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参与人类卵巢肿瘤的两个假定的11号染色体抑癌基因的染色体定位。

Chromosomal localisation of two putative 11p oncosuppressor genes involved in human ovarian tumours.

作者信息

Viel A, Giannini F, Tumiotto L, Sopracordevole F, Visentin M C, Boiocchi M

机构信息

Division of Experimental Oncology 1, Centro Riferimento Oncologico, Aviano (PN), Italy.

出版信息

Br J Cancer. 1992 Dec;66(6):1030-6. doi: 10.1038/bjc.1992.405.

Abstract

In this study, 44 primary or metastatic human ovarian tumours were tested for allelic deletions on the short arm of chromosome 11. Analysis of 12 polymorphic loci by Southern blotting evidenced loss of heterozygosity (LOH) in at least one locus in 41% of cases. Moreover, two hot spots of deletions were tentatively mapped on 11p13 and 11p15.5. Our results demonstrated that LOH at 11p is a common event in ovarian carcinomas and were indicative of the possible existence in 11p of two oncosuppressor genes involved in ovarian carcinogenesis. The similarity observed with 11p allelic losses in Wilms tumours, clustered in 11p13 and 11p15.5 too, suggests that deletion and possibly inactivation of the same growth regulatory genes (WT genes) could also contribute to development of the malignant phenotype in ovarian carcinomas. Finally, a statistically significant association (P = 0.005) between 11p deletions and hepatic involvement was suggested by the analysis of distribution of 11p LOH relative to different clinical and pathological parameters of the tumour patients.

摘要

在本研究中,对44例原发性或转移性人类卵巢肿瘤进行了11号染色体短臂上等位基因缺失的检测。通过Southern印迹法分析12个多态性位点,结果显示41%的病例中至少有一个位点存在杂合性缺失(LOH)。此外,初步将两个缺失热点定位在11p13和11p15.5。我们的结果表明,11p处的LOH在卵巢癌中是常见事件,提示11p可能存在两个参与卵巢癌发生的抑癌基因。在Wilms瘤中观察到的11p等位基因缺失也集中在11p13和11p15.5,这表明相同生长调节基因(WT基因)的缺失以及可能的失活也可能促成卵巢癌恶性表型的发展。最后,通过分析11p LOH相对于肿瘤患者不同临床和病理参数的分布情况,发现11p缺失与肝脏受累之间存在统计学显著关联(P = 0.005)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e8d/1978017/b851ac41c7f6/brjcancer00064-0054-a.jpg

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