<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(60)</volume><submitter>Bordron A</submitter><pubmed_abstract>The anti-CD20-specific monoclonal antibody rituximab (RTX), in combination with chemotherapy, is commonly used for primary treatment in chronic lymphocytic leukemia (CLL). However, relapses remain important and activation of the complement pathway is one of the mechanisms by which RTX generates the destruction of B cells directly by complement-dependent cytotoxicity (CDC), or indirectly by antibody-dependent cellular phagocytosis. In this study, the RTX capacity to induce CDC was established in 69 untreated CLL patients, this cohort including 34 patients tested before the initiation of RTX-chemotherapy. &lt;i>In vitro&lt;/i> CDC-resistance to RTX predicts lower response rates to RTX-chemotherapy and shorter treatment free survival. Furthermore, the predictive value of CDC-resistance was independ</pubmed_abstract><journal>Oncotarget</journal><pagination>31590-31605</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6114972</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Resistance to complement activation, cell membrane hypersialylation and relapses in chronic lymphocytic leukemia patients treated with rituximab and chemotherapy.</pubmed_title><pmcid>PMC6114972</pmcid><pubmed_authors>Bendaoud B</pubmed_authors><pubmed_authors>Deshayes S</pubmed_authors><pubmed_authors>Buors C</pubmed_authors><pubmed_authors>Bagacean C</pubmed_authors><pubmed_authors>Dalbies F</pubmed_authors><pubmed_authors>Pers JO</pubmed_authors><pubmed_authors>Renaudineau Y</pubmed_authors><pubmed_authors>Berthou C</pubmed_authors><pubmed_authors>Tempescul A</pubmed_authors><pubmed_authors>Bordron A</pubmed_authors><pubmed_authors>Mohr A</pubmed_authors><pubmed_authors>Saad H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Resistance to complement activation, cell membrane hypersialylation and relapses in chronic lymphocytic leukemia patients treated with rituximab and chemotherapy.</name><description>The anti-CD20-specific monoclonal antibody rituximab (RTX), in combination with chemotherapy, is commonly used for primary treatment in chronic lymphocytic leukemia (CLL). However, relapses remain important and activation of the complement pathway is one of the mechanisms by which RTX generates the destruction of B cells directly by complement-dependent cytotoxicity (CDC), or indirectly by antibody-dependent cellular phagocytosis. In this study, the RTX capacity to induce CDC was established in 69 untreated CLL patients, this cohort including 34 patients tested before the initiation of RTX-chemotherapy. &lt;i>In vitro&lt;/i> CDC-resistance to RTX predicts lower response rates to RTX-chemotherapy and shorter treatment free survival. Furthermore, the predictive value of CDC-resistance was independ</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Aug</publication><modification>2025-05-31T23:46:07.998Z</modification><creation>2019-03-26T23:54:09Z</creation></dates><accession>S-EPMC6114972</accession><cross_references><pubmed>30167081</pubmed><doi>10.18632/oncotarget.25657</doi></cross_references></HashMap>