Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E Huron Street, Chicago, IL, 60611, USA.
Department of Pathology, Northwestern University Feinberg School of Medicine, 251 E Huron Street, Chicago, IL, 60611, USA.
Hum Pathol. 2024 Jul;149:66-74. doi: 10.1016/j.humpath.2024.06.008. Epub 2024 Jun 13.
CSF3R activating mutation is a genetic hallmark of chronic neutrophilic leukemia (CNL), and is also present in a subset of atypical chronic myeloid leukemia (aCML), but infrequent in other myeloid neoplasms. However, the occurrence of CSF3R mutations in various myeloid neoplasms is not well studied. Here we evaluate the spectrum of CSF3R mutations and the clinicopathologic features of CSF3R mutated myeloid neoplasms. We retrospectively identified CSF3R mutations in a variety of myeloid neoplasms: two CNL, three atypical chronic myeloid leukemia (aCML), nine acute myeloid leukemia (AML), one chronic myelomonocytic leukemia, and one myeloproliferative neoplasm. The prototypic T618I mutation was found in 50% of cases: CNL (2/2), aCML (2/3) and AML (4/9). We observed a new recurrent CSF3R mutation Q776* in 25% of cases, and a potential-germline mutation in a 20-year-old patient. Co-occurring mutations were often in epigenetic modifier and spliceosome. IDH/RUNX1 and tumor suppressor mutations were frequent in AML but absent in CNL/aCML. All CNL/aCML patients succumbed within 2-years of diagnosis. We demonstrate that CSF3R mutations are not restricted to CNL. CNL and aCML show similar clinicopathologic and molecular features, suggesting that CNL may be best classified as myelodysplastic/myeloproliferative neoplasm rather than myeloproliferative neoplasm.
CSF3R 激活突变是慢性中性粒细胞白血病 (CNL) 的遗传标志,也存在于部分非典型慢性髓性白血病 (aCML) 中,但在其他髓性肿瘤中很少见。然而,CSF3R 突变在各种髓性肿瘤中的发生情况尚未得到充分研究。在这里,我们评估了 CSF3R 突变的谱以及 CSF3R 突变的髓性肿瘤的临床病理特征。我们回顾性地确定了各种髓性肿瘤中的 CSF3R 突变:2 例 CNL、3 例非典型慢性髓性白血病 (aCML)、9 例急性髓性白血病 (AML)、1 例慢性髓单核细胞白血病和 1 例骨髓增生性肿瘤。在 50%的病例中发现了典型的 T618I 突变:CNL(2/2)、aCML(2/3)和 AML(4/9)。我们观察到新的 CSF3R 突变 Q776*在 25%的病例中出现,并且在一名 20 岁的患者中存在潜在的种系突变。同时发生的突变通常在表观遗传调节剂和剪接体中。IDH/RUNX1 和肿瘤抑制基因突变在 AML 中很常见,但在 CNL/aCML 中不存在。所有的 CNL/aCML 患者在诊断后 2 年内都死亡了。我们证明 CSF3R 突变并不仅限于 CNL。CNL 和 aCML 表现出相似的临床病理和分子特征,这表明 CNL 可能最好被归类为骨髓增生性/骨髓增生异常性肿瘤,而不是骨髓增生性肿瘤。