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Methioninase Gene Therapy.

I'm not sure I've seen this approach to cancer before; this group used a gene therapy for methioninase to restrict the availability of methionine to cancer cells, which are apparently known to require more methionine than non-cancer cells. This treatment showed some interesting effects. I leave this for others on this distribution list to consider further.
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Somatic mutant clones colonize the human esophagus with age.

This looks like an interesting report of the accumulation of nuclear DNA mutants in human esophageal epithelium. This group found that somatic mutations accumulated during human aging in this tissue, with "a strong positive selection of clones carrying mutations in 14 cancer genes", with mutations in NOTCH1 and TP53 having relatively high prevalence (even higher than the rates found in esophageal cancers). These results make me wonder about the dynamics of cancer-related gene mutations during human aging. I wonder whether the age-related increase in cancer incidence is caused by the metabolic-abuse-area-under-the-curve associated with a longer time alive (living longer = more damage), or whether there is some positive selection process for cancer-associated gene mutations, or maybe the increased cancer incidence is caused mostly by a decline in immune function, or perhaps the explanation varies by cancer type.
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Thymic involution and rising disease incidence with age.

I found this abstract interesting. This group reports that the dramatic increases in age-related incidence of multiple diseases can be better modeled by functional decline in the thymus than by DNA mutation accumulation (an oft-assumed driver of age-related health decline).
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Every-other-day feeding extends lifespan but fails to delay many symptoms of aging in mice.

This large group of researchers report on experiments of every-other-day feeding in 200+ phenotypes of male C57BL/6J mice. The every-other-day feeding apparently extended lifespan, but from analysis of 20+ tissues, doesn't seem to delay histopathological aging more generally. They report that the protocol seems to delay neoplastic development and associated mortality, but not other aspects of aging. This may not be particularly relevant to damage identification and repair (the main interests of this distribution list), but I expect several recipients to be interested in these results.
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Persistent mTORC1 signaling in cell senescence results from defects in amino acid and growth factor sensing.

I suspect the results of this study may have very important implications for addressing cellular senescence with senolytics. I studied the paper in some detail. Basically, it appears that mTORC1 is constitutively expressed in senescent cells, such that amino acid starvation will not kill them. Their increased autophagy is counterbalanced with upregulated mTOR, to enhance their survivability. If I understand their results correctly, inhibition of mTORC1 causes autophagic apoptosis in senescent cells. The relevance to senolytics is that one might have to disable the constitutively expressed mTORC1 to get them to die (in greater numbers?) from senolytics. So I'm wondering if senolytics, combined with mTORC1 inhibition from something like rapamycin, might simultaneously enhance pro-apoptotic signals, and inhibit survival mechanisms (rapamycin disabling mTORC1), resulting in enhanced senolytic activity.
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The ageing genome, clonal mosaicism and chronic disease.

Clonal mosaicism refers to when one cell experiences a mutation, then divides a sufficient number of times such that this new mutation can be detected among cells without that mutation. These authors review this topic, and its potential relevance to chronic disease, including cancer. This topic seems relevant to the question of whether nuclear DNA damage (in this case, mutation) matter during a normal human lifespan.
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Free report on high blood pressure

The American Heart Association estimates more than 100 million Americans have high blood pressure, also known as “hypertension”. Learn more about the cause of high blood pressure and how you can reverse it in our free report.

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Free longevity biomarker report

Biomarker levels predict the risk of early death—and we can change them! Learn about some important longevity biomarkers in our free report.

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Free diabetes report

An estimated 50% of American adults have either prediabetes or type 2 diabetes. Learn more about the cause of type 2 diabetes, prediabetes, insulin resistance, and how to reverse them in our free report.

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