Title of article :
Effective response and delayed toxicities of refractory advanced diffuse large B-cell lymphoma treated by CD20-directed chimeric antigen receptor-modified T cells
Author/Authors :
Wang، نويسنده , , Yao and Zhang، نويسنده , , Wenying and Han، نويسنده , , Qing-wang and Liu، نويسنده , , Yang and Dai، نويسنده , , Han-ren and Guo، نويسنده , , Ye-lei and Bo، نويسنده , , Jian and Fan، نويسنده , , Hui and Zhang، نويسنده , , Yan and Zhang، نويسنده , , Yajing and Chen، نويسنده , , Mei-xia and Feng، نويسنده , , Kai-chao and Wang، نويسنده , , Quan-shun and Fu، نويسنده , , Xiao-Bing and Han، نويسنده , , Wei-dong، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
16
From page :
160
To page :
175
Abstract :
We conducted a trial testing a CD20-specific CAR coupled with CD137 and the CD3ζ moiety in patients with chemotherapy refractory advanced diffuse large B cell lymphomas (DLBCL). Seven patients were enrolled. One of the two patients with no bulky tumor obtained a 14-month durable and ongoing complete remission by cell infusion only, and another attained a 6-month tumor regression. Four of five patients with bulky tumor burden were evaluable for clinical efficacy, three of which attained 3- to 6-month tumor regression. Delayed toxicities related to cell infusion are directly correlated to tumor burden and tumor-harboring sites, and mainly included cytokine release symptoms, tumor lysis symptoms, massive hemorrhage of the alimentary tract and aggressive intrapulmonary inflammation surrounding extranodal lesions. These results show firstly that anti-CD20 CART cells can cause prolonged tumor regression in combination with debulking conditioning regimens for advanced DLBCL. This study is registered at www.clinicaltrials.gov as NCT01735604.
Keywords :
Refractory advanced , Diffuse large B-cell lymphoma (DLBCL) , Delayed toxicities , Anti-CD20 chimeric antigen receptor (CAR) T cells
Journal title :
Clinical Immunology
Serial Year :
2014
Journal title :
Clinical Immunology
Record number :
1857130
Link To Document :
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