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Competing interests The authors declare that they have no competing interests. Authors’ contributions LB and HE carried out the studies and drafted the manuscript. ME, PD, JFA and FE participated to the experimental studies. JLR participated in the design of the study and in the drafting. JB participated to the irradiation and help to draft the manuscript. JR and RFB participated in the drafting. All authors read and approved the final manuscript.”
“Background At present, identifying
targeted anticancer treatment suitable for a given patient OSI-906 mw requires the availability of accurate diagnostics. Diagnostic techniques therefore have a significant impact on patients’ survival and quality of life [1]. In recent years, it has become apparent that certain types of tumors undergo mutations that either originate from the aberrant physiology of the tumor or Selleck eFT508 are induced/selected by mutagenic cancer therapies [2–4]. Failure to detect mutations in important regulatory genes in tumor specimens may have serious consequences for the patients, because these alterations can significantly reduce the effectiveness Selleckchem Depsipeptide of certain biological and cytotoxic therapies. Mutations in the KRAS oncogene are often found in human cancers. They are most common in pancreatic cancer, which can exhibit mutation rates of 80 – 90%. KRAS mutations are also observed in
40 – 50% of colorectal cancers and 10 – 30% of Non-Small Cell Lung Cancers (NSCLCs). Recent studies have shown that some anticancer drugs are only effective against tumors in which the KRAS signaling pathway has not undergone oncogenic activation. These include the small-molecule epidermal growth factor receptor inhibitors erlotinib (Tarceva®) and gefitinib (Iressa®), which are used to treat NSCLC patients, and monoclonal antibody therapies such as cetuximab (Erbitux®) and panitumumab (Vectibix®), which are primarily used in the treatment of metastatic colorectal cancers (mCRC) [5–7]. According to the U.S. National Comprehensive Cancer Network (NCCN) guidelines from November 2008 ( http://www.nccn.org/about/news/newsinfo.asp?NewsID=194) and recommendations of the American Society of Clinical Oncology (ASCO) [8], screening of the status of the KRAS gene is mandatory when deciding whether or not a patient with colorectal cancer should receive anti-EGFR drugs. Similar rules are being considered for NSCLC where KRAS mutations have prognostic value for progressive disease in LY333531 adenocarcinoma [9, 10]. There are multiple methods for detecting KRAS mutations in patient tissues, with varying analytical parameters.