and reported modest associations for certain cancer types. The authors note that these findings are limited by short follow-up periods and potential reporting and detection biases, emphasizing the need for longer-term data.

The authors also discuss possible biological explanations for the reported patterns, including temporary immune changes, inflammation, or altered immune surveillance that could affect tumor behavior in people with undetected or controlled cancer. They place these observations within the broader context of how viral infections can interact with cancer biology.

“Establishing causality between SARS-CoV-2 infection, COVID-19 vaccination, and cancer requires a level of evidence far beyond temporal association.”

Overall, the review identifies significant gaps in current knowledge about possible associations between COVID-19 vaccination and cancer, including limited long-term cancer surveillance, lack of molecular data, and an incomplete understanding of individual susceptibility. The authors emphasize the need for carefully designed studies that integrate clinical, epidemiologic, and biological evidence. Finally, they conclude that examining these reported patterns is important for advancing cancer research and supporting informed public health discussions.

DOI - https://doi.org/10.18632/oncotarget.28824

Correspondence to - Charlotte Kuperwasser - charlotte.kuperwasser@tufts.edu, and Wafik S. El-Deiry - wafik@brown.edu

Abstract video - https://www.youtube.com/watch?v=5_-AaojOoR8

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Evaluation of Cancer Reports Following COVID-19 Vaccination and Infection

As we age, every tissue in the body undergoes gradual molecular changes. A long-standing question in aging research is whether these changes follow common patterns across tissues or whether each tissue ages on its own. While DNA-based “epigenetic clocks” can estimate age accurately across different tissues, identifying consistent patterns in gene expression has been much more challenging.

One reason for this difficulty is methodology. Most studies focus on whether genes increase or decrease their expression levels with age. However, genes do not function in isolation. They operate within complex networks, coordinating their activity with many others. Changes in these relationships may be important aspects of the aging process. 

To understand this, researchers from the University of São Paulo performed a study titled “A combination of differential expression and network connectivity analyses identifies a common set of RNA splicing and processing genes altered with age across human tissues.”

Full blog - https://aging-us.org/2026/01/a-common-aging-pattern-changes-in-rna-splicing-and-processing-across-human-tissues/

Paper DOI - https://doi.org/10.18632/aging.206347

Corresponding author - Nadja C. de Souza-Pinto - nadja@iq.usp.br

Abstract video - https://www.youtube.com/watch?v=A1slKwaSd6g

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Keywords - aging, gene expression, co-expression network analysis, RNA processing

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A Common Aging Pattern: Changes in RNA Splicing and Processing Across Human Tissues

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

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

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

Lower LRIG1 Expression Linked to Aggressive Gliomas

Oncotarget Podcast