DIFFUSE LARGE-CELL LYMPHOMAS EXHIBIT FREQUENT DELETIONS IN 9P21-22 AND 9Q31-34 REGIONS
DIFFUSE LARGE-CELL LYMPHOMAS EXHIBIT FREQUENT DELETIONS IN 9P21-22 AND 9Q31-34 REGIONS
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DOI：
10.1002/gcc.2870120106
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发表时间：
1995-01-01
影响因子：
3.7
通讯作者：
CHAGANTI, RSK
中科院分区：
文献类型：
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作者：
CHAGANTI, SR;GAIDANO, G;CHAGANTI, RSK
我们以前已经确定了一个大系列的非霍奇金淋巴瘤（NHL）的细胞遗传学分析中的9 p和9 q的缺失，这表明候选肿瘤抑制基因（TSGs）的损失。为了在分子水平上确定这些缺失，我们对一组配对的正常和肿瘤DNA进行了洛分析，包括13例弥漫性淋巴瘤伴大细胞成分（DLLC）和18例伯基特淋巴瘤（BL）。（D9 S33、D9 S25、IFNB、IFNA、IFNW、D9 S126、D9 S3和D9 S19）和定位于9 q的七个多态性探针（D9 S29、ASS、阿基、ABL、D9 S10、D9 S7和D9 S14）。在该分析中，在每个亚组的所有基因座信息的病例中，5/13（38%）DLLC和4/18（22%）BL在9 p基因座显示洛，而5/13（38%）DLLC和3/18（16%）BL在9 q基因座显示洛。在9 p位点中，在20-50%的DLLC信息病例中观察到D9 S25、IFNB、IFNA、IFNW、D9 S126和D9 S3的部分纯合或杂合丢失，而在BL中，这些位点的丢失范围为0%-11%。在9 q基因座中，在>20%的DLLC信息病例中观察到D9 S7（23%）和D9 S29（27%）的杂合丢失，而在BL中未观察到这两个基因座的丢失。这些数据表明DLLC中有高水平的分子缺失，但BL中没有，表明9号染色体上一个或多个TSG的缺失在DLLC的发展中起重要作用。(C)1995 Wiley-Liss，Inc.
We have previously identified deletions of 9p and 9q in a cytogenetic analysis of a large series of non-Hodgkin's lymphomas (NHLs), which suggested loss of candidate tumor suppressor genes (TSGs). In order to define these deletions at the molecular level, we performed an LOH analysis of a panel of paired normal and tumor DNAs comprising 13 cases of diffuse lymphoma with a large cell component (DLLC) and 18 cases of Burkitt's lymphoma (BL), The loci tested comprised eight polymorphic probes mapped to 9p (D9S33, D9S25, IFNB, IFNA, IFNW, D9S126, D9S3, and D9S19) and seven polymorphic probes mapped to 9q (D9S29, ASS, AKI, ABL, D9S10, D9S7, and D9S14). In this analysis, among cases informative for all loci in each subset, 5/13 (38%) DLLC and 4/18 (22%) BL showed LOH at 9p loci, whereas 5/13 (38%) DLLC and 3/18 (16%) BL showed LOH at 9q loci. Among the 9p loci partial homozygous or heterozygous losses were observed in 20-50% of informative cases of DLLC at D9S25, IFNB, IFNA, IFNW, D9S126, and D9S3, whereas in BL, losses at these loci ranged from 0% to 11%. Among the 9q loci, heterozygous losses were observed in >20% of informative cases of DLLC at D9S7 (23%) and D9S29 (27%), whereas no losses were seen at these two loci in BL. These data demonstrate a high level of molecular deletion in DLLC, but not in BL, suggesting that loss of one or more TSGs on chromosome 9 plays an important role in DLLC development. (C) 1995 Wiley-Liss, Inc.