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.
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. The role of a given gene in cancer progression may vary tremendously, depending on the stage and type of cancer involved.
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 (gene),
GPHN,
HIST1H4I,
HRAS,
HSPCA,
IL21R,
IIRF4,
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
rociowh:E
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. Since the compound DCA itself cannot be patented it could be an inexpensive alternative to other treatments, depending of course on whether the method of using DCA in the treatment of cancer is patentable. Clinical use of DCA will of course require further public/private investment for clinical trials. The initial research was funded by the Canadian Institutes of Health Research.
Another problem, according to the magazine, is that human tumors transplanted into lab rats "almost never metastasize", and yet metastatic cancers are reponsible for 90% of all cancer deaths. Robert Weinberg of the MIT recognizes that the inexistence of good animal models limits the rate of progress of cancer research.