<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>159(1)</volume><submitter>Sanchez-Beato M</submitter><pubmed_abstract>Different studies have already shown that the isolated inactivation of p21, p16, or p27 cyclin-dependent kinase inhibitors (CKIs) is associated with increased growth fraction, tumor progression, or decreased overall survival in cases of non-Hodgkin's lymphoma. In this study we linked molecular study of the p53 and p16 genes with immunohistochemical analysis of p27 expression in a group of aggressive B-cell lymphomas [large B-cell lymphomas (LBCLs) and Burkitt's lymphomas]. This was done to analyze the relationship between p53 and p16 silencing, p27 anomalous overexpression, and clinical follow-up, testing the hypothesis that the accumulation of CKI alterations could confer to the tumors a higher aggressivity. In a group of 62 patients, p53 inactivation as a result of mutation was observed </pubmed_abstract><journal>The American journal of pathology</journal><pagination>205-13</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1850429</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Overall survival in aggressive B-cell lymphomas is dependent on the accumulation of alterations in p53, p16, and p27.</pubmed_title><pmcid>PMC1850429</pmcid><pubmed_authors>Piris MA</pubmed_authors><pubmed_authors>Sanchez-Beato M</pubmed_authors><pubmed_authors>Camacho F</pubmed_authors><pubmed_authors>Villuendas R</pubmed_authors><pubmed_authors>Saez AI</pubmed_authors><pubmed_authors>Sanchez E</pubmed_authors><pubmed_authors>Algara P</pubmed_authors><pubmed_authors>Sanchez-Aguilera A</pubmed_authors><pubmed_authors>Navas IC</pubmed_authors><pubmed_authors>Sol Mateo M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Overall survival in aggressive B-cell lymphomas is dependent on the accumulation of alterations in p53, p16, and p27.</name><description>Different studies have already shown that the isolated inactivation of p21, p16, or p27 cyclin-dependent kinase inhibitors (CKIs) is associated with increased growth fraction, tumor progression, or decreased overall survival in cases of non-Hodgkin's lymphoma. In this study we linked molecular study of the p53 and p16 genes with immunohistochemical analysis of p27 expression in a group of aggressive B-cell lymphomas [large B-cell lymphomas (LBCLs) and Burkitt's lymphomas]. This was done to analyze the relationship between p53 and p16 silencing, p27 anomalous overexpression, and clinical follow-up, testing the hypothesis that the accumulation of CKI alterations could confer to the tumors a higher aggressivity. In a group of 62 patients, p53 inactivation as a result of mutation was observed </description><dates><release>2001-01-01T00:00:00Z</release><publication>2001 Jul</publication><modification>2025-04-26T03:11:16.67Z</modification><creation>2019-06-06T13:37:49Z</creation></dates><accession>S-EPMC1850429</accession><cross_references><pubmed>11438467</pubmed><doi>10.1016/S0002-9440(10)61686-0</doi></cross_references></HashMap>