Ueshima Y, Rowley J D, Variakojis D, Winter J, Gordon L
Blood. 1984 May;63(5):1028-38.
Cytogenetic studies were performed on three patients with chronic T cell leukemia and on one patient with T cell lymphoma. One of the patients had leukemic cells derived from a suppressor T cell clone, another expressed OKT3, 4, and 8, and cells of the other two were derived from a helper T cell clone. All patients had an abnormal karyotype in peripheral blood or bone marrow cultured with or without mitogen. Modal chromosome numbers were 42 and 44/45 in one patient each and 47 in the 2 others. The structural and numerical abnormalities involved almost all chromosomes, except no. 19 and the X chromosome. All patients had a rearrangement of the long arm of no. 14, with a break at band 14q11;3 patients also had a break at 14q32. An inversion of 14q occurred in two patients; a tandem translocation involving both no. 14 chromosomes and a translocation between no. 14 and no. 17 each occurred in one patient. The break in 14q at band q11 in our cases resembles the chromosome change reported in ataxia telangiectasia. This provides added support for the proposal that a 14q rearrangement involving band q11-12, with or without an accompanying break in 14q32, may confer a proliferative advantage on lymphocytes, especially on those of T cell origin.
对3例慢性T细胞白血病患者和1例T细胞淋巴瘤患者进行了细胞遗传学研究。其中1例患者的白血病细胞来源于抑制性T细胞克隆,另1例表达OKT3、4和8,其余2例患者的细胞来源于辅助性T细胞克隆。所有患者在有或无丝裂原培养的外周血或骨髓中均有异常核型。1例患者的众数染色体数为42,另1例为44/45,其余2例为47。结构和数目异常几乎累及所有染色体,除了19号染色体和X染色体。所有患者均有14号染色体长臂重排,断裂点在14q11;3例患者在14q32也有断裂。2例患者发生14q倒位;1例患者发生涉及两条14号染色体的串联易位,另1例患者发生14号与17号染色体之间的易位。我们病例中14q11带的断裂类似于共济失调毛细血管扩张症中报道的染色体改变。这为以下提议提供了更多支持,即涉及11-12带的14q重排,无论是否伴有14q32断裂,可能赋予淋巴细胞,尤其是T细胞来源的淋巴细胞增殖优势。