Aging-US

Dr. May Beydoun from the Laboratory of Epidemiology and Population Sciences, NIA/NIH/IRP, in Baltimore, MD, discusses a research paper she co-authored that was published by Aging (Aging-US) as the cover for Volume 14, Issue 13, entitled, “Epigenetic clocks and their association with trajectories in perceived discrimination and depressive symptoms among US middle-aged and older adults.”

DOI - https://doi.org/10.18632/aging.204150

Corresponding author - May A. Beydoun - [email protected]

Video version - https://www.youtube.com/watch?v=gkiDhjTL0YY

Abstract

Background: Perceived discrimination may be associated with accelerated aging later in life, with depressive symptoms acting as potential mediator.

Methods: A nationally representative sample of older adults was used [Health and Retirement Study 2010–2016, Age: 50–100 y in 2016, N = 2,806, 55.6% female, 82.3% Non-Hispanic White (NHW)] to evaluate associations of perceived discrimination measures [Experience of discrimination or EOD; and Reasons for Perceived discrimination or RPD) and depressive symptoms (DEP)] with 13 DNAm-based measures of epigenetic aging. Group-based trajectory and four-way mediation analyses were used.

Results: Overall, and mostly among female and NHW participants, greater RPD in 2010–2012 had a significant adverse total effect on epigenetic aging [2016: DNAm GrimAge, DunedinPoAm38 (MPOA), Levine (PhenoAge) and Horvath 2], with 20–50% of this effect being explained by a pure indirect effect through DEP in 2014–2016. Among females, sustained elevated DEP (2010–2016) was associated with greater LIN DNAm age (β ± SE: +1.506 ± 0.559, p = 0.009, reduced model), patterns observed for elevated DEP (high vs. low) for GrimAge and MPOA DNAm markers. Overall and in White adults, the relationship of the Levine clock with perceived discrimination in general (both EOD and RPD) was mediated through elevated DEP.

Conclusions: Sustained elevations in DEP and RPD were associated with select biological aging measures, consistently among women and White adults, with DEP acting as mediator in several RPD-EPICLOCK associations.

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Press release - https://www.aging-us.com/news_room/epigenetic-clocks-and-their-association-with-perceived-discrimination-and-depressive-symptoms

Keywords - aging, DNA methylation, epigenetic clocks, biological age, perceived discrimination, depressive symptoms

About Aging-US

Launched in 2009, 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-US 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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A new research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 17, entitled, “Extracellular microRNA and cognitive function in a prospective cohort of older men: The Veterans Affairs Normative Aging Study.”

Aging-related cognitive decline is an early symptom of Alzheimer’s disease and other dementias, and on its own can have substantial consequences on an individual’s ability to perform important everyday functions. Despite increasing interest in the potential roles of extracellular microRNAs (miRNAs) in central nervous system (CNS) pathologies, there has been little research on extracellular miRNAs in early stages of cognitive decline.

In a new study, researchers Nicole Comfort, Haotian Wu, Peter De Hoff, Aishwarya Vuppala, Pantel S. Vokonas, Avron Spiro, Marc Weisskopf, Brent A. Coull, Louise C. Laurent, Andrea A. Baccarelli, and Joel Schwartz from Columbia University Mailman School of Public Health, University of California San Diego, VA Boston Healthcare System, Boston University School of Medicine, and Harvard TH Chan School of Public Health leveraged the longitudinal Normative Aging Study (NAS) cohort to investigate associations between plasma miRNAs and cognitive function among cognitively normal men.

“In a cohort of older men from Massachusetts, we investigated associations between plasma miRNAs and global cognition and rate of global cognitive decline measured by the MMSE.”

Full press release - https://aging-us.net/2022/09/15/aging-extracellular-microrna-and-cognitive-function-in-a-prospective-cohort-of-older-men-the-veterans-affairs-normative-aging-study/

DOI: https://doi.org/10.18632/aging.204268

Corresponding Author: Nicole Comfort – [email protected]

Keywords: plasma, extracellular RNA, RNA-seq, microRNA, cognitive decline, cognitive impairment

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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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Listen to a blog summary of a trending review published by Aging (Aging-US), entitled, "New hallmarks of ageing: a 2022 Copenhagen ageing meeting summary."

