The RB and p53 pathways in cancer.

By C. Sherr, F. McCormick. Cancer Cell, 2002

1,792 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Ophthalmology

View Paper: https://www.semanticscholar.org/paper/a566bcd3435e21210fa91f95c1537f0f94a44460

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Citations in the corpus

Mutual exclusivity analysis identifies oncogenic network modules. (2012, methodology): “Because all genes in these two modules are members of the p53 signaling pathway (Sherr and McCormick 2002), we merged them and tested the resulting set of four genes for mutual exclusivity.”
Hallmarks of cancer: the next generation. (2011, neutral): “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).”
Sirt3-Mediated Deacetylation of Evolutionarily Conserved Lysine 122 Regulates MnSOD Activity in Response to Stress (2010, background): “Mammalian cells contain tumor suppressor (TS) genes, such as p53, and loss of TS function results in a damage-permissive phenotype (Sherr and McCormick, 2002) that is an early event in carcinogenesis.”
High-Dimensional Sparse Factor Modeling: Applications in Gene Expression Genomics (2008, background): “Structure Linked to p53 We begin with 25 genes known to participate in the p53 pathway (Sherr and McCormick 2002), none of which were included in Miller’s ﬁnal 32-gene signature.”
Cellular senescence: when bad things happen to good cells (2007, background): “p53 and pRB are transcriptional regulators, and the pathways they govern are frequently disrupted in cance”
Oxidative Stress in Aging Human Skin (2015, background): “The main candidate for the cell cycle arrest is p21 that is a very potent cyclin-dependent kinase inhibitor acting on CDK2 and CDK4 [343,349,352–355].”
Cell-cycle checkpoints and cancer (2004, background): “This is before the cells pass through the RB (retinoblastoma protein)/E2F (transcription factor)-controlled restriction point, after which they are committed to a round of DNA replication and cell divisio”
Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets (2007, background): “or by inhibiting its function (selective CDK kinase inhibitors”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “The Rb pathway In quiescent cells, hypophosphory-lated RB blocks proliferation by binding and sequestering the E2F family of transcription factors, which prevents the transactivation of genes essential for progression through the cell cycle (Sherr and McCormick 2002).”
RB1 methylation by SMYD2 enhances cell cycle progression through an increase of RB1 phosphorylation. (2012, background): “Importantly, most human tumors carry mutations that disable RB protein-mediated repression of E2F [5].”
Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence (2006, neutral): “dtd" [ ]> p53 limits the proliferation of primary diploid fibroblasts by inducing a state of growth arrest named replicative senescence — a process which protects against oncogenic transformation and requires integrity of the p53 tumour suppressor pathwa”