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The retinoblastoma (RB) tumor suppressor is mutated or functionally inactivated in the majority of human malignancies, and p16 INK4a -cyclin D1-cyclin-dependent kinase 4-RB pathway aberrations are present in nearly all cases of nonsmall cell lung cancer (NSCLC). Here, the distinct role of RB loss in tumorigenic proliferation and sensitivity to chemotherapeutics was determined in NSCLC cells. Attenuation of RB led to a proliferative advantage in vitro and aggressive tumorigenic growth indoi:10.1158/0008-5472.can-06-4753 pmid:17804741 fatcat:yulyxx2fevh3nmkdecdqpyim4q