Activation of caspase-3 and cleavage of Rb are associated with p16-mediated apoptosis in human non-small cell lung cancer cells.

Rb and p53 have roles in progression of primary non-small cell lung carcinoma

Retinoblastoma deficiency increases chemosensitivity in lung cancer.

simultaneous detection of p53, Rb, p16, and EGFR in a suspension microarray facilitates rapid diagnosis of lung cancer

Involvement of SNIP1 in progression of lung cancer by regulating the RB/HDAC1 interaction.

Genomic deregulation of the E2F/Rb pathway leads to activation of the oncogene EZH2 in small cell lung cancer.

RB1 polymorphism contributes to the efficacy of platinum-taxanes in advanced squamous cell lung cancer.

RB is lost in resistant EGFR mutant lung adenocarcinomas that transform to small-cell lung cancer.

These results indicate that the loss of RB1 and CDKN2A function induces distinctively different signaling cascades in non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma

The two most frequently mutated genes were TP53 (86%) and RB1 (58%); other frequently mutated genes (>10% patients) were involved in epigenetic regulation as well as the mTOR pathway.We found that small-cell lung cancer tumors harboring no mutation in RB1 had a poor response to chemotherapy.

Aberrant expressionof Rb is frequently occurred in lung adenocarcinoma patients with EGFR mutations.

MiR-661 promotes metastasis of non small cell lung cancer through RB/E2F1 signaling and epithelial-mesenchymal transition events.

Concurrent mutations, in genes such as CDKN2B or RB1, were associated with worse clinical outcome in lung adenocarcinoma patients with EGFR active mutations.

RB1 Loss Is Synthetic Lethal with Aurora B Kinase That Regulate Chromosomal Segregation in Small cell lung cancer.

a biomarker consisting of the phosphorylation of the retinoblastoma protein (Rb) on serine 249 combined with elevated p39 expression. This biomarker correlates with epithelial-to-mesenchymal transition traits in non-small cell lung carcinoma (NSCLC) cells.

Results found RB1 mutant status in 8.2% of a cohort of patients with non small cell lung cancer and strongly associated with worse outcomes.

Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EGFR-mutant tumors.

Silencing of KIF3A suppressed TNBC cell proliferation by repressing the Rb-E2F signaling pathway and inhibited migration and invasion by repressing epithelial-mesenchymal transition. The tumor size was smaller and the number of lung metastatic nodules was lower in KIF3A depletion MDA-MB-231 cell xenograft mice than in the negative control group. In addition, KIF3A overexpression correlated with chemoresistance.

FGFR1 Is Critical for RBL2 Loss-Driven tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell lung cancer.

The retinoblastoma gene Rb and its family member p130 suppress lung adenocarcinoma induced by oncogenic K-Ras.

p107 cooperates with Rb to protect against lung cancer

loss of Trp53 and Rb1 can efficiently transform neuroendocrine and SPC-expressing cells leading to small cell lung cancer.

NFIB overexpression interacts with Rb/p53 deletion to promote small cell lung cancer in a mouse model

Results show that ablation of the three members of the retinoblastoma family (RB1, p107 and p130) which targets a variety of adult lung epithelial cells, leads to spontaneous velopment of tumorlets, benign precancerous neuroendocrine (NE) lesions that do not progress to malignant tumors. Data imply the requirement of other oncogenic signaling pathways for full transformation in NE lung lesions mutant for the Rb family.