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Senescent cell populations re​-​awakened through aberrant patterns of methylation

from For the sake of reproducibility - a technical replicate by Tumor Necrosis Factor-alpha

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There are many a ways by which cells can be driven into proliferative, cancerous states
A classical model involves changes in DNA sequences, thus causing genomes to mutate

Although most mutations are of no consequences, provided they occur in non-coding regions

Problems may arise when these changes affect key players of DNA-repair or cell cycle regulation
Functional integrity of check point proteins may also be compromised by epigenetic modifications

Normal expression of tumor suppressor genes altered, silenced by aberrant methylation patterns
Repressive chromatin domain formation, from senescence to cell growth, the tables finally have turned

Specific repressing sites’ methylation resulting in transcriptional de-repression
CpG islands gains of methylation promoting cancerous proliferation
Generally senescent cell populations undergoing transcriptional de-repression
Awaiting their re-awakening through aberrant patterns of methylation

Ref: Cruickshanks HA et al. “Senescent cells harbour features of the cancer epigenome.” Nature Cell Biology 15, 1495-1506 (2013)

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Scientists, academics, gorefiends and grindheads of the world rejoice: Tumor Necrosis Factor-alpha unleashes its take on full blown Carcass-worship, topped with unique lyrical themes inspired by the most recent knowledge in state-of-the-art scientific research from the fields of cellular and molecular biology. ... more

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