Cell cycle, CDKs and cancer: a changing paradigm

By Marcos Malumbres, M. Barbacid. Nature Reviews. Cancer, 2009

3,805 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/ef65d6d99c7ffd12cf75a1f4ed2a3cdacfe1782c

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Citations in the corpus

Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “If the damage is irreparable due to excessive or continuous DNA damage, cells may enter senescence or undergo apoptosis (reviewed in Malumbres and Barbacid, 2009).”
Cdks, cyclins and CKIs: roles beyond cell cycle regulation (2013, background): “This increased Cdk complexity is thought to satisfy the requirement for a more elaborate control over the proliferation of different cell types during the advancement from unicellular to complex multicellular organisms (Malumbres and Barbacid, 2009).”
p21 in cancer: intricate networks and multiple activities (2009, background): “CDK1, at least in some tissues, may be the crucial target of p21 in tumorigenesi”
Programmed Cell Death in Animal Development and Disease (2011, neutral): “Other examples include the elimination of cells in response to viral infection, unrepaired DNA damage, cellcycle perturbations, and fate and differentiation defects (Abrams et al., 1993; Rossel and Capecchi, 1999; Derry et al., 2001, Vousden and Prives, 2009; Malumbres and Barbacid, 2009; Koto et al”
Subtype-specific genomic alterations define new targets for soft tissue sarcoma therapy (2010, neutral): “Furthermore, pharmacological inhibition of CDK4 in dedifferentiated liposarcoma cells with PD0332991, a selective CDK4 and CDK6 inhibitor currently in clinical trial”
The cell cycle and cancer (2012, background): “This releases the brakes on cell cycle progression, and further abrogation of checkpoint control mechanisms leads to the acquisition of genomic instability, which drives tumour evolution [12].”
Cyclin-dependent kinases (2014, background): “This simplified view is obscured owing to multiple non-consensus interactions between CDKs and cyclins and compensatory roles [6].”
Cell cycle kinases as therapeutic targets for cancer (2009, background): “In complex with cyclin A, CDK1 is abruptly activated at the transition from the second gap (G2) phase to the mitosis (M) phase to facilitate the commencement of mitosis through regulation of chromosome condensation and microtubule dynamic”
MONARCH 1, a phase 2 study of abemaciclib, a CDK4 and CDK6 inhibitor, as a single agent, in patients with refractory HR+/HER2− metastatic breast cancer (2017, background): “CDK4 and CDK6, together with D-type cyclins, phosphorylate the Retinoblastoma (Rb) tumor-suppressor protein, leading to release of Rb-bound E2F, which enables progression from the G1 to S phase of the cell cycle (15, 16).”