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<p>Promyelocytic blast crisis (BC) of CML is an extremely rare event, with only seven cases described as arising during therapy with TKIs. We present a 68-year-old male who developed promyelocytic blast crisis 12 months after CML diagnosis and start of Imatinib therapy, confirmed by the concomitant presence of the&#xa0;t(15;17) and&#xa0;t(9;22) translocations in the leukemic cells. Molecular remission for the <i>PML-RARA </i>clone was achieved with standard acute promyelocytic leukemia induction therapy with ATRA and idarubicin. However, <i>BCR-ABL</i> showed resistance to first-line Dasatinib and second-line Ponatinib, principally due to the presence of multiple mutations in ABL1 kinase domain, including T315I. Hematological and molecular response was achieved with Asciminib, a first‐in‐class STAMP (Specifically Targeting the ABL Myristoyl Pocket) inhibitor in combination with pulsed ATRA as post-remission strategy. Of the 7 cases of promyelocytic BC reported in the era of TKI therapy for CML, this is the first case effectively treated with Asciminib therapy.</p>

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Asciminib and pulsed ATRA as post-remission therapy in T315I mutated PML-RARA-positive blast crisis of chronic myeloid leukemia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月17日

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  • Roberta Mazzarella,
  • Laura Cicconi,
  • Salvatore Perrone,
  • Maria Domenica Divona,
  • Sara Ceccolini,
  • Anna Maria Nardozza,
  • Annalisa Biagi,
  • Tiziana Ottone,
  • Andrea Corbingi,
  • Paola Panetta,
  • Elettra Ortu La Barbera,
  • Luciano Fiori,
  • Azzurra Anna Romeo,
  • Giada Pacitto,
  • Ettore Cotroneo,
  • Massimo Breccia,
  • Maria Teresa Voso,
  • Alessandro Pulsoni

摘要

Promyelocytic blast crisis (BC) of CML is an extremely rare event, with only seven cases described as arising during therapy with TKIs. We present a 68-year-old male who developed promyelocytic blast crisis 12 months after CML diagnosis and start of Imatinib therapy, confirmed by the concomitant presence of the t(15;17) and t(9;22) translocations in the leukemic cells. Molecular remission for the PML-RARA clone was achieved with standard acute promyelocytic leukemia induction therapy with ATRA and idarubicin. However, BCR-ABL showed resistance to first-line Dasatinib and second-line Ponatinib, principally due to the presence of multiple mutations in ABL1 kinase domain, including T315I. Hematological and molecular response was achieved with Asciminib, a first‐in‐class STAMP (Specifically Targeting the ABL Myristoyl Pocket) inhibitor in combination with pulsed ATRA as post-remission strategy. Of the 7 cases of promyelocytic BC reported in the era of TKI therapy for CML, this is the first case effectively treated with Asciminib therapy.