作者: A Fernández-Barral , JL Orgaz , B Jiménez , None
DOI: 10.5772/19809
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摘要: Metastatic spread is achieved through changes in the tissue microenvironment driven by tumor cells that allow formation of various dissemination routes using a variety mechanisms; such as angiogenesis and vasculogenesis (hematogeneous routes), lymphangiogenesis (lymphatic some particular cases like melanoma, vasculogenic mimicry (vasculogenic channels lined melanoma cells) (Carmeliet, 2005; Hendrix et al., 2003; Kopp 2006; Tammela Alitalo, 2010). Building has to be coordinated with acquisition new capabilities enable them locally invade, intravasate into channels, survive circulation, extravasate, ultimately adapt foreign territory. All this complex cascade events orchestrated multiple cell types diverse families factors signaling circuits controlling intracellular well intercellular key communication (Nguyen 2009b). Interestingly, subset extracellular have dual capacity simultaneously impinge on modulate many properties themselves acquire order fulfill all steps required successfully colonize territory starting from primary lesion drastically different environment. This chapter focuses an angiostatic factor, pigment epithelium derived factor (PEDF), broader function allows it dually destroying more relevant counteracting metastatic cells. Understanding molecular cellular mechanisms progression become active field research over last five years unveiling intertwined relationship between present microenvironment, number mediators (Shackleton Quintana, 2010; Villanueva Herlyn, 2008). Plasticity for appropriate reprogramming underlying decision making process arbitrates