Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mod Pathol. 2018 Jul;31(7):1141-1154. doi: 10.1038/s41379-018-0014-x. Epub 2018 Feb 14.
The Philadelphia chromosome resulting from t(9;22)(q34;q11.2) or its variants is a defining event in chronic myeloid leukemia. It is also observed in several types of de novo acute leukemia, commonly in B lymphoblastic leukemia, and rarely in acute myeloid leukemia, acute leukemia of ambiguous lineage, and T lymphoblastic leukemia. Acquisition of the Philadelphia chromosome during therapy of acute leukemia and myelodysplastic syndrome is rare. We reported 19 patients, including 11 men and 8 women with a median age of 53 years at initial diagnosis. The diagnoses at initial presentation were acute myeloid leukemia (n = 11), myelodysplastic syndrome (n = 5), B lymphoblastic leukemia (n = 2), and T lymphoblastic leukemia (n = 1); no cases carried the Philadelphia chromosome. The Philadelphia chromosome was detected subsequently at relapse, or at refractory stage of acute leukemia or myelodysplastic syndrome. Of 14 patients evaluated for the BCR-ABL1 transcript subtype, 12 had the e1a2 transcript. In 11 of 14 patients, the diseases before and after emergence of the Philadelphia chromosome were clonally related by karyotype or shared gene mutations. Of 15 patients with treatment information available, 7 received chemotherapy alone, 5 received chemotherapy plus tyrosine kinase inhibitors, 2 received tyrosine kinase inhibitors only, and 1 patient was not treated. Twelve patients had follow-up after acquisition of the Philadelphia chromosome; all had persistent/refractory acute leukemia. Thirteen of 15 patients died a median of 3 months after the emergence of the Philadelphia chromosome. In summary, secondary Philadelphia chromosome acquired during therapy is rare, and is associated with the e1a2 transcript subtype, terminal disease stage, and poor outcome.
费城染色体源自 t(9;22)(q34;q11.2) 或其变体,是慢性髓性白血病的一个决定性事件。它也存在于几种新发的急性白血病中,通常见于 B 淋巴母细胞白血病,罕见于急性髓性白血病、急性混合谱系白血病和 T 淋巴母细胞白血病。在急性白血病和骨髓增生异常综合征的治疗过程中获得费城染色体的情况很少见。我们报告了 19 例患者,其中 11 例为男性,8 例为女性,初始诊断时的中位年龄为 53 岁。初始表现的诊断为急性髓性白血病(n=11)、骨髓增生异常综合征(n=5)、B 淋巴母细胞白血病(n=2)和 T 淋巴母细胞白血病(n=1);无费城染色体病例。费城染色体随后在复发时或急性白血病或骨髓增生异常综合征的难治期被检测到。在 14 例评估 BCR-ABL1 转录亚型的患者中,有 12 例为 e1a2 转录。在 14 例患者中有 11 例,在费城染色体出现前后的疾病通过核型或共享基因突变具有克隆相关性。在可获得治疗信息的 15 例患者中,7 例单独接受化疗,5 例接受化疗加酪氨酸激酶抑制剂,2 例仅接受酪氨酸激酶抑制剂,1 例未接受治疗。12 例患者在获得费城染色体后进行了随访;所有患者均为持续性/难治性急性白血病。在费城染色体出现后,中位时间为 3 个月,13 例患者死亡。综上所述,治疗过程中获得的继发性费城染色体很少见,与 e1a2 转录亚型、终末期疾病阶段和不良预后相关。