The EGFR pathway as an example for genotype: phenotype correlation in tumor genes.
Tumor-specific and germ-line variations of DNA significantly contribute to tumor growth and its ability to develop resistance. Among several mechanisms that cause resistance to cancer treatment, the genotype of certain growth factors, like epidermal growth factor receptor (EGFR), is critical. EGFR signals requests for proliferation and survival toward the nucleus of the cancer cell. Several polymorphic DNA sequences of EGFR and the mutational status of the Kirsten-Ras (KRAS) gene appear to be determinants of response to new drugs that inhibit EGFR. We describe the correlation between the EGFR genotype, including the KRAS mutation, and the consequences of the resulting genotype for anti-EGFR therapy in colorectal cancer.
Mogck
Ulrike
U
Department of Internal Medicine I, University Hospital Carl Gustav Carus, University Dresden, Dresden, Germany.
Goekkurt
Eray
E
Stoehlmacher
Jan
J
D000483:Alleles; D015179:Colorectal Neoplasms / Q000235:genetics; D004273:DNA, Neoplasm / Q000235:genetics; D066246:ErbB Receptors / Q000235:genetics*; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D011905:Genes, ras; D005838:Genotype; D006801:Humans; D009369:Neoplasms / Q000235:genetics*; D010641:Phenotype; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D017422:Sequence Analysis, DNA; D018631:ras Proteins / Q000235:genetics
D004273:DNA, Neoplasm; D066246:ErbB Receptors; D018631:ras Proteins