Cancer research

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Cancer research is research into cancer in order to identify causes and develop strategies for prevention, diagnosis, treatments and cure.

Cancer research ranges from epidemiology, molecular bioscience (bench research) to the performance of clinical trials to evaluate and compare applications of the various cancer treatment. These applications include surgery, radiation therapy, chemotherapy and hormone therapy, and combined treatment modalities such as chemo-radiotherapy. Starting in the mid-1990s, the emphasis in clinical cancer research shifted towards therapies derived from biotechnology research, such as immunotherapy and gene therapy.

1 Genes involved in cancer
2 Dichloroacetate
3 See also
4 References
5 External links

As the Cancer Genome Project stated in a 2004 review article, "a central aim of cancer research has been to identify the mutated genes that are causally implicated in oncogenesis (cancer genes)."^[1]

Several hereditary factors can increase the chance of cancer-causing mutations, including the activation of oncogenes or the inhibition of tumor suppressor genes. The functions of various onco- and tumor suppressor genes can be disrupted at different stages of tumor progression. Mutations in such genes can be used to classify the malignancy of a tumor.

In later stages, tumors can develop a resistance to cancer treatment. The identification of oncogenes and tumor suppressor genes is important to understand tumor progression and treatment success.

Genes and protein products that have been identified by at least two independent publications as being involved in cancer are: ABI1, ABL2, ACSL6, AF1Q, AF5Q31 (also known as MCEF), AKT1, ARNT, ASPSCR1, ATF1, ATIC, BCL10, BFHD, BIRC3, BMPR1A, BTG1, CBFA2T1, CBFA2T3, CBFB, CCND1, CDC2, CDK4, CHIC2, CHN1, COPEB, COX6C, CTNNB1, CYLD, DDB2, DDIT3, DEK, EIF4A2, EPS15, ERCC2, ERCC3, ERCC5, ERG, ETV4, ETV6, EWSR1, EXT1, EXT2, FANCC, FANCG, FGFR1OP, FGFR3, FH, FIP1L1, FUS, GAS7, GATA1, GMPS, GOLGA5, GPC, GPHN, HIST1H4I, HRAS, HSPCA, IL21R, IRF4, KRAS2, LASP1, LCP1, LHFP, LMO2, LYL1, MADH4, MLF1, MLH1, MLLT3, MLLT6, MNAT1, MSF, MSH2, MSN, MUTYH, MYC, NCOA4, NF2, NPM1, NRAS, PAX8, PCBD, PDGFB, PIM1, PLK2, PNUTL1, POU2F1, PPARG, PRCC, PRKACB, PRKAR1A, PTEN, PTPN11, RABEP1, RAD51L1, RAP1GDS1, RARA, RB1, RET, RHOH, RPL22, SBDS, SDHB, SEPTIN6, SET, SH3GL1, SS18L1, SSX1, SSX2, SSX4, STAT3, TAF15, TCF12, TCL1A, TFE3, TFEB, TFG, TFPT, TFRC, TNFRSF6, TP53, TPM3, TPM4, TRIP11, VHL, WAS, WT1, ZNF198, ZNF278, ZNF384, ZNFN1A1 based on a study by M. R Straton and co-workers " A census of human cancer genes".

In January 2007 researchers of the University of Alberta reported preliminary results of dichloroacetate (DCA) causing regression in several cancers in vitro, including lung, breast and brain tumors.^[2] Since DCA cannot be patented by any pharmaceutical company it could be an inexpensive alternative to other treatments; but would also require further public/private investment for clinical trials.^[3] The initial research was funded by the Canadian Institutes of Health Research.^[4]