Loss of heterozygosity in cervical carcinoma: subchromosomal localization of a putative tumor-suppressor gene to chromosome 11q22-q24.

Hampton, Garret M.; Penny, Laura A.; Baergen, Rebecca N.; Larson, Amy A.; Brewer, Carl G.; Liao, Shiping; Busby-Earle, R. M. C.; Williams, A. Wynn; Steel, C. M.; Bird, C. C.

doi:10.1073/pnas.91.15.6953

Cited by 120 publications

(69 citation statements)

References 28 publications

(26 reference statements)

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“…In contrast, LOH at markers from chromosome arm 11p did not exceed the 20% range (not shown) which, as previously mentioned above for chromosome 10 markers, correspond in our hands to a background of sporadic losses which does not allow the identi®cation of a particular region (Kerangueven et al, 1995a,b,c). The incidence of 50% is in close agreement with ®ndings by other groups (Carter et al, 1994;Hampton et al, 1994b;Koreth et al, 1995). The tumor samples could be separated into two distinct groups, according to their pattern of LOH.…”

Section: Loh At Markers From Chromosome 11supporting

confidence: 89%

“…LOH at markers of chromosome region 11q22-23 has been observed in several types of cancer, including bladder (Shaw and Knowles, 1995), cervical (Hampton et al, 1994b;Bethwaite et al, 1995) colorectal (Keldysh et al, 1993), lung (Iizuka et al, 1995), nasopharyngeal (Hui et al, 1996), ovarian (Foulkes et al, 1993;Davis et al, 1996;Gabra et al, 1996) and stomach (Ba a et al, 1996) carcinomas, and in melanomas (Tomlinson et al, 1993;Herbst et al, 1995), and thus may host at least one so-called multiple tumor suppressor gene, the activity of which is not restricted to breast epithelial cells. Further studies will aim at re®ning the localization of this important locus.…”

Section: Discussionmentioning

confidence: 99%

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Loss of heterozygosity in human breast carcinomas in the ataxia telangiectasia, Cowden disease and BRCA1 gene regions

et al. 1997

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To appreciate the involvement of known or potential susceptibility genes in sporadic breast tumors, we have searched for chromosomal deletions by studying loss of heterozygosity (LOH) at 43 microsatellite (CA) n markers from human chromosomes 10, 11 and 17, in 115 unselected consecutive samples of breast carcinoma with particular emphasis on speci®c regions. No site of consistent LOH was identi®ed on chromosome 10. Five regions of LOH were contained within bands q22-24 of chromosome 11 for which nearly 50% of the tumors had LOH at at least one marker. This region is thus a major site of deletion in breast cancer and several tumor suppressor genes seem to be involved. One of them may be the ataxia telangiectasia (ATM) gene which is located in one of the a ected regions. Five regions of LOH, one of which is within the BRCA1 gene area, were recognized along chromosome 17. LOH at three of these regions were found in highly proliferative tumors. When combined with a previous study of chromosome 13 with emphasis on BRCA2 and Rb1 genes, this work allowed to distinguish a total of 12 regions of LOH, variably a ected in breast tumors and correlated with prognostic parameters.

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Section: Loh At Markers From Chromosome 11supporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Loss of heterozygosity in human breast carcinomas in the ataxia telangiectasia, Cowden disease and BRCA1 gene regions

et al. 1997

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“…The smallest region of loss could be mapped to 11q22-qter. We have previously mapped the smallest region of chromosome loss on 11q in cervical cancers as 11q22 -24 (Allen et al, 2000) and an identical region has been previously mapped by LOH studies in cervical cancer (Hampton et al, 1994). These data indicate that, in contrast to genes on 3q, those on 3p and 11q may be related to development and progression of anogenital SCC independent of HPV status.…”

Section: Discussionsupporting

confidence: 63%

“…Loss of 3p is also frequently seen in cervical SCC, by CGH and LOH analysis (Heselmeyer et al, 1996(Heselmeyer et al, , 1997bLarson et al, 1997;Wistuba et al, 1997;Kersemaekers et al, 1998;Steenbergen et al, 1998;Dellas et al, 1999;Kirchoff et al, 1999;Allen et al, 2000). Loss of 11q has been documented in cervical and other malignancies not related to HPV infection, including breast, colorectal and ovarian cancers and malignant melanoma (Hampton et al, 1994;Kersemaekers et al, 1998;Allen et al, 2000). Loss of 11q was frequently documented in our series of vulvar cancers and was not related to HPV status.…”

Section: Discussionsupporting

confidence: 52%

Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers

Hammet

et al. 2002

Br J Cancer

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Squamous cell carcinoma of the vulva is a disease of significant clinical importance, which arises in the presence or absence of human papillomavirus. We used comparative genomic hybridisation to document non-random chromosomal gains and losses within human papillomavirus positive and negative vulvar cancers. Gain of 3q was significantly more common in human papillomavirus-positive cancers compared to human papillomavirus-negative cancers. The smallest area of gain was 3q22 -25, a chromosome region which is frequently gained in other human papillomavirus-related cancers. Chromosome 8q was more commonly gained in human papillomavirus-negative compared to human papillomavirus-positive cancers. 8q21 was the smallest region of gain, which has been identified in other, non-human papillomavirus-related cancers. Chromosome arms 3p and 11q were lost in both categories of vulvar cancer. This study has demonstrated chromosome locations important in the development of vulvar squamous cell carcinoma. Additionally, taken together with previous studies of human papillomaviruspositive cancers of other anogenital sites, the data indicate that one or more oncogenes important in the development and progression of human papillomavirus-induced carcinomas are located on 3q. The different genetic changes seen in human papillomavirus-positive and negative vulvar squamous cell carcinomas support the clinicopathological data indicating that these are different cancer types.

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“…Hampton et al (1994) found the smallest region of overlapping LOH at 1 lq22-24. Bethwaite et al (1995) found LOH on 1 1q23, but only with one marker in this region.…”

mentioning

confidence: 89%

Loss of heterozygosity for defined regions on chromosomes 3, 11 and 17 in carcinomas of the uterine cervix

Kersemaekers

Hermans²,

Fleuren³

et al. 1998

Br J Cancer

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Summary 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 11 q22 (46%) and 11 q23.3 (43%). LOH on chromosome 11p was not frequent. On chromosome 17p1 3.3, a marker (Dl 7S513) 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 f-catenin gene is located in this chromosomal region. Therefore, expression of f-catenin protein was studied in 39 cases using immunohistochemistry. Staining of 1-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 ,B-catenin in this one case, but (an)other tumour-suppressor gene(s) must also be present in this region. For the other chromosomes studied, 1 3q (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, 1 1 q and 1 7p. 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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Loss of heterozygosity in cervical carcinoma: subchromosomal localization of a putative tumor-suppressor gene to chromosome 11q22-q24.

Cited by 120 publications

References 28 publications

Loss of heterozygosity in human breast carcinomas in the ataxia telangiectasia, Cowden disease and BRCA1 gene regions

Loss of heterozygosity in human breast carcinomas in the ataxia telangiectasia, Cowden disease and BRCA1 gene regions

Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers

Loss of heterozygosity for defined regions on chromosomes 3, 11 and 17 in carcinomas of the uterine cervix

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