Lkb1 Loss Promotes Tumor Progression of BRAFV600E-Induced Lung Adenomas

摘要: Aberrant activation of MAP kinase signaling pathway and loss tumor suppressor LKB1 have been implicated in lung cancer development progression. Although oncogenic KRAS mutations are frequent, BRAF (BRAFV600E) found 3% human non-small cell cancers. Contrary to mutant tumors, BRAFV600E-induced tumors benign adenomas that fail progess. Interestingly, supressor coexists with synergizes formation progression, however, its cooperation BRAFV600E oncogene is unknown. Our results describe a population neonates mice where expression leads adenoma development. Importantly, concomitant the only single-copy Lkb1, overcomes senencence–like features BRAFV600E-mutant leading malignization carcinomas. These posit haploinsufficiency as risk factor for progression mutated patients.