{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Haertle L"],"funding":["Deutsche Forschungsgemeinschaft","Instituto de Salud Carlos III"],"pagination":["e110"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11237348"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(7)"],"pubmed_abstract":["Multiple myeloma (MM) is a genetically heterogeneous disease and the management of relapses is one of the biggest clinical challenges. <i>TP53</i> alterations are established high-risk markers and are included in the current disease staging criteria. <i>KRAS</i> is the most frequently mutated gene affecting around 20% of MM patients. Applying Clonal Competition Assays (CCA) by co-culturing color-labeled genetically modified cell models, we recently showed that mono- and biallelic alterations in <i>TP53</i> transmit a fitness advantage to the cells. Here, we report a similar dynamic for two mutations in <i>KRAS</i> (G12A and A146T), providing a biological rationale for the high frequency of <i>KRAS</i> and <i>TP53</i> alterations at MM relapse. Resistance mutations, on the other hand, did n"],"journal":["HemaSphere"],"pubmed_title":["Clonal competition assays identify fitness signatures in cancer progression and resistance in multiple myeloma."],"pmcid":["PMC11237348"],"funding_grant_id":["FIS No. PI21/00314","544189139","Miguel Servet CP22/00082","442740310","493951700"],"pubmed_authors":["Muller N","Stuhmer T","Vogt C","Hernandez HNC","Steinbrunn T","Hoschle C","Han S","Heckel T","Buenache N","Zhou X","Munawar U","Bassermann F","Barrio S","Martin L","Rasche L","Bischler T","Haertle L","Martin Kortum K","Arroyo-Barea A","Cuenca I","Del Campo PL","Waldschmidt J","Martinez-Lopez J"],"additional_accession":[]},"is_claimable":false,"name":"Clonal competition assays identify fitness signatures in cancer progression and resistance in multiple myeloma.","description":"Multiple myeloma (MM) is a genetically heterogeneous disease and the management of relapses is one of the biggest clinical challenges. <i>TP53</i> alterations are established high-risk markers and are included in the current disease staging criteria. <i>KRAS</i> is the most frequently mutated gene affecting around 20% of MM patients. Applying Clonal Competition Assays (CCA) by co-culturing color-labeled genetically modified cell models, we recently showed that mono- and biallelic alterations in <i>TP53</i> transmit a fitness advantage to the cells. Here, we report a similar dynamic for two mutations in <i>KRAS</i> (G12A and A146T), providing a biological rationale for the high frequency of <i>KRAS</i> and <i>TP53</i> alterations at MM relapse. Resistance mutations, on the other hand, did n","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-01T13:30:50.473Z","creation":"2025-04-05T15:47:25.29Z"},"accession":"S-EPMC11237348","cross_references":{"pubmed":["38993727"],"doi":["10.1002/hem3.110"]}}