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Humans battle a number of biological processes with age that lead to the gradual deterioration of cells and tissues. Frailty, disability, disease, and death are all costly fates of aging. Researchers who study aging aim to change this fate, however, the mechanisms of aging are still all but fully understood.

In 2013, López-Otín and colleagues attempted to identify these biological processes and proposed the original nine hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, loss of proteostasis, deregulated nutrient-sensing, cellular senescence, stem cell exhaustion, and altered intercellular communication. These hallmarks of aging have helped to provide a framework for thought about the causes and consequences of aging, as well as potential targets for therapeutic interventions. Now, nine years later, the hallmarks of aging have been updated in light of recent discoveries.

“In the nearly past 10 years, our in-depth exploration on ageing research has enabled us to formulate new hallmarks of ageing which are compromised autophagy, microbiome disturbance, altered mechanical properties, splicing dysregulation, and inflammation, among other emerging ones.”

This update was presented on March 22, 2022, at the “New Hallmarks of Ageing” research symposium in Copenhagen, Denmark. On August 29, 2022, a review paper summarizing the symposium was published in Aging (Aging-US), entitled, “New hallmarks of ageing: a 2022 Copenhagen ageing meeting summary.”

Full blog - https://aging-us.org/2022/09/the-2022-new-hallmarks-of-ageing-research-symposium/

DOI - https://doi.org/10.18632/aging.204248

Corresponding authors - Tinna Stevnsner - [email protected], Lene Juel Rasmussen - [email protected], Evandro F. Fang - [email protected]

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Keywords - aging, hallmarks of ageing, neurodegeneration, healthspan, longevity, autophagy

About Aging-US

Launched in 2009, 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-US 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.

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

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In the fourth episode of the Longevity & Aging Series, Dr. Carly Bobak from Dartmouth College, Dr. Cristian Coarfa from Baylor College of Medicine, and Dr. Andrew DiNardo from Baylor College of Medicine, discuss a research paper they co-authored that was published in Volume 14, Issue 5, of Aging (Aging-US), entitled, “Increased DNA methylation, cellular senescence and premature epigenetic aging in guinea pigs and humans with tuberculosis.”

DOI - https://doi.org/10.18632/aging.203936

Corresponding Authors - Carly A. Bobak - [email protected], Cristian Coarfa - [email protected], and Andrew R. DiNardo - [email protected]

Abstract

Background: Tuberculosis (TB) is the archetypical chronic infection, with patients having months of symptoms before diagnosis. In the two years after successful therapy, survivors of TB have a three-fold increased risk of death.

Methods: Guinea pigs were infected with Mycobacterium tuberculosis (Mtb) for 45 days, followed by RRBS DNA methylation analysis. In humans, network analysis of differentially expressed genes across three TB cohorts were visualized at the pathway-level. Serum levels of inflammation were measured by ELISA. Horvath (DNA methylation) and RNA-seq biological clocks were used to investigate shifts in chronological age among humans with TB.

Results: Guinea pigs with TB demonstrated DNA hypermethylation and showed system-level similarity to humans with TB (p-value = 0.002). The transcriptome in TB in multiple cohorts was enriched for DNA methylation and cellular senescence. Senescence associated proteins CXCL9, CXCL10, and TNF were elevated in TB patients compared to healthy controls. Humans with TB demonstrate 12.7 years (95% CI: 7.5, 21.9) and 14.38 years (95% CI: 10.23–18.53) of cellular aging as measured by epigenetic and gene expression based cellular clocks, respectively.

Conclusions: In both guinea pigs and humans, TB perturbs epigenetic processes, promoting premature cellular aging and inflammation, a plausible means to explain the long-term detrimental health outcomes after TB.

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Longevity & Aging Series

Aging (Aging-US) and FOXO Technologies have teamed up for a special collaboration on aging research with a monthly video series: Longevity & Aging Series. This series invites Aging researchers to speak with host Dr. Brian Chen, an adjunct faculty member at the University of California San Diego and Chief Science Officer of FOXO Technologies.

Learn more - https://www.aging-us.com/longevity

Keywords - aging, tuberculosis, multi-cohort analysis, network analysis, DNA methylation, senescence, Cavia porcellus, DNA hypermethylation, epigenetic aging

About Aging-US

Launched in 2009, 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-US 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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A new research paper was published in Aging (“Aging (Albany NY)” by Medline/PubMed, “Aging-US” by Web of Science) Volume 14, Issue 16, entitled, “Systemic lipolysis promotes physiological fitness in Drosophila melanogaster.”

