{"title":"Ikaros as a downstream mediator of BCR blockade therapy in B-cell non-Hodgkin lymphoma.","authors":"Marcelo Lima Ribeiro, Emmanuel Normant, Gaël Roué","doi":"10.18632/oncoscience.568","DOIUrl":null,"url":null,"abstract":"B cell receptor (BCR) complex is essential for B cell development and function, being its downstream effectors involved in the regulation of several biological process such as immune response, cell growth, adhesion, differentiation, survival, cytoskeletal remodeling, and apoptosis [1]. Genetic events leading to BCR constitutive activation and consequent enhancement of tumor cell proliferation and survival, are frequently observed in B-cell non-Hodgkin lymphoma (B-NHL) patients [2]. In the last decade, numerous studies have highlighted that pharmacological targeting of Bruton’s tyrosine kinase (BTK), an apical component of the BCR axis, represents an excellent anti-tumor strategy in chronic lymphocytic leukemia (CLL) and in determined subtype of B-NHL including mantle cell lymphoma (MCL) and follicular lymphoma (FL). Most BTK inhibitors bind irreversibly to the ATP binding site of BTK at the Cys481 amino acid residue, forming a covalent bond that impairs the Editorial","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9708099/pdf/","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oncoscience","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.18632/oncoscience.568","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
B cell receptor (BCR) complex is essential for B cell development and function, being its downstream effectors involved in the regulation of several biological process such as immune response, cell growth, adhesion, differentiation, survival, cytoskeletal remodeling, and apoptosis [1]. Genetic events leading to BCR constitutive activation and consequent enhancement of tumor cell proliferation and survival, are frequently observed in B-cell non-Hodgkin lymphoma (B-NHL) patients [2]. In the last decade, numerous studies have highlighted that pharmacological targeting of Bruton’s tyrosine kinase (BTK), an apical component of the BCR axis, represents an excellent anti-tumor strategy in chronic lymphocytic leukemia (CLL) and in determined subtype of B-NHL including mantle cell lymphoma (MCL) and follicular lymphoma (FL). Most BTK inhibitors bind irreversibly to the ATP binding site of BTK at the Cys481 amino acid residue, forming a covalent bond that impairs the Editorial
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