PRJNA419878
A genome-wide forward genetic screen in transposon mutagenized human colorectal carcinomas cells
The Ras pathway genes KRAS, BRAF or ERBBs have somatic mutations in ~60% of human colorectal carcinomas. At present, it is unknown whether the remaining cases lack mutations activating the Ras pathway, or whether they have acquired mutations in genes hitherto not known to belong to the pathway. To address the second possibility, and extend the compendium of Ras pathway genes, we used genome-wide transposon mutagenesis of the colorectal cancer cell systems deprived of their activating KRAS or BRAF allele to identify genes enabling growth in low glucose, a Ras pathway phenotype, when targeted.