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Pocket protein function in melanocyte homeostasis and neoplasia

机译：口袋蛋白在黑素细胞稳态和瘤形成中的功能

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Melanoma is the most lethal of human skin cancers and its incidence is increasing worldwide [L.K. Dennis (1999). Arch. Dermatol. 135, 275; C. Garbe et al. (2000). Cancer 89, 1269]. Melanomas often metastasize early during the course of the disease and are then highly intractable to current therapeutic regimens [M.F. Demierre and G. Merlino (2004). Curr. Oncol. Rep. 6, 406]. Consequently, understanding the factors that maintain melanocyte homeostasis and prevent their neoplastic transformation into melanoma is of utmost interest from the perspective of therapeutic interdiction. This review will focus on the role of the pocket proteins (PPs), Rb1 (retinoblastoma protein), retinoblastoma-like 1 (Rbl1 also known as p107) and retinoblastoma-like 2 (Rbl2 also known as p130), in melanocyte homeostasis, with particular emphasis on their functions in the cell cycle and the DNA damage repair response. The potential mechanisms of PP deregulation in melanoma and the possibility of PP-independent pathways to melanoma development will also be considered. Finally, the role of the PP family in ultraviolet radiation (UVR)-induced melanoma and the precise contribution that each PP family member makes to melanocyte homeostasis will be discussed in the context of a number of genetically engineered mouse models.(1)
机译：黑色素瘤是最致命的人类皮肤癌，在世界范围内其发病率正在增加。丹尼斯（1999）。拱。皮肤病135、275; C. Garbe等。 （2000）。巨蟹座89，1269年]。黑色素瘤通常在疾病过程的早期转移，然后对于当前的治疗方案非常难治[M.F. Demierre和G. Merlino（2004）。 Curr。 Oncol。 Rep。6，406]。因此，从治疗阻滞的观点来看，了解维持黑素细胞稳态并防止其向黑素瘤的肿瘤转化的因素是最重要的。这项审查将侧重于口袋蛋白（PPs），Rb1（成视网膜细胞瘤蛋白），类成视网膜细胞瘤1（Rbl1也称为p107）和成视网膜细胞瘤样2（Rbl2也称为p130）在黑素细胞稳态中的作用。特别强调它们在细胞周期和DNA损伤修复反应中的功能。黑色素瘤中PP失调的潜在机制以及与黑色素瘤发展无关的PP通路的可能性也将被考虑。最后，将在许多基因工程小鼠模型的背景下讨论PP家族在紫外线（UVR）诱导的黑色素瘤中的作用以及每个PP家族成员对黑色素细胞稳态的精确贡献。（1）

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