AFP, ErbB4, MMP-2, Amphiregulin, FGF basic, MMP-3, Angiopoietin-1, FoxC2 , MMP-9, ANGPTL4, FKHR, MSP/MST1, ENPP-2/Autotaxin, Galectin-3, MUC-1, AXL, GM-CSF, Nectin-4, BCL-X, HCG, Osteopontin, CA125/MUC-16, HGF R/c-Met, p27/Kip1, E-Cadherin, HIF-1alpha, p53, VE-Cadherin, HNF-3beta, PDGF-AA, CAP-G, HO-1/HMOX1, CD31/PECAM-1, CA-9, ICAM-1/CD54, Progesterone R, Cathepsin B, CD25/IL-2 R alpha, Progranulin, Cathepsin D, IL-6, Prolactin, Cathepsin S, CXCL8/IL-8, Prostasin, CEACAM-5, IL-18 Bpa, E-Selectin, Decorin, KLK-3/PSA, Maspin, DKK-1, KLK-5, PAI-1/Serpin E1, DLL-1, KLK-6, SNAIL, EGF R/ErbB1, Leptin (OB), SPARC, Endoglin/CD105, Lumican, Survivin, Endostatin, CCL2/MCP-1, Tenascin-C, Enolase 2, CCL8/MCP-2, THBS-1, eNOS, CCL7/MCP-3, TIE-2, EpCAM, M-CSF, UPA-1, ER-alpha, Mesothelin, VCAM-1, ErbB2, CCL3/MIP-1alpha, VEGF, ErbB3, CCL20/MIP-3alpha, Vimentin
A large number of genes with diverse normal functions are involved in human cancer. More than 500 genes have been identified as strongly implicated in the process of transforming normal cells to cancer cells. The expression of these genes in normal cells contributes to normal growth, survival and function, whereas dysregulated expression, including overexpression, loss of expression or expression of a defect protein, in cancer cells contributes to ungoverned tumor growth. Altered gene expression can be caused by coarse structural and numerical chromosomal rearrangements, specific gene amplifications, silencing of transcription through methylation and mutations, e.g. point mutations with single base substitutions and small inserts or deletions, that lead to loss or gain of function of the corresponding protein.