c-src is consistently conserved in the chromosomal deletion (20q) observed in myeloid disorders.
c-src is consistently conserved in the chromosomal deletion (20q) observed in myeloid disorders.
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c-src 在骨髓疾病中观察到的染色体缺失 (20q) 中始终保守。
DOI：
10.1073/pnas.82.19.6692
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发表时间：
1985
影响因子：
11.1
通讯作者：
Rowley,JD
中科院分区：
文献类型：
--
作者：
LeBeau,MM;Westbrook,CA;Diaz,MO;Rowley,JD
原癌基因c-src已被定位到人类染色体上的两条带，1p36和20q13，这两条带都参与了人类肿瘤的重排。尤其是20号染色体的长臂del(20q)的缺失(一条染色体的一部分丢失)，在血液系统的恶性疾病中很常见。用c-src探针与3例Del(20Q)白血病患者骨髓细胞制备的中期细胞进行染色体原位杂交，观察到每例患者缺失的染色体上都有特异的标记，表明c-src基因座是保守的。C-src基因重排后的染色体通常位于20q的最远端，这表明c-src基因的缺失并不是染色体形态上的末端缺失，而是间质缺失。C-src在这些缺失中相对于远端断裂点的位置未知。使用v-src探针对3例del(20Q)患者的基因组DNA进行Southern杂交分析，发现在与v-src同源的区域内没有发生重大的基因组重排或c-src基因的扩增。我们观察到c-src在这些重排的染色体中持续保持，提示该基因可能在某些髓系疾病的发病机制中发挥作用。
The proto-oncogene c-src has been mapped to two bands in human chromosomes, 1p36 and 20q13, both of which are involved in rearrangements in human tumors. In particular, deletions (loss of part of a chromosome) of the long arm of chromosome 20, del(20q), are commonly observed in hematologic malignant diseases. By using in situ chromosomal hybridization of a c-src probe to metaphase cells prepared from leukemic bone marrow cells of three patients with a del(20q), we observed specific labeling on the deleted chromosome in each patient, indicating that the c-src locus was conserved. The presence on the rearranged chromosomes of c-src, which is normally located on the most distal band of 20q, indicated that the deletions were not terminal as they appeared to be on the basis of chromosome morphology, but rather that they were interstitial. The location of c-src relative to the distal breakpoint in these deletions is unknown. By using the v-src probe in Southern blot analysis of genomic DNA from three patients with a del(20q), we found that no major genomic rearrangements or amplification of the c-src genes had occurred within the regions homologous to v-src. Our observation that c-src is consistently preserved in these rearranged chromosomes suggests that this gene may play a role in the pathogenesis of some myeloid disorders.