Treatment with interferon α-1b, interleukin-2, and thalidomide for persistent RUNX1::RUNX1T1 in a patient with KIT-mutated acute myeloid leukemia after allogeneic hematopoietic stem cell transplantation: a case report and literature review
10.3760/cma.j.cn121090-20250331-00160
- VernacularTitle:干扰素α-1b、IL-2联合沙利度胺治疗allo-HSCT后RUNX1::RUNX1T1持续阳性的伴KIT突变急性髓系白血病1例报告并文献复习
- Author:
Ruihua MI
1
;
Lin CHEN
1
;
Lin WANG
1
;
Yixuan MA
1
;
Yuewen FU
1
;
Xudong WEI
1
Author Information
1. 郑州大学附属肿瘤医院/河南省肿瘤医院，郑州 450000
- Publication Type:Journal Article
- From:
Chinese Journal of Hematology
2025;46(11):1060-1063
- CountryChina
- Language:Chinese
-
Abstract:
Here we report the case of a CBF-AML patient with KIT p.D816V mutation who failed avapritinib induction therapy and subsequently underwent bridging allogeneic hematopoietic stem cell transplantation (allo-HSCT), along with a literature review. The patient was a 64-year-old male who did not achieve remission after induction therapy with the DA regimen (Daunorubicin + Cytarabine). After reinduction with avapritinib combined with the DCHG regimen (Decitabine + Homoharringtonine + Cytarabine + Granulocyte colony-stimulating factor), he attained complete remission (CR) and flow cytometry minimal residual disease (MRD) negativity, but the RUNX1::RUNX1T1 fusion gene remained positive. During consolidation therapy, flow MRD reappeared, and the fusion gene level progressively increased. The patient then underwent a 9/10 HLA-matched unrelated donor allo-HSCT. Post-transplant, the fusion gene persisted, prompting treatment with the "ITI" regimen (with dose adjustments, including sequential addition of interferon and interleukin-2, pomalidomide incorporation, and standard vs. escalated dosing of "ITI" regimen). Currently, MRD negativity has been maintained for over 5 months, with good treatment tolerance. This finding suggest that the "ITI" regimen may serve as a novel and well-tolerated therapeutic option for CBF-AML patients with persistent RUNX1::RUNX1T1 fusion gene positivity after allo-HSCT and KIT p.D816V mutation, particularly in cases of avapritinib treatment failure.
