Manickam Janakiraman

TL;DR: KRAS mutations are identified as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of KRAS mutant clones can be detected non-invasively months before radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance.

TL;DR: The model that inhibition of ERK signalling by RAF inhibitors is dependent on levels of RAS–GTP too low to support RAF dimerization is supported and a novel mechanism of acquired resistance in patients is identified: expression of splicing isoforms of BRAF(V600E) that dimerize in a RAS-independent manner.

TL;DR: The results demonstrate the feasibility of using whole-genome sequencing in the clinical setting to identify previously occult biomarkers of drug sensitivity that can aid in the identification of patients most likely to respond to targeted anticancer drugs.

TL;DR: An assay panel for mass spectrometry genotyping encompassing the most significant oncogenes in this disease encompassing 111 mutations in RET, BRAF, NRAS, HRAS, KRAS, PIK3CA, AKT1, and other related genes was designed to obtain comprehensive genetic information on advanced thyroid cancers.

TL;DR: Inactivating somatic mutations and frequent intragenic deletions of PARK2 in human malignancies are described and strongly point to PARK2 as a tumor suppressor on 6q25.2–q27 in cancer.