Loss of heterozygosity and amplification on chromosome 11q in human ovarian cancer.
Loss of heterozygosity and amplification on chromosome 11q in human ovarian cancer.
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DOI：
10.1038/bjc.1993.51
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发表时间：
1993-02
影响因子：
8.8
通讯作者：
Trowsdale, J
中科院分区：
文献类型：
--
作者：
Foulkes, W D;Campbell, I G;Stamp, G W;Trowsdale, J
11q13 染色体区域编码与多种人类癌症相关的癌基因以及与 1 型多发性内分泌肿瘤有关的抑癌基因。此外，映射到 11q13.3-13.5 的高亲和力叶酸受体 (FOLR1) 在超过 80% 的非粘液性上皮性卵巢癌表面表达水平升高。在许多癌症中还发现了端粒 11q 断点。我们通过寻找肿瘤特异性杂合性丢失 (LOH) 以及可能解释 FOLR1 过度表达的扩增或重排，研究了 11q 标记在卵巢癌中的参与情况。 28 例上皮性卵巢癌以及来自同一个体的淋巴细胞 DNA 被用于使用来自 11q 的多态性探针进行 Southern 印迹分析。还使用了 11q23.3 的 PCR 引物。 28 种癌症中有 4 种 11q13 带被扩增。在这四种情况之一中，扩增子包括探针 D11S146 以及 FGF3（以前称为 INT2）和 FOLR1，从而跨越了 bcl1 易位断点。 16 例 FGF3 (11q13) 病例中，有 3 例出现 LOH。在 11q23.3-qter 处发现了更高频率的 LOH (8/12)，这意味着该区域存在肿瘤抑制基因。
The 11q13 chromosomal region encodes oncogenes relevant to a variety of human cancers as well as a tumour suppressor gene implicated in multiple endocrine neoplasia type 1. In addition, high affinity folate receptor (FOLR1), which maps to 11q13.3-13.5, is expressed at an elevated level on the surface of over 80% of nonmucinous epithelial ovarian cancers. Further telomeric, 11q breakpoints are found in many cancers. We studied the involvement of 11q markers in ovarian cancer by looking for tumour-specific loss of heterozygosity (LOH), as well as amplification or rearrangements that might explain the overexpression of FOLR1. Twenty eight epithelial ovarian cancers, along with lymphocyte DNA from the same individual were used for Southern blotting with polymorphic probes from 11q. PCR primers from 11q23.3 were also used. The 11q13 band was amplified in four out of 28 cancers. The amplicon included the probe D11S146 as well as FGF3 (formerly INT2) and FOLR1 in one out of these four cases, thus crossing the bcl1 translocation breakpoint. LOH was seen in three out of 16 cases with FGF3 (11q13). A much higher frequency of LOH (8/12) was found at 11q23.3-qter, implying the presence of a tumour suppressor gene in this region.