A large body of literature shows that lipid metabolism exerts profound regulatory effects on aging and affects stress responses. Interventions such as caloric restriction or fasting robustly promote lipid catabolism and improve aging-related phenotypical markers.

Researchers Linshan Shang, Elizabeth Aughey, Huiseon Kim, Timothy D. Heden, Lu Wang, Charles P. Najt, Nicholas Esch, Sophia Brunko, Juan E. Abrahante, Marissa Macchietto, Mara T. Mashek, Todd Fairbanks, Daniel E. L. Promislow, Thomas P. Neufeld, and Douglas G. Mashek from the University of Minnesota and University of Washington investigated the direct effect of increased lipid catabolism via overexpression of bmm (brummer, FBgn0036449), the major triglyceride hydrolase in Drosophila, on lifespan and physiological fitness.

Comprehensive characterization was carried out using RNA-seq, lipidomics and metabolomics analysis. Global overexpression of bmm strongly promoted numerous markers of physiological fitness, including increased female fecundity, fertility maintenance, preserved locomotion activity, increased mitochondrial biogenesis and oxidative metabolism. Since bmm drives fatty acid oxidation, the data in this study implicated differential partitioning of glucose into the pentose phosphate pathway and purine biosynthesis between males and females. However, the underlying mechanisms through which bmm elicits these sex-specific effects remains to be determined.

“Increased bmm robustly upregulated the heat shock protein 70 (Hsp70) family of proteins, which equipped the flies with higher resistance to heat, cold, and ER [endoplasmic reticulum] stress via improved proteostasis.”

Despite improved physiological fitness, bmm overexpression did not extend lifespan. Taken together, these data show that bmm overexpression has broad beneficial effects on physiological fitness, but not lifespan.

“Collectively, these studies reveal diverse beneficial effects of global elevation of lipolysis on physiological fitness. This work provides additional rationale for pursuing therapeutic approaches, as done previously [39], that enhance lipolysis to mitigate metabolic and aging-related diseases.”

DOI: https://doi.org/10.18632/aging.204251

Corresponding Author: Douglas G. Mashek – Email: [email protected]

Keywords: brummer, lipolysis, physiological fitness, stress resistance, proteostasis

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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.

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

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For media inquiries, please contact [email protected]

A new research paper was published in Aging (“Aging (Albany NY)” by Medline/PubMed, “Aging-US” by Web of Science) on the cover of Volume 14, Issue 16, entitled, “Synergism of BCL-2 family inhibitors facilitates selective elimination of senescent cells.”

Cellular senescence, a complex cellular response to stress characterized by a halt of cell cycle progression, is one factor contributing to aging. Accumulation of senescent cells in tissues with advancing age participates in the pathogenesis of several human age-associated diseases.

Specific senescent secretome, the resistance of senescent cells to apoptotic stimuli, and lack of immune system response contribute to the accumulation of senescent cells and their adverse effects in tissues. Inhibition of antiapoptotic machinery, augmented in senescent cells, by BCL-2 protein family inhibitors represents a promising approach to eliminate senescent cells from tissues.

“In this study, with the goal of decreasing the toxicity and potential onset of resistance to senolytic BCL-2 inhibitor monotherapy, we explored the effects of combined treatment covering both BCL-2 and MCL-1 anti-apoptotic factors in human cells.”

Researchers David Rysanek, Pavla Vasicova, Jayaprakash Narayana Kolla, David Sedlak, Ladislav Andera, Jiri Bartek, and Zdenek Hodny from the Czech Academy of Sciences and the Danish Cancer Society Research Center aimed to explore synergistic and selective senolytic effects of anti-apoptotic BCL-2 family targeting compounds, particularly BH3 mimetics.

“Using human non-transformed cells RPE-1, BJ, and MRC-5 brought to ionizing radiation-, oncogene-, drug-induced and replicative senescence, we found synergy in combining MCL-1 selective inhibitors with other BH3 mimetics.”

