Ebook and shit

BUFFALO, NY- March 12, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Associations of prenatal one-carbon metabolism nutrients and metals with epigenetic aging biomarkers at birth and in childhood in a US cohort.”

Epigenetic gestational age acceleration (EGAA) at birth and epigenetic age acceleration (EAA) in childhood may be biomarkers of the intrauterine environment. In this new study, researchers Anne K. Bozack, Sheryl L. Rifas-Shiman, Andrea A. Baccarelli, Robert O. Wright, Diane R. Gold, Emily Oken, Marie-France Hivert, and Andres Cardenas from Stanford University School of Medicine, Harvard Medical School, Harvard T.H. Chan School of Public Health, Columbia University, and Icahn School of Medicine at Mount Sinai investigated the extent to which first-trimester folate, B12, 5 essential and 7 non-essential metals in maternal circulation are associated with EGAA and EAA in early life. 

“[...] we hypothesized that OCM [one-carbon metabolism] nutrients and essential metals would be positively associated with EGAA and non-essential metals would be negatively associated with EGAA. We also investigated nonlinear associations and associations with mixtures of micronutrients and metals.”

Bohlin EGAA and Horvath pan-tissue and skin and blood EAA were calculated using DNA methylation measured in cord blood (N=351) and mid-childhood blood (N=326; median age = 7.7 years) in the Project Viva pre-birth cohort. A one standard deviation increase in individual essential metals (copper, manganese, and zinc) was associated with 0.94-1.2 weeks lower Horvath EAA at birth, and patterns of exposures identified by exploratory factor analysis suggested that a common source of essential metals was associated with Horvath EAA. The researchers also observed evidence of nonlinear associations of zinc with Bohlin EGAA, magnesium and lead with Horvath EAA, and cesium with skin and blood EAA at birth. Overall, associations at birth did not persist in mid-childhood; however, arsenic was associated with greater EAA at birth and in childhood. 

“Prenatal metals, including essential metals and arsenic, are associated with epigenetic aging in early life, which might be associated with future health.”

DOI - https://doi.org/10.18632/aging.205602

Corresponding author - Andres Cardenas - andres.cardenas@stanford.edu

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Keywords - aging, epigenetic age acceleration, metals, folate, B12, prenatal exposures

About Aging-US

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases. 

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Aging (Aging-US)

Association of Prenatal Vitamins and Metals With Epigenetic Aging at Birth and in Childhood

BUFFALO, NY- June 10, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Relationships of depression and antidepressant use with epigenetic age acceleration and all-cause mortality among postmenopausal women.”

In this new study, researchers May A. Beydoun, Hind A. Beydoun, Jason Ashe, Michael F. Georgescu, Steve Horvath, Ake Lu, Anthony S. Zannas, Aladdin H. Shadyab, Su Yon Jung, Sylvia Wassertheil-Smoller, Ramon Casanova, Alan B. Zonderman, and Robert L. Brunner from the National Institute on Aging, U.S. Department of Veterans Affairs (Washington, DC), University of Texas Health Science Center at Houston, University of California Los Angeles, University of North Carolina at Chapel Hill, University of California San Diego, Albert Einstein College of Medicine, Wake Forest University School of Medicine, and University of Nevada Reno investigated relations of depressive symptoms, antidepressant use, and epigenetic age acceleration with all-cause mortality risk among postmenopausal women. 

“Frequently under-recognized depression is a major contributor to the Global Burden of Diseases [1, 2] while being the most prevalent mental illness among geriatric populations [2].”

Data were analyzed from ≤1,900 participants in the Women's Health Initiative study testing four-way decomposition models. After a median 20.4y follow-up, 1,161 deaths occurred. Approximately 11% had elevated depressive symptoms (EDS+), 7% were taking antidepressant medication at baseline (ANTIDEP+), while 16.5% fell into either category (EDS_ANTIDEP+). 

Baseline ANTIDEP+, longitudinal transition into ANTIDEP+ and accelerated epigenetic aging directly predicted increased mortality risk. GrimAge DNA methylation age acceleration (AgeAccelGrim) partially mediated total effects of baseline ANTIDEP+ and EDS_ANTIDEP+ on all-cause mortality risk in socio-demographic factors-adjusted models (Pure Indirect Effect >0, P < 0.05; Total Effect >0, P < 0.05). Thus, higher AgeAccelGrim partially explained the relationship between antidepressant use and increased all-cause mortality risk, though only prior to controlling for lifestyle and health-related factors. 

“Antidepressant use and epigenetic age acceleration independently predicted increased all-cause mortality risk. Further studies are needed in varying populations.”

DOI - https://doi.org/10.18632/aging.205868

Corresponding author - May A. Beydoun - baydounm@mail.nih.gov

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Keywords - aging, depressive symptoms, epigenetic age acceleration, mortality

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

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Depression, Antidepressants, Epigenetic Age Acceleration, and Mortality in Postmenopausal Women

BUFFALO, NY- October 16, 2024 – A new #review was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Molecular chaperones: Guardians of tumor suppressor stability and function.”

