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Extra info for Cancer Epigenetics: Biomolecular Therapeutics for Human Cancer
The senescence phenotype was first observed in cultures of normal human fibroblasts, reflecting the limitation in the number of population doublings (Hayflick and Moorhead, 1961; Hayflick, 1965). , 2003), pointing to a link between senescence and activation of DNA damage response pathways. Meanwhile, it is obvious that DNA damage plays a general role. , 1999). , 2006). Cancer Epigenetics: Biomolecular Therapeutics for Human Cancer, First Edition. Edited by Antonio Giordano and Marcella Macaluso.
2002). , 1997). The inhibitory effect of the CDK inhibitor p21CIP1 is potentiated through cooperating functions of p27KIP1. p27KIP1 displays high affinity for cyclin E–CDK2 complexes. , 1999). , 1999). Accordingly, inhibition of CDK2 activity by p21CIP1 favors an accumulation of p27KIP1 in an autoregulatory feedback loop as is typically found in senescent cells. Binding of p27KIP1 and p21CIP1 to cyclin D–CDK4/6 complexes does not necessarily block the kinase activity.
Downregulation of cyclin/CDK (cyclin-dependent kinase) activity in response to the absence of mitogens leads to accumulation of hypophosphorylated pRb, which has higher affinity for HDAC1 and displaces it from MyoD . Pathways that remove epigenetic events like recruitment of demethylases or by histone variant exchange are subsequently activated. Transcription is achieved by the binding of MyoD to its cognate sequences (E-box, CANNTG), and consequent recruitment of HATs, SWI/SNF chromatinremodeling complexes, and polymerase II-activating kinases [3,16,24,25].
Cancer Epigenetics: Biomolecular Therapeutics for Human Cancer by Antonio Giordano, Marcella Macaluso