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<p>Due to its rarity, no large studies have evaluated the outcomes of p230-CML patients treated with tyrosine kinase inhibitors (TKI). We describe the clinical course of two patients with p210/p230 co-expressed CML and provide a comprehensive review of 65 cases of p230-CML. Case-1 was a 35-year old male diagnosed with p210/p230-CML in chronic phase (CP) who progressed to extramedullary blast crises (EMBC) in the form of leukemia cutis (LC) after 4-years of imatinib therapy. TK domain (TKD) mutation was negative. Treatment with dasatinib resulted in resolution of LC, but patient defaulted treatment and died. Case-2 was a 25-year old male with p210/p230-CML in accelerated phase (AP) who progressed to EMBC-LC (T315I<sup>+</sup>) after 1-year of imatinib therapy. He responded transiently to dasatinib, but succumbed to progressive disease. Literature review revealed that patients with p230-CML had female predominance, a lower total leucocyte count and higher platelets at presentation than p210-CML. About 18% had extreme thrombocytosis (&gt; 1000 × 10<sup>9</sup>/L) and 29.5% had additional cytogenetic abnormalities at diagnosis. The proportion of transformations to AP/BC (30% vs. 25%) and deaths (37.5% vs. 27%) was similar in the pre-TKI and TKI era. As compared to imatinib, frontline treatment with 2nd -generation TKI improved the median survival.</p>

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Inferior Outcomes of p230-CML with Imatinib: a Report of 2 Cases of p210/p230 Co-Expressed CML Showing Rapid Progression To Leukaemia Cutis along with the Systematic Review

  • 期刊论文

  • 发表日期：

    2025年9月10日

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  • Ankur Jain,
  • Sumita Chaudhry,
  • Monica Sharma,
  • J. M. Khunger

摘要

Due to its rarity, no large studies have evaluated the outcomes of p230-CML patients treated with tyrosine kinase inhibitors (TKI). We describe the clinical course of two patients with p210/p230 co-expressed CML and provide a comprehensive review of 65 cases of p230-CML. Case-1 was a 35-year old male diagnosed with p210/p230-CML in chronic phase (CP) who progressed to extramedullary blast crises (EMBC) in the form of leukemia cutis (LC) after 4-years of imatinib therapy. TK domain (TKD) mutation was negative. Treatment with dasatinib resulted in resolution of LC, but patient defaulted treatment and died. Case-2 was a 25-year old male with p210/p230-CML in accelerated phase (AP) who progressed to EMBC-LC (T315I+) after 1-year of imatinib therapy. He responded transiently to dasatinib, but succumbed to progressive disease. Literature review revealed that patients with p230-CML had female predominance, a lower total leucocyte count and higher platelets at presentation than p210-CML. About 18% had extreme thrombocytosis (> 1000 × 109/L) and 29.5% had additional cytogenetic abnormalities at diagnosis. The proportion of transformations to AP/BC (30% vs. 25%) and deaths (37.5% vs. 27%) was similar in the pre-TKI and TKI era. As compared to imatinib, frontline treatment with 2nd -generation TKI improved the median survival.