<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>125(10)</volume><submitter>Aliagas E</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>There is no effective therapy for patients with malignant pleural mesothelioma (MPM) who progressed to platinum-based chemotherapy and immunotherapy.&lt;h4>Methods&lt;/h4>We aimed to investigate the antitumor activity of CDK4/6 inhibitors using in vitro and in vivo preclinical models of MPM.&lt;h4>Results&lt;/h4>Based on publicly available transcriptomic data of MPM, patients with CDK4 or CDK6 overexpression had shorter overall survival. Treatment with abemaciclib or palbociclib at 100 nM significantly decreased cell proliferation in all cell models evaluated. Both CDK4/6 inhibitors significantly induced G1 cell cycle arrest, thereby increasing cell senescence and increased the expression of interferon signalling pathway and tumour antigen presentation process in culture models of M</pubmed_abstract><journal>British journal of cancer</journal><pagination>1365-1376</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8576019</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Efficacy of CDK4/6 inhibitors in preclinical models of malignant pleural mesothelioma.</pubmed_title><pmcid>PMC8576019</pmcid><pubmed_authors>Llatjos R</pubmed_authors><pubmed_authors>Hernandez-Madrigal M</pubmed_authors><pubmed_authors>Varela M</pubmed_authors><pubmed_authors>Ruffinelli JC</pubmed_authors><pubmed_authors>Vidal A</pubmed_authors><pubmed_authors>Sanchez-Cespedes M</pubmed_authors><pubmed_authors>Sharkley AJ</pubmed_authors><pubmed_authors>Pros E</pubmed_authors><pubmed_authors>Aliagas E</pubmed_authors><pubmed_authors>Palmero R</pubmed_authors><pubmed_authors>Aso S</pubmed_authors><pubmed_authors>Nadal E</pubmed_authors><pubmed_authors>Padrones S</pubmed_authors><pubmed_authors>Dawson A</pubmed_authors><pubmed_authors>Escobar I</pubmed_authors><pubmed_authors>Sole X</pubmed_authors><pubmed_authors>Villanueva A</pubmed_authors><pubmed_authors>Munoz-Pinedo C</pubmed_authors><pubmed_authors>Saigi M</pubmed_authors><pubmed_authors>Dorca E</pubmed_authors><pubmed_authors>Ramos R</pubmed_authors><pubmed_authors>Alay A</pubmed_authors><pubmed_authors>Busacca S</pubmed_authors><pubmed_authors>Cordero D</pubmed_authors><pubmed_authors>Martinez-Iniesta M</pubmed_authors><pubmed_authors>Fennell D</pubmed_authors><pubmed_authors>Gausachs M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Efficacy of CDK4/6 inhibitors in preclinical models of malignant pleural mesothelioma.</name><description>&lt;h4>Background&lt;/h4>There is no effective therapy for patients with malignant pleural mesothelioma (MPM) who progressed to platinum-based chemotherapy and immunotherapy.&lt;h4>Methods&lt;/h4>We aimed to investigate the antitumor activity of CDK4/6 inhibitors using in vitro and in vivo preclinical models of MPM.&lt;h4>Results&lt;/h4>Based on publicly available transcriptomic data of MPM, patients with CDK4 or CDK6 overexpression had shorter overall survival. Treatment with abemaciclib or palbociclib at 100 nM significantly decreased cell proliferation in all cell models evaluated. Both CDK4/6 inhibitors significantly induced G1 cell cycle arrest, thereby increasing cell senescence and increased the expression of interferon signalling pathway and tumour antigen presentation process in culture models of M</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Nov</publication><modification>2026-05-08T11:20:28.054Z</modification><creation>2025-04-19T11:44:19.528Z</creation></dates><accession>S-EPMC8576019</accession><cross_references><pubmed>34588615</pubmed><doi>10.1038/s41416-021-01547-y</doi></cross_references></HashMap>