Clinical translational research of chimeric antigen receptor-T (CAR-T) cells for the treatment of relapsed and refractory B-cell lymphoma/leukemia / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 1137-1141, 2014.
Article
in Chinese
| WPRIM
| ID: wpr-302332
ABSTRACT
B-cell lymphoma and leukemia are the most common subtypes of malignant lymphomas. Relapse and refractory to multiple therapy are the main reasons of treatment failure. As the classical anti-tumor methods, surgery, radiation, chemotherapy and palliative therapy have cured lots of cancer patients. However, each year many patients still died of different kinds of hard-to-treat cancers. Although the ratio of complete remission of B-cell lymphoma/leukemia patients particularly with CD20 positive mature B cell malignancies has been largely increased after the application of Rituximab in clinic, nearly 20%-40% patients still died due to relapse and refractory to the treatment. During last five years, the development of chimeric antigen receptor-T (CAR-T) cells, especially CD19 CAR-T cells, which can recognize CD19 specifically expressed on B cells and have been demonstrated to be significantly effective to relapsed and refractory B cell lymphoma/leukemia in clinical trials, has gradually attracted extensively concerning from researchers and clinicians. Many medical institutions all over the world (besides in China) have registered the clinical trials for B-cell lymphoma/leukemia patients by use of CAR-T cells. In this review, we summarize the developmental history, the main ongoing clinical trials and proved potential adverse affects of CD19 CAR-T cells for the treatment of patients with B-cell lymphoma/leukemia.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Therapeutics
/
Remission Induction
/
Receptors, Antigen, T-Cell
/
Lymphoma, B-Cell
/
Therapeutic Uses
/
Allergy and Immunology
/
Translational Research, Biomedical
/
Cell- and Tissue-Based Therapy
Limits:
Humans
Language:
Chinese
Journal:
Journal of Experimental Hematology
Year:
2014
Type:
Article
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