Bertness V L, Felix C A, McBride O W, Morgan R, Smith S D, Sandberg A A, Kirsch I R
Navy Medical Oncology Branch, National Cancer Institute, Bethesda, MD 20814-5105.
Cancer Genet Cytogenet. 1990 Jan;44(1):47-54. doi: 10.1016/0165-4608(90)90196-h.
The leukemic cells and derivative cell line from a 74-year-old male with T-cell acute lymphoblastic leukemia showed chromosomal abnormalities including a t(14;14)(q11.2;q32). This translocation is characteristic of a variety of T-cell malignancies, particularly T-cell prolymphocytic leukemia and the clonal proliferations of peripheral T cells in patients with ataxia-telangiectasia. Using DNA probes that spanned the T-cell receptor alpha chain (TCRA) joining (J) locus, the DNA rearrangement caused by the translocation was identified, cloned, and sequenced. The breakpoint shows site-specific juxtaposition of a TCRA joining segment and DNA from a region of 14q32 centromeric to the immunoglobulin heavy chain locus. Comparison of restriction map and nucleotide sequence from this translocation with other related chromosomal breakpoints suggests a dispersion of breakpoints throughout the 14q32 region.
一名74岁患T细胞急性淋巴细胞白血病男性的白血病细胞及衍生细胞系显示出染色体异常，包括t(14;14)(q11.2;q32)。这种易位是多种T细胞恶性肿瘤的特征，尤其是T细胞幼淋巴细胞白血病以及共济失调-毛细血管扩张症患者外周T细胞的克隆性增殖。使用跨越T细胞受体α链（TCRA）连接（J）基因座的DNA探针，鉴定、克隆并测序了由该易位引起的DNA重排。断点显示了一个TCRA连接片段与来自14q32着丝粒区域至免疫球蛋白重链基因座的DNA的位点特异性并列。将该易位的限制性图谱和核苷酸序列与其他相关染色体断点进行比较，表明断点分散在整个14q32区域。
