<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12</volume><submitter>Kim SH</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Abemaciclib, a CDK4/6 inhibitor, is well-established for treating hormone receptor-positive and HER2-negative (HR&lt;sup>+&lt;/sup>/HER2&lt;sup>-&lt;/sup>) human breast cancer by inducing G1 cell cycle arrest. However, its antitumor effects in other cancers, including canine melanoma, remain largely unexplored. Canine melanoma often harbors CDK4/6 copy number gains and cell cycle dysregulation, suggesting it may be a suitable target for abemaciclib.&lt;h4>Methods&lt;/h4>Five canine melanoma cell lines (CMeC1, KMeC, LMeC, UCDK9M4, and UCDK9M5) were used to evaluate the antitumor effects of abemaciclib. Cell viability and migration were assessed using Cell Counting Kit-8 and wound healing assays, respectively. Cell cycle distribution was analyzed by flow cytometry, and the expression of c</pubmed_abstract><journal>Frontiers in veterinary science</journal><pagination>1603686</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12240792</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Abemaciclib induces G1 arrest and lysosomal dysfunction in canine melanoma cells: synergistic effects with fenbendazole.</pubmed_title><pmcid>PMC12240792</pmcid><pubmed_authors>Kim SH</pubmed_authors><pubmed_authors>Song KH</pubmed_authors><pubmed_authors>Choi JY</pubmed_authors><pubmed_authors>Ryu MO</pubmed_authors><pubmed_authors>Suh YH</pubmed_authors><pubmed_authors>Seo KW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Abemaciclib induces G1 arrest and lysosomal dysfunction in canine melanoma cells: synergistic effects with fenbendazole.</name><description>&lt;h4>Introduction&lt;/h4>Abemaciclib, a CDK4/6 inhibitor, is well-established for treating hormone receptor-positive and HER2-negative (HR&lt;sup>+&lt;/sup>/HER2&lt;sup>-&lt;/sup>) human breast cancer by inducing G1 cell cycle arrest. However, its antitumor effects in other cancers, including canine melanoma, remain largely unexplored. Canine melanoma often harbors CDK4/6 copy number gains and cell cycle dysregulation, suggesting it may be a suitable target for abemaciclib.&lt;h4>Methods&lt;/h4>Five canine melanoma cell lines (CMeC1, KMeC, LMeC, UCDK9M4, and UCDK9M5) were used to evaluate the antitumor effects of abemaciclib. Cell viability and migration were assessed using Cell Counting Kit-8 and wound healing assays, respectively. Cell cycle distribution was analyzed by flow cytometry, and the expression of c</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-07-15T12:48:26.633Z</modification><creation>2026-07-04T03:16:11.576Z</creation></dates><accession>S-EPMC12240792</accession><cross_references><pubmed>40642276</pubmed><doi>10.3389/fvets.2025.1603686</doi></cross_references></HashMap>