Human ABL1 deficiency syndrome (HADS) is a recognizable syndrome distinct from ABL1-related congenital heart defects and skeletal malformations syndrome.
The interplay between telomeric complex members and BCR::ABL1 oncogenic tyrosine kinase in the maintenance of telomere length in chronic myeloid leukemia.
Emergence of a BCR::ABL1 rearrangement following a uniquely complex clonal evolution pattern in a patient undergoing Fms-like tyrosine kinase 3 inhibitor therapy for acute myeloid leukemia.
Deep sequencing reveals the spectrum of BCR-ABL1 mutations upon front-line therapy resistance in chronic myeloid leukemia: An Eastern-Indian cohort study.
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