Clonal Evolution and Lineage Switch from T-Cell Acute Lymphoblastic Leukemia to Acute Myeloid Leukemia in Therapy-Resistant Leukemia.
[BACKGROUND] -positive T-ALL is rare and associated with poor prognosis.
APA
Kawamura M, Sadato D, et al. (2026). Clonal Evolution and Lineage Switch from T-Cell Acute Lymphoblastic Leukemia to Acute Myeloid Leukemia in Therapy-Resistant Leukemia.. EJHaem, 7(1), e70217. https://doi.org/10.1002/jha2.70217
MLA
Kawamura M, et al.. "Clonal Evolution and Lineage Switch from T-Cell Acute Lymphoblastic Leukemia to Acute Myeloid Leukemia in Therapy-Resistant Leukemia.." EJHaem, vol. 7, no. 1, 2026, pp. e70217.
PMID
41584902
Abstract
[BACKGROUND] -positive T-ALL is rare and associated with poor prognosis. Lineage switch to AML is exceptionally uncommon, particularly after long-term remission.
[CASE PRESENTATION] We report an adolescent -positive T-ALL with a cortical thymocyte, non-ETP phenotype. The patient achieved complete remission but relapsed as AML 6 years later. Cytogenetics revealed del(5q), del(17p), and 17q gain. Mutational profiling demonstrated mutations with LOH in and , a hemizygous mutation, and a hemizygous mutation detected only after subsequent therapy.
[CONCLUSION] This case illustrates that therapy-resistant progenitors can persist during remission and re-emerge as AML through lineage switch. The sequential acquisition of cooperating genetic lesions supports clonal evolution and highlights the need for molecular monitoring and novel therapeutic strategies.
[TRIAL REGISTRATION] The authors have confirmed clinical trial registration is not needed for this submission.
[CASE PRESENTATION] We report an adolescent -positive T-ALL with a cortical thymocyte, non-ETP phenotype. The patient achieved complete remission but relapsed as AML 6 years later. Cytogenetics revealed del(5q), del(17p), and 17q gain. Mutational profiling demonstrated mutations with LOH in and , a hemizygous mutation, and a hemizygous mutation detected only after subsequent therapy.
[CONCLUSION] This case illustrates that therapy-resistant progenitors can persist during remission and re-emerge as AML through lineage switch. The sequential acquisition of cooperating genetic lesions supports clonal evolution and highlights the need for molecular monitoring and novel therapeutic strategies.
[TRIAL REGISTRATION] The authors have confirmed clinical trial registration is not needed for this submission.