In an attempt to uncover the mechanism of such synergy, the team revealed that the surviving subpopulation of cells resistant to individually applied ABT-737/ABT-263, MIK665, ABT-199, and S63845 BCL-2 family inhibitors showed elevated MCL-1 compared to untreated control cells indicating the presence of a subset of cells expressing high MCL-1 levels and, therefore, resistant to BCL-2 inhibitors within the original population of senescent cells.

Overall, the researchers found that combining BCL-2 inhibitors can be beneficial for eliminating senescent cells, thereby enabling use of lower, potentially less toxic, doses of drugs compared to monotherapy, thereby overcoming the resistance of the subpopulation of senescent cells to monotherapy.

DOI: https://doi.org/10.18632/aging.204207

Corresponding Author: Jiri Bartek, Zdenek Hodny – Email: [email protected], [email protected]

Keywords: homoharringtonine, cellular senescence, BCL-2, MCL-1, senolytics

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About Aging-US

Launched in 2009, 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-US 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.

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

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Listen to a blog summary of a trending research paper published by Aging, entitled, "Regulation of microglial activation in stroke in aged mice: a translational study.“

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A stroke can occur when the blood supply in and around the brain becomes interrupted. A hemorrhagic stroke is when a blood vessel bursts in or near the brain. An ischemic stroke is caused when a blood vessel carrying oxygen and nutrients to the brain is obstructed—usually by a clot. The most common type of stroke is ischemic, which accounts for approximately 87% of all strokes in humans. A major risk factor for an ischemic stroke is aging.

Inflammation (a chronic condition among the elderly) is a key contributing factor to strokes, and microglia are the primary immune cells in the brain. Researchers recently identified a role for the microglial IRF5-IRF4 regulatory axis in mediating responses after stroke. However, whether or not aged microglia also undergo the same regulatory mechanisms after a stroke had previously not been determined.

“Microglial activation plays a central role in initiating and perpetuating the post-stroke inflammation, and acts as a ‘double-edged’ sword to confer both detrimental and beneficial effects [9].”

In a recent study, researchers Conelius Ngwa, Abdullah Al Mamun, Shaohua Qi, Romana Sharmeen, Yan Xu, and Fudong Liu from The University of Texas Health Science Center at Houston investigated aged mice and the role of the microglial IRF5-IRF4 regulatory axis after a stroke. On August 12, 2022, their research paper was published in Aging’s Volume 14, Issue 15, and entitled, “Regulation of microglial activation in stroke in aged mice: a translational study.“

Full blog - https://aging-us.org/2022/08/stroke-outcomes-mediated-by-these-2-mechanisms/

DOI - https://doi.org/10.18632/aging.204216

Corresponding author - Fudong Liu - [email protected]

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Keywords - aging, inflammation, IRF, inflammation, microglia, stroke

About Aging-US

Launched in 2009, 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-US 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.

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

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In the third episode of the Longevity & Aging Series, Dr. Steve Horvath, Professor of Human Genetics and Biostatistics at UCLA, and Principal Investigator at Altos Labs, discusses the evolution of aging research and epigenetic clocks with host Brian Chen.

Special Collection on Steve Horvath's Publications in Aging - https://www.aging-us.com/special-collections-archive/steve-horvath

Author contact - Steve Horvath - [email protected]

Longevity & Aging Series - https://www.aging-us.com/longevity

Transcript - https://aging-us.net/2022/08/23/longevity-aging-series-ep-3-dr-steve-horvath-epigenetic-clocks/

About Aging-US

Launched in 2009, 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-US 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.

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

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Listen to a blog summary of a trending research paper featured as the cover for Volume 14, Issue 15 of Aging (Aging-US), entitled, "Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival."

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Successful, or healthy, aging may be the result of adherence to several protective factors simultaneously within all three of the well-being domains. Previously, the majority of research on healthy aging has been limited to a single domain per study. In a new study, researchers Marguerita Saadeh, Xiaonan Hu, Serhiy Dekhtyar, Anna-Karin Welmer, Davide L. Vetrano, Weili Xu, Laura Fratiglioni, and Amaia Calderón-Larrañaga (from Karolinska Institutet, Karolinska University Hospital, Stockholm University, Lund University, and Stockholm Gerontology Research Center) believe that the vast heterogeneity in aging phenotypes cannot be explained by one domain of well-being alone. On July 18, 2022, their research paper was published on the cover of Aging’s Volume 14, Issue 15, and entitled, “Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival.”

