Chronic Myelogenous Leukemia (CML)

Overview

Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasm defined by the BCR-ABL1 fusion gene arising from the Philadelphia chromosome t(9;22)(q34;q11). The BCR-ABL1 fusion constitutively activates ABL1 tyrosine kinase, driving clonal myeloid proliferation. CML is highly responsive to ABL1 tyrosine kinase inhibitors (imatinib, dasatinib, nilotinib, bosutinib, ponatinib), which have transformed it into a chronic, manageable disease for most patients.

Cohorts in the corpus

  • mixed_pipseq_2017 — PIPseq pediatric pan-cancer cohort (Columbia University Medical Center), which includes a CML case among 101 high-risk pediatric patients PMID:28007021.

Recurrent alterations

  • PIPseq cohort: BCR-ABL1 fusion confirmed by RNA-seq as diagnostic of CML (PIPID 14-85546); imatinib is the first-line TKI target; the same sequencing run identified a BCR-ABL1-like RNA-seq signature in a separate BLL patient PMID:28007021.

Subtypes

  • Chronic phase, accelerated phase, blast crisis (myeloid or lymphoid); blast crisis CML carries AML/ALL-like biology.

Therapeutic landscape

  • BCR-ABL1 TKIs (imatinib, dasatinib, nilotinib, bosutinib, ponatinib) are standard of care; palliative imatinib used in the pediatric PIPseq CML case PMID:28007021.

Sources

  • PMID:28007021 — Oberg et al. PIPseq pediatric pan-cancer sequencing program (n=101).

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