Takamasa Katagiri

TL;DR: A highly biased set of mutations is evidence of Darwinian selection in the failed bone marrow environment and might not necessarily have predicted the response to therapy and long-term survival among individual patients.

TL;DR: It is shown that a substantial proportion of AA patients harbor clonal hematopoiesis characterized by the presence of acquired copy number-neutral loss of heterozygosity (CNN-LOH) of the 6p arms (6pLOH).

TL;DR: Preemptive PFA therapy is safe, but as HHV-6 DNAemia can abruptly develop before neutrophil engraftment in UCBT recipients, prophylactic PFA administration from day 7 or earlier after UCBT may be needed.

TL;DR: The markedly high prevalence of leukocytes lacking HLA-B4002 as a result of either 6pLOH or structural gene mutations, or both, suggests that antigen presentation by hematopoietic stem/progenitor cells to cytotoxic T cells via the HLA -B allele plays a critical role in the pathogenesis of AA.

TL;DR: It is suggested that myelodysplastic syndrome-unclassified with del(13q) is a benign bone marrow failure subset characterized by good response to immunosuppressive therapy and a high prevalence of increased glycosylphosphatidylinositol-anchored protein-deficient cells, and should not be considered an intermediate-risk chromosomal abnormality.