Cellular mechanisms of tumour suppression by the retinoblastoma gene

By Deborah L. Burkhart, Julien Sage. Nature Reviews. Cancer, 2008

998 citations recorded by the source corpus.

The retinoblastoma (RB) tumour suppressor gene is functionally inactivated in a broad range of paediatric and adult cancers, and a plethora of cellular functions and partners have been identified for the RB protein. Data from human tumours and studies from mouse models indicate that loss of RB function contributes to both cancer initiation and progression. However, we still do not know the identity of the cell types in which RB normally prevents cancer initiation in vivo, and the specific functions of RB that suppress distinct aspects of the tumorigenic process are poorly understood.

Subfields: Molecular Biology, Oncology, Ophthalmology

View Paper: https://www.semanticscholar.org/paper/42ff8c0bb2ea6d8b0a0e8324d110835f542694af

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Citations in the corpus

Dedifferentiation, transdifferentiation and reprogramming: three routes to regeneration (2011, background): “RB is a member of the pocket protein family and is crucial for arresting cell cycle progression by inhibiting E2F transcription factors and stabilizing the cell cycle inhibitor p27 (Ref”
Cell cycle regulation: p53-p21-RB signaling (2022, background): “Later, many tumor types were found to hold inactivated RB arising also from spontaneous alterations, particularly in small-cell lung cancer, glioma, esophageal cancer, and liver tumors [2].”
Adipogenesis: from stem cell to adipocyte. (2012, background): “Upon hyperphosphorylation of Rb (⇒ pRb) by cyclindependent kinases, E2F is released and promotes transcriptional activation of genes that encode cell-cycle regulators required for Sphase entry and progression of the cell cycle (70).”
Hallmarks of cancer: the next generation. (2011, positive): “The RB protein integrates signals from diverse extracellular and intracellular sources and, in response, decides whether or not a cell should proceed through its growth-and-division cycle (Burkhart and Sage, 2008; Deshpande et al., 2005; Sherr and McCormick, 2002).”
Emerging roles of E2Fs in cancer: an exit from cell cycle control (2009, neutral): “The RB tumour suppressor and the RB-related pocket proteins p107 and p130 directly associate with E2Fs and can be co-recruited to E2F-responsive promoters to modulate gene expressio”
RB1 methylation by SMYD2 enhances cell cycle progression through an increase of RB1 phosphorylation. (2012, background): “Although RB has been reported to be inactivated in more than 90% of human small cell lung carcinomas [1], most human cancers express wild-type RB that is predominantly at a phosphorylated state because of the deregulation of CDKs.”
Early Adaptation and Acquired Resistance to CDK4/6 Inhibition in Estrogen Receptor–Positive Breast Cancer (2016, positive): “The release of E2F transcription factors initiates an Sphase transcriptional programpromoting E-type cyclin andCDK2 expression and cell-cycle progression (7).”