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egulation of cell cycle. Chegini and Kornberg [52] demonstrated that GnRHa therapyresulted in a noticeable decrease in FAK in ULs cells. These data suggested that ULsregression induced by GnRHa is mediated in part through a mechanism involving growthfactors and adhesion molecules. The TNS1 gene associated on FAK signaling acts inextracellular matrix production. Therefore, the current study showing that up-regulation ofTNS1 associated with genomic amplifications gives an additional support for treatment withGnRH analogs in ULs.Heterotrimeric G proteins are the key players in transmembrane signaling by couplinga multitude of receptors to enzymes, channel proteins and other effector molecules. TheCALCRL gene encodes the receptor-like calcitonin that forms complexes with protein-G. TheCALCRL mediates the effects of adrenomedullin (AM), which is an angiogenic factorinduced by hypoxia. Despite its benign nature, ULs have aberrant angiogenesis, essential stepfor the growth and proliferation [for review 4]. Nikitenko et al. [53] reported an increasedactivity of CALCRL in the vascular endothelium of ULs suggesting that CALCRL could be apotential therapeutic target for angiogenesis inhibitors in ULs. In agreement with the findings,CALCRL gains and up-regulation could explain the angiogenesis phenotype detected in ULs.The hepatic fibrosis/hepatic stellate cell activation pathways revealed an association ofCOL3A1, FGFR1, and IGFBP5. Hepatic fibrosis is a chronic liver disease associated with theextracellular matrix accumulation, very similar to pathological conditions of ULs. Theinhibitor of tyrosine kinase activity of FGFR1 (NP603) recently described, inhibits theproliferation of myofibroblasts associated with liver fibrosis in rats [54]. In ULs, the increasedtyrosine kinase activity of FGFR1 in association with IGFBP5 in response to FGF1, IGF-1 orTGF-beta might trigger cell proliferation, while increased activity of COL3A1, in response toET-1 could lead to extracellular matrix accumulation and collagen deposition. Additional14