On cellular senescence and tumor treatment and theory of Traditional Chinese Medicine Kidney_0.docVIP
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On cellular senescence and tumor treatment and theory of Traditional Chinese Medicine Kidney_0
PAGE \* MERGEFORMAT 13
On cellular senescence and tumor treatment and theory of Traditional Chinese Medicine Kidney
Keywords:] theory of cell aging kidney cancer medicine
With cell proliferation, differentiation, apoptosis, like cell senescence (cell senescence) is one of the basic activities cells. Cell senescence initially Hayflick in normal fibroblast cells observed in vitro and found that under the conditions of normal cell proliferation in vitro 50 to 70 on behalf of the division into a state of senescence, cells can lose the ability to continue the further proliferation of subculture, but still alive, a phenomenon known as the “Hayflick limit.” cell aging and cancer are closely related, cell senescence tumor formation is the main host defense barrier of one of the .2005, a number of research studies published in professional journals indicated that the K-rasV12 cancer gene, p-ten knockout, BRAF mutation and other factors induced by the process of tumor formation, if the occurrence of cell senescence simultaneously, greatly reducing the risk of cancer incidence, and in the formation of tumor cells, almost all have some degree of senescence barriers, particularly the activation of telomerase, the ability of tumor cell senescence and treatment effect is also closely related.
1 cell senescence
Currently, the academic community will Hayflick found to increase the cell proliferation caused by passages called the proliferation of old age (replicative senescence), this phenomenon also exists in vivo, despite the discovery of a long time, but until recent years, great progress was made. cell proliferation and senescence at the molecular level of the main ends of chromosomes telomeres (Telomer) and related TP53 → CDKN1a → pRB → E2F signaling pathway, the role of telomeres in the maintenance of chromosome structural integrity during replication of normal cells per 1 loss to split the rate of approximately 100 bp sequence of gradual loss of telomere ends
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