Arsenic induced complete remission in a refractory T-ALL patient with a distinct T-cell clonal evolution without molecular complete remission: A case report.
Currently, arsenic trioxide therapy is widely used for the treatment of acute promyelocytic leukemia (APL), relapsed and refractory adult T-cell leukemia/lymphoma and myelodysplastic syndrome. Regarding the broad antitumor activity of arsenic, certain studies have been undertaken to test its efficacy in treating acute T-cell lymphoblastic leukemia (T-ALL) cell lines and patients; however, to the best of our knowledge, no reports document that arsenic is able to induce the remission of T-ALL patients. The present study reports the case of young male patient diagnosed with T-ALL, with no significant response to common chemotherapy regimens, who finally achieved complete remission without minimal residual disease (as detected by flow cytometry) due to arsenic treatment. This result is encouraging, and the present study has shown that malignant TCRαβ+cell clones can be detected at the molecular level using reverse transcription-polymerase chain reaction (PCR) combined with the GeneScan technique. The result is mainly based on the T-cell receptor (TCR) Vβ1 clone (a 190-base pair PCR product that with the same complementarity determining region 3 length can be detected for all samples collected during various statuses) and on undetectable TCR Vγ subfamily members, at the time of disease diagnosis. It is important to analyze the dynamically changing TCR pool in leukemia patients during therapy. Although the molecular mechanism through which arsenic contributes to malignant clone elimination remains unclear in the case presented, the use of arsenic is expected to be effective for clinically treating refractory and relapsed T-ALL patients.
Department of Hematology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Suijing
S
Wu
Institute of Hematology, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Ling
L
Xu
Department of Hematology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Xin
X
Huang
Department of Hematology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Suxia
S
Geng
Institute of Hematology, Jinan University, Guangzhou, Guangdong 510632, P.R. China; Key Laboratory for Regenerative Medicine, Ministry of Education, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Yan
Y
Xu
Institute of Hematology, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Shaohua
S
Chen
Institute of Hematology, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Lijian
L
Yang
Institute of Hematology, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Xiuli
X
Wu
Department of Hematology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Janyu
J
Weng
Department of Hematology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Xin
X
DU
Institute of Hematology, Jinan University, Guangzhou, Guangdong 510632, P.R. China; Key Laboratory for Regenerative Medicine, Ministry of Education, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Yangqiu
Y
Li
T-cell clonality; T-cell receptor; acute T-lymphocyte leukemia; arsenic trioxide; minimal residual disease