In the British Journal of Cancer this week, researchers in the US and Europe describe their comparison of three methods for detecting KRAS mutations in preserved colorectal cancer samples. The team used the Cobas KRAS Mutation Test, the Qiagen Therascreen KRAS Kit, and Sanger sequencing on 120 colorectal cancer samples, and found that the Cobas test detected six mutations not found by Sanger sequencing and eight mutations not found by the Qiagen kit. "The Cobas test was reproducible between sites, and detected several mutations that were not detected by the Therascreen test or Sanger," the authors write. "Sanger sequencing had poor sensitivity for low levels of mutation."
Also in the British Journal of Cancer this week, researchers in Singapore and the UK describe their morpho-molecular prognostic model for hepatocellular carcinoma. Using immunohistochemistry on tissue microarrays containing 121 primary hepatocellular carcinoma samples, the team evaluated 13 biomarkers related to the etiopathogenesis of the disease. They found that p53, alpha fetaprotein, CD44 and CD31, tumor size and vascular invasion were significant predictors for worse survival in patients, and constructed a morpho-molecular prognostic model based on these factors. "[The model] was a significant independent predictor for overall survival and relapse-free survival," the authors write. "The MMPM, based on the expression of selected proteins and clinicopathological parameters, can be used to classify HCC patients between good vs poor prognosis and high vs low risk of recurrence following hepatic resection."
Finally in the British Journal of Cancer this week, UK researchers report on the use of ATR inhibition to target radiation-resistant hypoxic tumor cells. The team used a highly selective inhibitor called VE-821 and found that it inhibited ATR-mediated signaling in response to severe hypoxia-induced replication arrest. VE-821 also induced DNA damage and increased phosphorylation of H2AX and KAP1. "Consistently, ATR inhibition sensitized tumor cell lines to a range of oxygen tensions," the authors write. "Most importantly, VE-821 increased radiation-induced loss of viability in hypoxic conditions. Using this inhibitor we have also demonstrated for the first time a link between ATR and the key regulator of the hypoxic response, HIF-1."