Deletion of chromosome 11p13-11p15.5 sequences in invasive human ovarian cancer is a subclonal progression factor.

Deletion of chromosome 11p13-11p15.5 sequences in invasive human ovarian cancer is a subclonal progression factor.
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侵袭性人类卵巢癌中染色体 11p13-11p15.5 序列的缺失是亚克隆进展因素。

DOI:
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发表时间:
1992
期刊:
影响因子:
11.2
通讯作者:
J. D. Greve
J. D. Greve
中科院分区:
医学1区
文献类型:
--
作者:
B. Vandamme;Willy Lissens;K. Amfo;P. D. Sutter;Claire Bourgain;E. Vamos;J. D. Greve

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在人类卵巢癌中,可以通过细胞遗传学分析或分子技术(例如限制性片段长度多态性探测)发现多个特定的染色体缺失。这项工作在 19 名患者的 32 个样本或细胞系中确定,在 2 例浸润性卵巢癌病例中,有 1 例 HRAS 等位基因缺失。其他多态性探针的结果表明共有缺失可能包括 11p15.5-11p13。抑癌基因可能位于缺失区域,并且该基因的缺失可能在疾病进展中发挥作用。对个体患者不同肿瘤部位的 DNA 检查表明恶性细胞群中的克隆异质性,表明 11p 序列的丢失是疾病进展的晚期事件。一名患者不同疾病部位交替 11p 等位基因的丢失与当前抑癌基因失活的模型不一致。 11p 缺失似乎仅限于年轻患者的卵巢癌。当前的分析中包括了八种新型永久性卵巢癌细胞系,这些细胞系以前未在文献中描述过,并且源自五名患者的肿瘤部位。
In human ovarian cancer, multiple specific chromosomal deletions can be found by cytogenetic analysis or molecular techniques such as restriction fragment length polymorphism probing. This work confirms the loss of HRAS alleles in 1 out of 2 cases of invasive ovarian cancer as determined in 32 samples or cell lines derived from 19 patients. Results with other polymorphic probes indicate that a consensus deletion probably includes 11p15.5-11p13. Tumor suppressor genes might be located in the deleted area, and deletion of the gene might then play a role in disease progression. Examination of DNA from distinct tumor sites of individual patients indicates clonal heterogeneity in the malignant cell population, indicating that loss of 11p sequences is a late event in the disease progression. Loss of alternate 11p alleles at different disease sites in one patient is inconsistent with the current model of tumor suppressor gene inactivation. The 11p deletion seems to be limited to ovarian cancers in younger patients. Eight novel permanent ovarian cancer cell lines, previously not described in the literature and derived from tumor sites from five patients, were included in the current analysis.
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