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人类宫颈癌中c-Ha-ras基因的体细胞缺失和突变

Somatic deletions and mutations of c-Ha-ras gene in human cervical cancers.

作者信息

Riou G, Barrois M, Sheng Z M, Duvillard P, Lhomme C

机构信息

Laboratoire de Pharmacologie Clinique et Moléculaire, Institut Gustave Roussy, Villejuif, France.

出版信息

Oncogene. 1988 Sep;3(3):329-33.

PMID:3060795
Abstract

The c-Ha-ras-1 locus was analysed in cervical cancers and shown to exhibit the loss of one allele in 36% of heterozygous tumours and a mutation at codon 12 in 24% of tumours at advanced stages. 40% of tumours with mutation contained also a deletion. A c-myc gene activation was found in 100% and 70% of tumours containing mutation and deletion respectively. This suggests that the two proto-oncogenes cooperate for the progression of cervical cancers. Furthermore as more than 90% of these tumours contained also human papillomavirus sequences, our data strongly suggest that multiple genetic events are involved in the genesis and progression of most cervical cancers.

摘要

对宫颈癌中的c-Ha-ras-1基因座进行了分析,结果显示,在36%的杂合性肿瘤中存在一个等位基因缺失,在24%的晚期肿瘤中密码子12处发生了突变。40%发生突变的肿瘤还存在缺失。在分别含有突变和缺失的肿瘤中,c-myc基因激活的发现率分别为100%和70%。这表明这两个原癌基因在宫颈癌进展过程中相互协作。此外,由于这些肿瘤中超过90%还含有人类乳头瘤病毒序列,我们的数据强烈表明,大多数宫颈癌的发生和进展涉及多个基因事件。

相似文献

1
Somatic deletions and mutations of c-Ha-ras gene in human cervical cancers.人类宫颈癌中c-Ha-ras基因的体细胞缺失和突变
Oncogene. 1988 Sep;3(3):329-33.
2
High correlation between molecular alterations of the c-myc oncogene and carcinoma of the uterine cervix.c-myc癌基因的分子改变与子宫颈癌之间存在高度相关性。
Cancer Res. 1987 Aug 1;47(15):4173-7.
3
[c-myc and c-Ha-ras proto-oncogenes in cervical cancer: prognostic value].[宫颈癌中的c-myc和c-Ha-ras原癌基因:预后价值]
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Clin Cancer Res. 1995 Mar;1(3):359-65.
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[Alterations of c-myc and c-Ha-ras-1 oncogenes in human ovarian cancer].[人类卵巢癌中c-myc和c-Ha-ras-1癌基因的改变]
Eksp Onkol. 1990;12(6):47-9.
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[Presence of papillomavirus genomes and amplification of the c-myc and C-Ha-ras oncogenes in invasive cancers of the uterine cervix].[子宫颈浸润癌中乳头瘤病毒基因组的存在以及c-myc和C-Ha-ras癌基因的扩增]
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C-myc, N-myc, N-ras, and c-erb-B: lack of amplification or rearrangement in human medullary thyroid carcinoma and a derivative cell line.C-myc、N-myc、N-ras和c-erb-B:在人甲状腺髓样癌及其衍生细胞系中缺乏扩增或重排。
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引用本文的文献

1
The long noncoding RNA lnc-FANCI-2 intrinsically restricts RAS signaling in human papillomavirus type 16-infected cervical cancer cells.长链非编码RNA lnc-FANCI-2在人乳头瘤病毒16型感染的宫颈癌细胞中内在地限制RAS信号传导。
Elife. 2025 Aug 29;13:RP102681. doi: 10.7554/eLife.102681.
2
Characterization of c-Kit expression and activation in KSHV-infected endothelial cells.卡波西肉瘤相关疱疹病毒(KSHV)感染的内皮细胞中c-Kit表达及激活的特征分析
Virology. 2009 Aug 1;390(2):174-85. doi: 10.1016/j.virol.2009.05.011. Epub 2009 Jun 6.
3
Cervical keratinocytes containing stably replicating extrachromosomal HPV-16 are refractory to transformation by oncogenic H-Ras.
含有稳定复制的染色体外人乳头瘤病毒16型(HPV-16)的宫颈角质形成细胞对致癌性H-Ras介导的转化具有抗性。
Virology. 2006;356(1-2):68-78. doi: 10.1016/j.virol.2006.07.039. Epub 2006 Aug 30.
4
Molecular analysis of ras oncogenes in CIN III and in stage I and II invasive squamous cell carcinoma of the uterine cervix.子宫颈CIN III级及I期和II期浸润性鳞状细胞癌中ras癌基因的分子分析。
J Clin Pathol. 1998 Aug;51(8):576-82. doi: 10.1136/jcp.51.8.576.
5
Ras-related TC21 is activated by mutation in a breast cancer cell line, but infrequently in breast carcinomas in vivo.与Ras相关的TC21在一种乳腺癌细胞系中因突变而被激活,但在体内乳腺癌中很少发生这种情况。
Br J Cancer. 1998 Aug;78(3):296-300. doi: 10.1038/bjc.1998.490.
6
A possible role for human papillomaviruses in head and neck cancer.人乳头瘤病毒在头颈癌中可能发挥的作用。
Cancer Metastasis Rev. 1996 Mar;15(1):91-112. doi: 10.1007/BF00049489.
7
Population genetics of the HRAS1 minisatellite locus.HRAS1微卫星基因座的群体遗传学
Am J Hum Genet. 1993 Dec;53(6):1298-305.
8
Cervical carcinoma: low frequency of allele loss at loci implicated in other common malignancies.宫颈癌:在与其他常见恶性肿瘤相关的基因座上,等位基因缺失频率较低。
Br J Cancer. 1993 Jan;67(1):71-5. doi: 10.1038/bjc.1993.11.
9
Cellular proteins involved in papillomavirus-induced transformation.参与乳头瘤病毒诱导转化的细胞蛋白。
Arch Virol. 1994;138(1-2):105-15. doi: 10.1007/BF01310042.
10
Deletion and translocation of chromosome 11q13 sequences in cervical carcinoma cell lines.
Am J Hum Genet. 1995 Mar;56(3):705-15.