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乳腺癌中IGF-II受体基因拷贝数的分析。

Analysis of the IGF-II receptor gene copy number in breast carcinoma.

作者信息

Hébert E, Herbelin C, Bougnoux P

机构信息

Centre de Biophysique Moléculaire et Université d'Orléans, France.

出版信息

Br J Cancer. 1994 Jan;69(1):120-4. doi: 10.1038/bjc.1994.19.

DOI:10.1038/bjc.1994.19
PMID:8286193
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1968763/
Abstract

Insulin and the insulin-like growth factors (IGFs) may be important regulators of breast cancer growth. The IGF-II receptor is identical to the mannose 6-phosphate (Man-6-P) receptor, which is involved in lysosomal enzyme pathways. In order to determine whether the Man-6-P/IGF-II receptor gene copy number is altered in breast cancer we analysed specimens of invasive breast carcinoma from 51 patients by Southern blotting. No amplification of the receptor gene was observed whatever the clinical presentation of the tumour and irrespective of a concomitant amplification of c-erbB2 or int-2 genes in several tumours. As indicated by Northern blotting, the gene is transcribed in breast tumour tissues and non-tumour breast tissue. These results suggest that the receptor gene is stable in breast carcinoma and that, if anything, the receptor involvement in breast cancer progression may be the result of a disregulation of its expression at a post-transcriptional or post-translational level.

摘要

胰岛素及胰岛素样生长因子(IGFs)可能是乳腺癌生长的重要调节因子。IGF-II受体与甘露糖6-磷酸(Man-6-P)受体相同,后者参与溶酶体酶途径。为了确定Man-6-P/IGF-II受体基因拷贝数在乳腺癌中是否改变,我们通过Southern印迹法分析了51例浸润性乳腺癌患者的标本。无论肿瘤的临床表现如何,也无论在一些肿瘤中c-erbB2或int-2基因是否同时扩增,均未观察到受体基因的扩增。如Northern印迹法所示,该基因在乳腺肿瘤组织和非肿瘤乳腺组织中均有转录。这些结果表明,该受体基因在乳腺癌中是稳定的,并且如果存在任何情况,受体参与乳腺癌进展可能是其在转录后或翻译后水平表达失调的结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/1cac9f90d74b/brjcancer00191-0124-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/62569ed72a9f/brjcancer00191-0123-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/145e31511fb8/brjcancer00191-0123-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/7d8cca1e400d/brjcancer00191-0123-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/4334b1f68ee3/brjcancer00191-0124-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/1cac9f90d74b/brjcancer00191-0124-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/62569ed72a9f/brjcancer00191-0123-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/145e31511fb8/brjcancer00191-0123-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/7d8cca1e400d/brjcancer00191-0123-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/4334b1f68ee3/brjcancer00191-0124-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9c/1968763/1cac9f90d74b/brjcancer00191-0124-b.jpg

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引用本文的文献

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Br J Cancer. 1995 Nov;72(5):1189-93. doi: 10.1038/bjc.1995.484.

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