AI Article Synopsis

  • Allogeneic hematopoietic cell transplantation (allo-HCT) is the most effective treatment for acute myeloid leukemia (AML) with complex karyotype (CK), but CK is diverse and can impact prognosis differently.
  • In a study involving 236 patients, those with a pure hyperdiploid karyotype (pHDK) had significantly better 2-year outcomes (50% leukemia-free survival and 57% overall survival) compared to those with other cytogenetic abnormalities (HDK+) which had lower survival rates (31% and 36% respectively).
  • pHDK AML is likely a separate cytogenetic category from HDK+ and has better treatment outcomes post-allo-HCT, highlighting

Article Abstract

Allogeneic hematopoietic cell transplantation (allo-HCT) remains the best consolidation strategy for acute myeloid leukemia (AML) with complex karyotype (CK). However, CK is a heterogenous and highly diverse entity. Numerical abnormalities have been associated with a controversial prognosis and AML with only multiple numerical abnormalities known as pure hyperdiploid karyotype (HDK) may have a distinct prognosis after allo-HCT compared to non-pure HDK CK AML. A total of 236 patients were identified within the EBMT registry as having HDK comprising 95 pure (pHDK) and 141 with other cytogenetic abnormalities (HDK+). The 2-year probability of leukemia-free survival (LFS) was 50% for pHDK and 31% for HDK+ (p = 0.003). The 2-year probability of overall survival (OS) was 57% for pHDK and 36% for HDK+ (p = 0.007). The 2-year cumulative incidence of relapse (RI) was 22% for pHDK and 44% for HDK+ (p = 0.001). The 2-year probability of graft-versus-host disease (GvHD)-free and relapse-free survival (GRFS) was 36% for pHDK and 21% for HDK+ (p = 0.01). On multivariate analysis, pHDK remained associated with significantly better LFS, OS and GRFS and lower RI (all p-values <0.004). pHDK AML constitutes probably a distinct cytogenetic entity from HDK+ or other non-hyperdiploid CK AML with better outcomes after allo-HCT.

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Source
http://dx.doi.org/10.1038/s41409-023-02167-1DOI Listing

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