ArticleBritish journal of cancer1998
Loss of heterozygosity for defined regions on chromosomes 3, 11 and 17 in carcinomas of the uterine cervix.
Article in British journal of cancer, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 71 citations in OpenAlex.
- Mutational analysis of beta-catenin gene in Japanese ovarian carcinomas: frequent mutations in endometrioid carcinomas.Japanese journal of cancer research : Gann · 1999Trial
- NFrontiers in oncology · 2021Article
- Characterization of genomic changes in the cervical pre-cancerous lesions and tumors induced by different types of human papillomaviruses.Virusdisease · 2016Article
- Assessment of the frequency of genetic alterations (LOH/MSI) in patients with intraepithelial cervical lesions with HPV infection: a pilot study.Medical oncology (Northwood, London, England) · 2016Article
- Deletions in chromosome 4 differentially associated with the development of cervical cancer: evidence of slit2 as a candidate tumor suppressor gene.Human genetics · 2007Article
- Combined array-comparative genomic hybridization and single-nucleotide polymorphism-loss of heterozygosity analysis reveals complex genetic alterations in cervical cancer.BMC genomics · 2007Article
- Smad4 deficiency in cervical carcinoma cells.Oncogene · 2005Article
- Differential deletions of chromosome 3p are associated with the development of uterine cervical carcinoma in Indian patients.Molecular pathology : MP · 2003Article
- Pathologic aspects of AIDS malignancies.Oncogene · 2003Review
- Mapping common deleted regions on 5p15 in cervical carcinoma and their occurrence in precancerous lesions.Molecular cancer · 2002Article
- Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers.British journal of cancer · 2002Article
- Postmodern cancer: the role of human immunodeficiency virus in uterine cervical cancer.Molecular pathology : MP · 2002Review
- Loss of sequences on the short arm of chromosome 17 is a late event in squamous carcinoma of the cervix.Molecular pathology : MP · 2001Article
- Progressive genetic aberrations detected by comparative genomic hybridization in squamous cell cervical cancer.British journal of cancer · 2000Article
- The molecular genetics of cervical carcinoma.British journal of cancer · 1999Review
- Localization of tumor suppressor activity important in nonsmall cell lung carcinoma on chromosome 11q.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Loss of heterozygosity (LOH) frequently occurs in squamous cell carcinomas of the uterine cervix and indicates the probable sites of tumour-suppressor genes that play a role in the development of this tumour. To define the localization of these tumour-suppressor genes, we studied loss of heterozygosity in 64 invasive cervical carcinomas (stage IB and IIA) using the polymerase chain reaction with 24 primers for polymorphic repeats of known chromosomal localization. Chromosomes 3, 11, 13, 16 and 17, in particular, were studied. LOH was frequently found on chromosome 11, in particular at 11q22 (46%) and 11q23.3 (43%). LOH on chromosome 11p was not frequent. On chromosome 17p13.3, a marker (D17S513) distal to p53 showed 38% LOH, whereas p53 itself showed only 20% LOH. On the short arm of chromosome 3, LOH was frequently found (41%) at 3p21.1. The beta-catenin gene is located in this chromosomal region. Therefore, expression of beta-catenin protein was studied in 39 cases using immunohistochemistry. Staining of beta-catenin at the plasma membrane of tumour cells was present in 38 cases and completely absent in only one case. The tumour-suppressor gene on chromosome 3p21.1 may be beta-catenin in this one case, but (an)other tumour-suppressor gene(s) must also be present in this region. For the other chromosomes studied, 13q (BRCA-2) and 16q (E-cadherin), only sporadic losses (< 15% of cases) were found. Expression of E-cadherin was found in all of 37 cases but in six cases the staining was very weak. No correlation was found between clinical and histological parameters and losses on chromosome 3p, 11q and 17p. In addition to LOH, microsatellite instability was found in one tumour for almost all loci and in eight tumours for one to three loci. In conclusion, we have identified three loci with frequent LOH, which may harbour new tumour-suppressor genes, and found microsatellite instability in 14% of cervical carcinomas.
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