<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Papadimitriou M</submitter><funding>NCI NIH HHS</funding><pubmed_abstract>Recent data highlight genomic events driving antigen escape as a recurring cause of chimeric antigen receptor T-cell (CAR-T) and bispecific T-cell engager (TCE) resistance in multiple myeloma (MM). Yet, it remains unclear if these events, leading to clonal dominance at progression, result from acquisition under treatment selection or selection of pre-existing undetectable clones. This differentiation gains importance as these immunotherapies progress to earlier lines of treatment, prompting the need for innovative diagnostic testing to detect these events early on. By reconstructing phylogenetic trees and exploring chemotherapy mutational signatures as temporal barcodes in 11 relapsed refractory MM patients with available whole genome sequencing data before and after CART/TCE treatment, we</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2024.05.22.595383</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11142165</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Timing antigenic escape in multiple myeloma treated with T-cell redirecting immunotherapies.</pubmed_title><pmcid>PMC11142165</pmcid><funding_grant_id>P30 CA240139</funding_grant_id><pubmed_authors>Neri P</pubmed_authors><pubmed_authors>Truger M</pubmed_authors><pubmed_authors>Diamond B</pubmed_authors><pubmed_authors>Ziccheddu B</pubmed_authors><pubmed_authors>Bahlis NJ</pubmed_authors><pubmed_authors>Lee H</pubmed_authors><pubmed_authors>Durante M</pubmed_authors><pubmed_authors>Landgren O</pubmed_authors><pubmed_authors>Papadimitriou M</pubmed_authors><pubmed_authors>Rasche L</pubmed_authors><pubmed_authors>McIntyre J</pubmed_authors><pubmed_authors>Maura F</pubmed_authors><pubmed_authors>Ahn S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Timing antigenic escape in multiple myeloma treated with T-cell redirecting immunotherapies.</name><description>Recent data highlight genomic events driving antigen escape as a recurring cause of chimeric antigen receptor T-cell (CAR-T) and bispecific T-cell engager (TCE) resistance in multiple myeloma (MM). Yet, it remains unclear if these events, leading to clonal dominance at progression, result from acquisition under treatment selection or selection of pre-existing undetectable clones. This differentiation gains importance as these immunotherapies progress to earlier lines of treatment, prompting the need for innovative diagnostic testing to detect these events early on. By reconstructing phylogenetic trees and exploring chemotherapy mutational signatures as temporal barcodes in 11 relapsed refractory MM patients with available whole genome sequencing data before and after CART/TCE treatment, we</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 May</publication><modification>2026-06-05T03:24:18.423Z</modification><creation>2026-06-05T03:11:57.498Z</creation></dates><accession>S-EPMC11142165</accession><cross_references><pubmed>38826396</pubmed><doi>10.1101/2024.05.22.595383</doi></cross_references></HashMap>