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BCL2 mutations do not confer adverse prognosis in follicular lymphoma patients treated with rituximab
Author(s) -
Huet Sarah,
SzaferGlusman Edith,
Tesson Bruno,
Xerri Luc,
Fairbrother Wayne J.,
Mukhyala Kiran,
Bolen Chris,
Punnoose Elizabeth,
To Laurie,
ChassagneClément Catherine,
Feugier Pierre,
Viari Alain,
Jardin Fabrice,
Salles Gilles,
Sujobert Pierre
Publication year - 2017
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.24701
Subject(s) - activation induced (cytidine) deaminase , rituximab , cytidine deaminase , follicular lymphoma , medicine , context (archaeology) , adverse effect , regimen , somatic hypermutation , lymphoma , cohort , mutation , oncology , prospective cohort study , biology , immunology , genetics , antibody , gene , b cell , paleontology
BCL2 mutations have been suggested to confer an adverse prognosis to follicular lymphoma (FL) patients, but their prognostic value has not been assessed in patients treated with a rituximab‐containing regimen. Here we evaluated the prognostic value of BCL2 mutations in a large prospective cohort of 252 patients with FL treated with immunochemotherapy in the PRIMA randomized trial. Using a DNA‐targeted sequencing approach, we detected amino acid altering mutations in 135 patients (54%) and showed that these mutations were probably mediated by the over‐activation of AICDA (activation‐induced cytidine deaminase) in the context of the t(14;18) translocation. The BCL2 variants identified in PRIMA patients affected the BH1, BH2, and BH3 functional motifs at a lower frequency than the N‐terminus and flexible loop domain, with mostly conservative aminoacid changes. With a median follow‐up of 6.7 years, we did not observe any impact of BCL2 mutations either on overall survival or progression‐free survival.