Full blog - https://aging-us.org/2022/08/3-domains-of-well-being-extend-elderly-mobility-and-longevity/

DOI - https://doi.org/10.18632/aging.204182

Corresponding author - Marguerita Saadeh - [email protected]

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Keywords - aging, mobility, survival, well-being, older adults, successful aging

About Aging-US

Launched in 2009, 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-US 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.

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

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Aging (Aging-US) Volume 14, Issue 15:

https://www.aging-us.com/issue/v14i15

Research Paper (Cover): “Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival”

https://doi.org/10.18632/aging.204182

Editorial: “Sex difference in epigenomic instability during human aging”

https://doi.org/10.18632/aging.204199

Editorial: “NAD+ to assess health in aging humans”

https://doi.org/10.18632/aging.204220

Editorial: “T cell senescence by N-glycan branching”

https://doi.org/10.18632/aging.204239

Research Paper: “mtDNA variability determines spontaneous joint aging damage in a conplastic mouse model”

https://doi.org/10.18632/aging.204153

Research Paper: “Senolytic drugs relieve pain by reducing peripheral nociceptive signaling without modifying joint tissue damage in spontaneous osteoarthritis”

​​https://doi.org/10.18632/aging.204204

Research Paper: “Ascorbic acid induces salivary gland function through TET2/acetylcholine receptor signaling in aging SAMP1/Klotho (-/-) mice”

https://doi.org/10.18632/aging.204213

Research Paper: “Regulation of microglial activation in stroke in aged mice: a translational study”

https://doi.org/10.18632/aging.204216

Research Paper: “PDCD10 promotes the aggressive behaviors of pituitary adenomas by up-regulating CXCR2 and activating downstream AKT/ERK signaling”

https://doi.org/10.18632/aging.204206

Research Paper: “Influence of cardiovascular risk burden on pulmonary function trajectory: role of physical and social activities”

https://doi.org/10.18632/aging.204201

Research Paper: “miRNA-338-3p inhibits the migration, invasion and proliferation of human lung adenocarcinoma cells by targeting MAP3K2”

https://doi.org/10.18632/aging.204198

Research Paper: “Serial neurocognitive changes following transcatheter aortic valve replacement: comparison between low and intermediate-high risk groups”

https://doi.org/10.18632/aging.204202

Research Paper: “MAB21L1 promotes survival of lens epithelial cells through control of αB-crystallin and ATR/CHK1/p53 pathway”

https://doi.org/10.18632/aging.204203

Research Paper: “Interleukin-17D promotes lung cancer progression by inducing tumor-associated macrophage infiltration via the p38 MAPK signaling pathway”

​​https://doi.org/10.18632/aging.204208

Research Paper: “A signature constructed with mitophagy-related genes to predict the prognosis and therapy response for breast cancer”

https://doi.org/10.18632/aging.204209

Research Paper: “Artemisia argyi exhibits anti-aging effects through decreasing the senescence in aging stem cells”

https://doi.org/10.18632/aging.204210

Research Paper: “SIAH1-mediated RPS3 ubiquitination contributes to chemosensitivity in epithelial ovarian cancer”

https://doi.org/10.18632/aging.204211

Research Paper: “CBXs-related prognostic gene signature correlates with immune microenvironment in gastric cancer”

https://doi.org/10.18632/aging.204214

Research Paper: “Targeting circRNA-MAP4K2 for the treatment of diabetes-induced retinal vascular dysfunction”

https://doi.org/10.18632/aging.204215

Research Paper: “The comprehensive expression and functional analysis of m6A modification “readers” in hepatocellular carcinoma”

https://doi.org/10.18632/aging.204217

Research Paper: “Establishing and validating an ADCP-related prognostic signature in pancreatic ductal adenocarcinoma”

https://doi.org/10.18632/aging.204221

Research Paper: “SAAL1, a novel oncogene, is associated with prognosis and immunotherapy in multiple types of cancer”

https://doi.org/10.18632/aging.204224

Research Paper: “Comprehensive pan-cancer analysis reveals the prognostic value and immunological role of SPIB”

https://doi.org/10.18632/aging.204225

Research Paper: “Clinical outcomes and potential therapies prediction of subgroups based on a ferroptosis-related long non-coding RNA signature for gastric cancer”

https://doi.org/10.18632/aging.204227

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