Testa J R, Kinnealey A, Rowley J D, Golde D W, Potter D
Blood. 1978 Nov;52(5):868-77.
Detailed clinical and cytogenetic studies were performed in five patients who had abnormal hematopoiesis and an acquired deletion of an F-group chromosome. Cytogenetic analyses, with banding techniques, of cells from bone marrow, spleen, or unstimulated peripheral blood showed a partial deletion of the long arm of one chromosome 20 [del(20)(q11)] in all five patients. Three patients had myeloproliferative disorders of uncertain classification, the fourth had possible preleukemia, and the fifth had acute myelomonocytic leukemia. Although the five cases showed certain similarities, the clinical and hematologic findings seen with the 20q- abnormality were not specific. None of the patients showed evidence of polycythemia vera or idiopathic acquired refractory sideroblastic anemia, two diseases previously associated with the 20q-. Our studies indicate that the 20q- abnormality is not limited to diseases primarily affecting erythropoiesis but that it can be found in the broader spectrum of myeloid disorders. In polycythemia vera, the 20q- has sometimes been regarded as a possible result of previous therapy with cytotoxic agents; however, four of our patients were untreated when the deletion was first noted.
对5例造血异常且获得性F组染色体缺失的患者进行了详细的临床和细胞遗传学研究。采用显带技术对骨髓、脾脏或未受刺激的外周血中的细胞进行细胞遗传学分析,结果显示所有5例患者均存在一条20号染色体长臂部分缺失[del(20)(q11)]。3例患者患有分类不明的骨髓增殖性疾病,第4例可能患有白血病前期,第5例患有急性粒单核细胞白血病。虽然这5例病例有一定相似性,但20q-异常相关的临床和血液学表现并不具有特异性。患者中无真性红细胞增多症或特发性获得性难治性铁粒幼细胞贫血的证据,这两种疾病以前曾与20q-相关。我们的研究表明,20q-异常并不局限于主要影响红细胞生成的疾病,而是可见于更广泛的髓系疾病谱中。在真性红细胞增多症中,20q-有时被认为是先前细胞毒性药物治疗的可能结果;然而,我们的4例患者在首次发现缺失时未接受治疗。