CDKN1A


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CDKN1A

A gene on chromosome 6p21.2 that encodes a cyclin-dependent kinase inhibitor, which binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, thus acting as a regulator of cell cycle progression at G1. CDKN1A expression is controlled by p53, a tumour suppressor that mediates p53-dependent cell cycle G1-phase arrest in response to various stress stimuli. CDKN1A is specifically cleaved by CASP3-like caspases, activating CDK2 and possibly also the apoptosis pathway.
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Other genes that have emerged as significantly mutated genes in whole-exome sequencing studies of serous endometrial carcinomas are SPOP, a putative tumor suppressor gene; CDKN1A [cyclin-dependent kinase inhibitor 1A (p21, Cip1)], a bona fide cancer gene; TAF1; HCFC1R1 [host cell factor C1 regulator 1 (XPO1 dependent)]; CTDSPL [CTD (carboxy-terminal domain, RNA polymerase II, polypeptide A) small phosphatase-like]; YIPF3 (Yip1 domain family, member 3); and FAM132A (family with sequence similarity 132, member A) (17, 18).
Postmenopausal hormone therapy is associated with a reduced risk of colorectal cancer lacking CDKN1A expression.
It was also shown to increase the expression of CDKN1A (p21), a gene that inhibits prostate cancer.
A second variant identified was in a gene called CDKN1A which governs a number of tumour suppressing biological pathways.
The wide array of molecular-based PCa markers includes proliferation index (Ki-67), microvessel density, nuclear morphometry, tumor suppressor genes (eg, TP53, CDKN1A, CDKN1B, NKX3-1, PTEN, and the retinoblastoma gene Rb), oncogenes (eg, BCL2, MYC, EZH2, and ERBB2 [formerly HER2/neu]), adhesion molecules (eg, CD44 and E-cadherin), the PI3K/Akt/mTOR (mammalian target of rapamycin) pathway, (30,31) apoptosis regulators (eg, survivin and transforming growth factor p1), androgen receptor status, neuroendocrine differentiation markers, and prostate tissue lineage-specific markers (PSA, prostate-specific acid phosphatase, and prostate-specific membrane antigen).
The formula also increased expression of CDKN1A, a gene that fights prostate cancer by inhibiting cancer-promoting cellular mechanisms.
The formula also significantly increased the expression of a gene that fights against prostate cancer, CDKN1A, which works by specifically inhibiting other cancer-promoting cellular mechanisms.
miR-106b, which has been shown to be part of an oncogenic miRNA cluster that regulates PTEN, has been suggested to have a regulatory effect on CDKN1A (40).
Immunohistochemical labeling of several genes including CDKN1A, (12) PSCA, (7,13) MMP7, (14) MUC4, (15,16) CLDN18, (17) ANXA2, (18) BIRC5, (19,20) MUC5, (7) and S100P (21) in multiple PanIN lesions has shown a progressive increase in their expression from low- to high-grade PanINs and leading into invasive cancer.