<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gu SS</submitter><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>263</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7559192</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Immune checkpoint blockade (ICB) therapy has improved patient survival in a variety of cancers, but only a minority of cancer patients respond. Multiple studies have sought to identify general biomarkers of ICB response, but elucidating the molecular and cellular drivers of resistance for individual tumors remains challenging. We sought to determine whether a tumor with defined genetic background exhibits a stereotypic or heterogeneous response to ICB treatment.&lt;h4>Results&lt;/h4>We establish a unique mouse system that utilizes clonal tracing and mathematical modeling to monitor the growth of each cancer clone, as well as the bulk tumor, in response to ICB. We find that tumors derived from the same clonal populations showed heterogeneous ICB response and diverse response pa</pubmed_abstract><journal>Genome biology</journal><pubmed_title>Clonal tracing reveals diverse patterns of response to immune checkpoint blockade.</pubmed_title><pmcid>PMC7559192</pmcid><funding_grant_id>P50 CA206963</funding_grant_id><funding_grant_id>P50 CA101942</funding_grant_id><funding_grant_id>K99 CA248953</funding_grant_id><funding_grant_id>U01 CA226196</funding_grant_id><funding_grant_id>R01 CA234018</funding_grant_id><pubmed_authors>Long H</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Hu X</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Liu XS</pubmed_authors><pubmed_authors>Jiang P</pubmed_authors><pubmed_authors>Cejas P</pubmed_authors><pubmed_authors>Tang Q</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Meyer C</pubmed_authors><pubmed_authors>Xing X</pubmed_authors><pubmed_authors>Zeng Z</pubmed_authors><pubmed_authors>Gu SS</pubmed_authors><pubmed_authors>Kroger B</pubmed_authors><pubmed_authors>Zhang W</pubmed_authors><pubmed_authors>Traugh N</pubmed_authors><pubmed_authors>Freeman GJ</pubmed_authors><pubmed_authors>Sahu AD</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Bu X</pubmed_authors><pubmed_authors>Brown M</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Fu J</pubmed_authors><pubmed_authors>Lim K</pubmed_authors><pubmed_authors>Ouyang Z</pubmed_authors><pubmed_authors>Tokheim C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Clonal tracing reveals diverse patterns of response to immune checkpoint blockade.</name><description>&lt;h4>Background&lt;/h4>Immune checkpoint blockade (ICB) therapy has improved patient survival in a variety of cancers, but only a minority of cancer patients respond. Multiple studies have sought to identify general biomarkers of ICB response, but elucidating the molecular and cellular drivers of resistance for individual tumors remains challenging. We sought to determine whether a tumor with defined genetic background exhibits a stereotypic or heterogeneous response to ICB treatment.&lt;h4>Results&lt;/h4>We establish a unique mouse system that utilizes clonal tracing and mathematical modeling to monitor the growth of each cancer clone, as well as the bulk tumor, in response to ICB. We find that tumors derived from the same clonal populations showed heterogeneous ICB response and diverse response pa</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Oct</publication><modification>2025-04-22T14:58:43.981Z</modification><creation>2020-10-29T12:36:02Z</creation></dates><accession>S-EPMC7559192</accession><cross_references><pubmed>33059736</pubmed><doi>10.1186/s13059-020-02166-1</doi></cross_references></HashMap>