Cancer Epigenetics: Biomolecular Therapeutics for Human by Antonio Giordano, Marcella Macaluso

By Antonio Giordano, Marcella Macaluso

Melanoma Epigenetics: Biomolecular Therapeutics in Human melanoma is the single source to target biomolecular ways to melanoma treatment. Its presentation of the newest learn in melanoma biology displays the interdisciplinary nature of the sector and goals to facilitate collaboration among the fundamental, translational, and scientific sciences.

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1993) Deficiency in rhabdomyosarcomas of a factor required for MyoD activity and myogenesis. Science; 259:1450–1453. 30. Barr FG. (2001) Gene fusions involving PAX and FOX family members in alveolar rhabdomyosarcoma. Oncogene; 20:5736–5746. 31. Keleti J, Quezado MM, Abaza MM, Raffeld M, Tsokos M. (1996) The MDM2 oncoprotein is overexpressed in rhabdomyosarcoma cell lines and stabilizes wild-type p53 protein. Am J Pathol; 149:143–151. 1 FROM REPLICATIVE SENESCENCE TO DNA DAMAGE RESPONSE Cellular senescence is defined as the entry of cells into an irreversible G1/S growth arrest.

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]. 5 Histone Acetylation. When differentiation is induced, the cAMP responsive element binding protein (CREB) transcription factor is upregulated and phosphorylated on serine 133 and, after this step, CREB is able to promote the recruitment of HATs p300 and PCAF by MyoD direct physical interaction [23].

An indirect action of mitogen-activated cyclin/cdks can be envisioned via hyperphosphorylation of pRb, which prevents interactions with class I HDACs, thereby favoring MyoD–HDAC1 association in myoblasts. It is still not known if all Rb in differentiated myotubes is inactive or in association with the histone deacetylase transcriptional repressors such as HDAC1 [22]. The physical interaction between the hypophosphorylated form of pRb and HDAC1 in growtharrested cells has suggested an additional mechanism of cooperation between pRb and MyoD in the absence of a direct interaction.

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