<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gazinska P</submitter><funding>Cancer Research UK</funding><funding>Breast Cancer Now</funding><funding>National Institute for Health Research (NIHR)</funding><pagination>4494-4508</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9561554</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>28(20)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>To identify potential immune targets in post-neoadjuvant chemotherapy (NAC)-resistant triple-negative breast cancer (TNBC) and ER+HER2- breast cancer disease.&lt;h4>Experimental design&lt;/h4>Following pathology review, 153 patients were identified as having residual cancer burden (RCB) II/III disease (TNBC n = 80; ER+HER2-n = 73). Baseline pre-NAC samples were available for evaluation for 32 of 80 TNBC and 36 of 73 ER+HER2- cases. Bright-field hematoxylin and eosin assessment allowed for tumor-infiltrating lymphocyte (TIL) evaluation in all cases. Multiplexed immunofluorescence was used to identify the abundance and distribution of immune cell subsets. Levels of checkpoints including PD-1/PD-L1 expression were also quantified. Findings were then validated using expression profil</pubmed_abstract><journal>Clinical cancer research : an official journal of the American Association for Cancer Research</journal><pubmed_title>Dynamic Changes in the NK-, Neutrophil-, and B-cell Immunophenotypes Relevant in High Metastatic Risk Post Neoadjuvant Chemotherapy-Resistant Early Breast Cancers.</pubmed_title><pmcid>PMC9561554</pmcid><funding_grant_id>24869</funding_grant_id><funding_grant_id>C56773 / A24869</funding_grant_id><funding_grant_id>DRCRPGTD-Nov21\100001</funding_grant_id><funding_grant_id>CL-2015-22-002</funding_grant_id><pubmed_authors>Melcher A</pubmed_authors><pubmed_authors>Naidoo K</pubmed_authors><pubmed_authors>Buus R</pubmed_authors><pubmed_authors>Wesseling J</pubmed_authors><pubmed_authors>Roxanis I</pubmed_authors><pubmed_authors>Ward J</pubmed_authors><pubmed_authors>Lips E</pubmed_authors><pubmed_authors>Khan A</pubmed_authors><pubmed_authors>Milton C</pubmed_authors><pubmed_authors>Alaguthurai T</pubmed_authors><pubmed_authors>Gillett C</pubmed_authors><pubmed_authors>Iacovacci J</pubmed_authors><pubmed_authors>Gazinska P</pubmed_authors><pubmed_authors>Marafioti T</pubmed_authors><pubmed_authors>Dowsett M</pubmed_authors><pubmed_authors>Irshad S</pubmed_authors><pubmed_authors>Graham R</pubmed_authors><pubmed_authors>Akarca A</pubmed_authors><pubmed_authors>Salgado R</pubmed_authors><pubmed_authors>Haider S</pubmed_authors><pubmed_authors>Tutt A</pubmed_authors><pubmed_authors>Cheang M</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dynamic Changes in the NK-, Neutrophil-, and B-cell Immunophenotypes Relevant in High Metastatic Risk Post Neoadjuvant Chemotherapy-Resistant Early Breast Cancers.</name><description>&lt;h4>Purpose&lt;/h4>To identify potential immune targets in post-neoadjuvant chemotherapy (NAC)-resistant triple-negative breast cancer (TNBC) and ER+HER2- breast cancer disease.&lt;h4>Experimental design&lt;/h4>Following pathology review, 153 patients were identified as having residual cancer burden (RCB) II/III disease (TNBC n = 80; ER+HER2-n = 73). Baseline pre-NAC samples were available for evaluation for 32 of 80 TNBC and 36 of 73 ER+HER2- cases. Bright-field hematoxylin and eosin assessment allowed for tumor-infiltrating lymphocyte (TIL) evaluation in all cases. Multiplexed immunofluorescence was used to identify the abundance and distribution of immune cell subsets. Levels of checkpoints including PD-1/PD-L1 expression were also quantified. Findings were then validated using expression profil</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2026-05-28T03:45:45.788Z</modification><creation>2025-04-06T00:51:07.62Z</creation></dates><accession>S-EPMC9561554</accession><cross_references><pubmed>36161312</pubmed><doi>10.1158/1078-0432.CCR-22-0543</doi></cross_references></HashMap>