Combined KRAS and TP53 mutation status is not predictive in CAPOX-treated metastatic colorectal cancer

Autor: Menno T, De Bruijn, Daniëlle A E, Raats, Jolien, Tol, John, Hinrichs, Steven, Teerenstra, Cornelis J A, Punt, Inne H M Borel, Rinkes, Onno, Kranenburg
Rok vydání: 2011
Předmět:
Zdroj: Anticancer research. 31(4)
ISSN: 1791-7530
Popis: The response of colorectal tumours to chemotherapy is highly variable. Preclinical work has shown that the Kirsten ras (KRAS) oncogene sensitizes colorectal tumour cells to oxaliplatin and capecitabine in a wild-type tumour suppressor p53 (TP53)-dependent manner. Therefore, whether or not the combined mutation status of KRAS and TP53 could predict response to chemotherapy in metastatic colorectal cancer was tested.A subgroup of patients from the CAIRO2 study (randomized phase III study on capecitabine, oxaliplatin, bevacizumab with or without cetuximab in first-line advanced colorectal cancer) that received capecitabine plus oxaliplatin (CAPOX) treatment in combination with bevacizumab was selected. The tumours were analyzed for KRAS and TP53 mutations by PCR/sequencing. The relationship between tumour response and genotype was analyzed.The following KRAS/TP53 genotypes were identified: KRASmut/TP53mut n=21, KRASmut/TP53wt n=20, KRASwt/TP53mut n=25, KRASwt/TP53wt n=15. No genotype was associated with a significantly better or worse progression-free or overall survival.The combined mutation status of KRAS and TP53 does not predict response to CAPOX in patients with metastasized colorectal cancer.
Databáze: OpenAIRE