دورية أكاديمية
أعرض في EDS

Resistance to complement activation, cell membrane hypersialylation and relapses in chronic lymphocytic leukemia patients treated with rituximab and chemotherapy.

التفاصيل البيبلوغرافية
العنوان: Resistance to complement activation, cell membrane hypersialylation and relapses in chronic lymphocytic leukemia patients treated with rituximab and chemotherapy.
المؤلفون: Bordron A; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France., Bagacean C; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France.; Laboratory of Immunology and Immunotherapy, CHRU Brest, Hôpital Morvan, Brest, France., Mohr A; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France., Tempescul A; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France.; Department of Haematology, CHRU Brest, Hôpital Morvan, Brest, France., Bendaoud B; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France.; Laboratory of Immunology and Immunotherapy, CHRU Brest, Hôpital Morvan, Brest, France., Deshayes S; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France., Dalbies F; Department of Haematology, CHRU Brest, Hôpital Morvan, Brest, France., Buors C; Laboratory of Haematology, CHRU Brest, Hôpital Morvan, Brest, France., Saad H; Department of Haematology, CHRU Brest, Hôpital Morvan, Brest, France., Berthou C; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France.; Department of Haematology, CHRU Brest, Hôpital Morvan, Brest, France., Pers JO; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France., Renaudineau Y; U1227 B Lymphocytes and Autoimmunity, Université de Brest, INSERM, IBSAM, Labex IGO, Networks IC-CGO and REpiCGO from 'Canceropole Grand Ouest, Brest, France.; Laboratory of Immunology and Immunotherapy, CHRU Brest, Hôpital Morvan, Brest, France.
المصدر: Oncotarget [Oncotarget] 2018 Aug 03; Vol. 9 (60), pp. 31590-31605. Date of Electronic Publication: 2018 Aug 03 (Print Publication: 2018).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Impact Journals Country of Publication: United States NLM ID: 101532965 Publication Model: eCollection Cited Medium: Internet ISSN: 1949-2553 (Electronic) Linking ISSN: 19492553 NLM ISO Abbreviation: Oncotarget Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Albany, N.Y. : Impact Journals
مستخلص: 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. In vitro CDC-resistance to RTX predicts lower response rates to RTX-chemotherapy and shorter treatment free survival. Furthermore, the predictive value of CDC-resistance was independent from the clinical, cytogenetic and FcγR3A V158F polymorphism status. In contrast, CLL cell resistance to CDC predominates in IGHV unmutated patients and was related to an important α2-6 sialyl transferase activity, which in turn increases cell surface α2-6 hypersialylation. Suspected factors associated with resistance to CDC (CD20, CD55, CD59, factor H, GM1, and sphingomyelin) were not differentially expressed or recruited between the two CLL groups. Altogether, results provide evidence that testing RTX capacity to induce CDC in vitro represents an independent predictive factor of therapeutic effects of RTX, and that α2-6 hypersialylation in CLL cells controls RTX response through the control of the complement pathway. At a time when CLL therapy is moving towards chemo-free treatments, further experiments are required to determine whether performing an initial in vitro assay to appreciate CLL CDC resistance might be useful to select patients.
Competing Interests: CONFLICTS OF INTEREST The authors declare no financial conflicts of interest.
التعليقات: Comment in: Oncotarget. 2018 Aug 28;9(67):32732-32733. (PMID: 30214679)
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فهرسة مساهمة: Keywords: chronic lymphocytic leukemia; complement-dependent cytotoxicity; progression-free survival; rituximab; sialylation
تواريخ الأحداث: Date Created: 20180901 Latest Revision: 20220408
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC6114972
DOI: 10.18632/oncotarget.25657
PMID: 30167081
قاعدة البيانات: MEDLINE
الوصف
تدمد:1949-2553
DOI:10.18632/oncotarget.25657