Saturday 29 November 2003
CDKN1A plays a critical role in the cellular response to DNA damage, and its overexpression results in cell cycle arrest.
Upregulation of CDKN1A mRNA and protein following ionizing radiation is dependent on p53 (TP53; 191170), and CDKN1A mediates cell cycle arrest in response to the p53 checkpoint pathway.
CDKN1A (p21) and CDKN1B (p27 or KIP1) block the cell cycle by binding to cyclin-CDK complexes. p21 is induced by the tumor suppressor p53 (TP53).
CDKN1B (p27 or KIP1) responds to growth suppressors such as transforming growth factor-β (TGFBs).
Expression of p21 protein predicts clinical outcome in DLBCL patients older than 60 years treated with R-CHOP but not CHOP (#20371683#).
- p21 protein expression emerged as an important independent predictor of a favorable clinical outcome when rituximab was added to CHOP therapy.
- rituximab-related effects on lymphoma survival pathways may be functionally linked to p21 activity.
Cip/Kip family: CDKN1A (p21) and CDKN1B (p27 or KIP1)
Rowland BD, Peeper DS. KLF4, p21 and context-dependent opposing forces in cancer. Nat Rev Cancer. 2006 Jan;6(1):11-23. PMID: #16372018#
Gartel AL, Radhakrishnan SK. Lost in transcription: p21 repression, mechanisms, and consequences. Cancer Res. 2005 May 15;65(10):3980-5. PMID: #15899785#
Kumar R, Hung MC. Signaling intricacies take center stage in cancer cells. Cancer Res. 2005 Apr 1;65(7):2511-5. PMID: #15805240#
Coqueret O. New roles for p21 and p27 cell-cycle inhibitors: a function for each cell compartment? Trends Cell Biol. 2003 Feb;13(2):65-70. PMID: #12559756#