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2018
DOI: 10.1007/s11845-018-1751-z
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p16, p21, and p53 proteins play an important role in development of pancreatic intraepithelial neoplastic

Abstract: Background Deregulation of cell cycle takes place during the development of many cancers as well as pancreatic ductal adenocarcinoma (PDA), which develops from precursor lesions, most frequently including pancreatic intraepithelial neoplasia (PanIN). Aims The aim of this study was to evaluate and compare the expression of p16, p21, and p53 proteins taking part in the regulation of the cell cycle in normal pancreatic ducts and pancreatic intraepithelial neoplasia at its various advancing stages. Methods The exp… Show more

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Cited by 15 publications
(10 citation statements)
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“…A crucial checkpoint, controlled by the CDK4/6-cyclin D-Rb pathway, is the transition from G1 to S phase [ 144 ]. Consequently, dysregulation of the Rb pathway results in enhanced proliferation [ 145 , 146 , 147 , 148 ]. Against the background of a high frequency of KRAS mutations, which is the case in PDAC, the CDK4/6 inhibitor encoding function of the CDKN2A locus is principally relevant [ 26 ].…”
Section: The Role Of Cdks In Pancreatic Cancermentioning
confidence: 99%
“…A crucial checkpoint, controlled by the CDK4/6-cyclin D-Rb pathway, is the transition from G1 to S phase [ 144 ]. Consequently, dysregulation of the Rb pathway results in enhanced proliferation [ 145 , 146 , 147 , 148 ]. Against the background of a high frequency of KRAS mutations, which is the case in PDAC, the CDK4/6 inhibitor encoding function of the CDKN2A locus is principally relevant [ 26 ].…”
Section: The Role Of Cdks In Pancreatic Cancermentioning
confidence: 99%
“…Furthermore, ZNF655 knockdown resulted in downregulation of CCND1 expression and inhibition of PI3K/AKT signaling pathway in pancreatic cancer cells. Additionally, the characteristics of early lesions also include the inactivation of the tumor suppressor gene CDKN2A and the overexpression of the oncogene CDKN1A, which promote the transition of the cell cycle from the G1 phase to the S phase [36]. In later lesions, two key tumor suppressor genes, Smad4 and TP53, were inactivated.…”
Section: Discussionmentioning
confidence: 99%
“…The tumor suppressor p53 is a pivotal nuclear transcription factor that is activated by various cellular stress reactions such as oxidative stress and DNA damage and accumulates in the nucleus, thereby playing an important role in regulation of cell cycle and induction of irreversible apoptosis [53]. The cyclin-dependent kinase inhibitor (CDKI) p21 is a downstream effector of p53, and its activation under oxidative stress indicates that p53-dependent cell cycle arrest is completely triggered [54]. The interaction amongst cyclins, cyclin-dependent kinases (CDK), and CDKI is involved in the regulation of cell cycle.…”
Section: Discussionmentioning
confidence: 99%