Cyclins are proteins that regulate the progression through the cell cycle, i.e., the transition of G1 to S phase. It is well known that high cyclin expression may lead to cell proliferation states, which is closely associated with cancer progression. Moreover, the blockage of cyclins may have an anti-carcinogenic effect by inhibiting the progression through the cell cycle. MAP kinases are serine/threonine kinases that regulate the progression through the cell cycle by phosphorylating a variety of substrates during cell proliferation. In consequence, phosphatases that inactivate MAPK kinases (i.e., by dephosphorylation) may have an anticarcinogenic effect. The p53 is a tumor suppressor protein involved in diverse cellular processes including DNA repair, cycle arrest and programmed cell death. This protein (p53) is activated by phosphorylation at target residues and phosphatases inactivate it, thereby the blockage of its degradation may have an anticarcinogenic effect. Oncogene activation (i.e., the expression of oncogenes), may alter diverse cellular processes including DNA replication, and thereby may lead to cancer development. The G-protein α subunit is a GTPase that hydrolyses GTP and thus has a major role in controlling the kinetics of the G-protein signaling cascade. Platelet-derived growth factor receptors (PDGFR) are kinase receptors that play roles in regulating cellular differentiation, cell proliferation and cell growth. PDGFR receptors are present on the surface of normal cells, however, it has been shown that mutations of the PDGFR genes that lead to their high expression lead to uncontrolled cell growth and consequently cause cancer (i.e., by increasing PDGF signaling).
In some cases, skin cancers are hereditary and an increased risk of developing the disease can be passed from parent to child. If members of the same or multiple members being diagnosed the chance it being passed down to your children is higher.