As highlighted in the abstract of this paper, "tumor suppressor" describes a diverse set of genes typically involved in suppressing metastasis, but which can lead to tumorigenesis when loss-of-function mutations occur. Despite the varied structures and functions of tumor suppressor proteins, many share a common regulatory mechanism—they are "clients" of molecular chaperones, and they rely on an intracellular network of chaperones and co-chaperones to maintain their stability. Mutations in tumor suppressors that disrupt proper chaperoning prevent cells from maintaining sufficient protein levels for normal physiological function.

In their review, researchers Jennifer A. Heritz, Sarah J. Backe, and Mehdi Mollapour from SUNY Upstate Medical University and New York VA Health Care in Syracuse, New York, discuss the role of molecular chaperones Hsp70 and Hsp90 in maintaining the stability and functional integrity of tumor suppressors. They also detail the contributions of co-chaperones prefoldin, HOP, Aha1, p23, FNIP1/2, and Tsc1, as well as the chaperonin TRiC, to tumor suppressor stability.

“Overall, it is clear that oncogenesis can result from the dysregulation of tumor suppressor stabilization by chaperones.”

DOI - https://doi.org/10.18632/oncotarget.28653

Correspondence to - Mehdi Mollapour - mollapom@upstate.edu

Video short - https://www.youtube.com/watch?v=V5OFjeqaH3A

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Keywords - cancer, molecular chaperone, tumor suppressor, renal cell carcinoma, Birt-Hogg-Dubé (BHD) syndrome, TSC syndrome

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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Oncotarget

Molecular Chaperones: Guardians of Tumor Suppressor Stability

By studying epigenetics you can find new directions in developing improved treatments for addiction. Epigenetic studies can identify drug-related genes, provide in vivo research of transcriptional mechanisms, and can give unique insight into the mechanisms of long-lasting adaptations that underlie addiction.

Drug Use and Epigenetic Changes

Oncotarget Volume 11, Issue 27 reported that Epithelial-mesenchymal transition (EMT) and its reverse process mesenchymal-epithelial transition are central to metastatic aggressiveness and therapy resistance in solid tumors.

While molecular determinants of both processes have been extensively characterized, the heterogeneity in the response of tumor cells to EMT and MET inducers has come into focus recently and has been implicated in the failure of anti-cancer therapies.

Recent experimental studies have shown that some cells can undergo an irreversible EMT depending on the duration of exposure to EMT-inducing signals.

While the irreversibility of MET, or equivalently, resistance to EMT, has not been studied in as much detail, evidence supporting such behavior is slowly emerging.

Here, the authors identify two possible mechanisms that can underlie resistance of cells to undergo EMT: epigenetic feedback in ZEB1/GRHL2 feedback loop and stochastic partitioning of biomolecules during cell division.

Identifying the ZEB1/GRHL2 axis as a key determinant of epithelial-mesenchymal plasticity across many cancer types, the authors use mechanistic mathematical models to show how GRHL2 can be involved in both the above-mentioned processes, thus driving an irreversible MET. This study highlights how an isogenic population may contain subpopulation with varying degrees of susceptibility or resistance to EMT, and proposes a next set of questions for detailed experimental studies characterizing the irreversibility of MET/resistance to EMT.

Dr. Herbert Levine from The Center for Theoretical Biological Physics at Rice University as well as The Department of Physics at Northeastern University and Dr. Mohit Kumar Jolly from The Centre for BioSystems Science and Engineering at The Indian Institute of Science said: "Epithelial-Mesenchymal Transition (EMT) is a cell biological process involved in driving cancer metastasis and therapy resistance the two grand clinically unsolved challenges."

These hybrid E/M phenotypes may drive collective cell migration as clusters of tumor cells and can be more aggressive than cells in pure epithelial or mesenchymal phenotypes.

Recent experiments decoding the dynamics of EMT/MET using live-cell imaging and/or induction and withdrawal of various EMT-inducing external signals such as TGF? or tuning the levels of EMT-specific transcription factors have provided important insights into the reversibility of EMT and MET. Cells induced to undergo EMT for shorter durations may revert to an epithelial state after withdrawal of the signal/stimulus.

However, similar investigations about the irreversibility of MET, or in other words, the resistance of epithelial cells to undergo EMT in response to EMT-inducing signals, remain to be done.

Here, the authors' propose two independent mechanism that may explain the resistance of epithelial tumor cells to undergo EMT:

1) epigenetic feedback mediated via GRHL2?an MET-inducing transcription factor ; and
2) stochastic partitioning of parent cell biomolecules among the daughter cells at the time of cell division.
Conversely, here, the authors' show that incorporating this epigenetic feedback loop acting on the inhibition of ZEB1 by GRHL2 can cause an irreversible MET. Cells undergoing irreversible MET may exhibit resistance in undergoing EMT when exposed to EMT-inducing signals.

The Levine/Jolly Research Team concluded in their Oncotarget Research Paper that their results offer mechanistic insights into two possible mechanisms that may drive varying degrees of susceptibility and resistance to undergoing EMT in response to an EMT-inducing signal in a given isogenic population.
Full text - https://www.oncotarget.com/article/27651/text/

Oncotarget: Volume 11, Issue 27

Oncotarget Podcast: Epigenetic feedback and stochastic partitioning can drive resistance to EMT

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/