Chromosome changes in a squamous cell carcinoma of the vagina

Atkin, N. B.; Fox, Margaret

doi:10.1016/0165-4608(91)90071-2

Cancer Genetics and Cytogenetics

1991

DOI: 10.1016/0165-4608(91)90071-2

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Chromosome changes in a squamous cell carcinoma of the vagina

N. B. Atkin

Margaret Fox

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1992

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Cited by 6 publications

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“…In the case of vulvar SCC and its precursor lesions, there are few karyotypic or DNA content analyses to document whether chromosomal aberrations are significant in its genesis. 2,[12][13][14][15][16][17][18][19][20] To determine whether chromosomal abnormalities occur in vulvar cancers and their surrounding skin, we used fluorescent in situ (FISH) methods to visualize abnormalities in chromosome 17 copy number in a prospective study of vulvar SCCs. Chromosome 17 was chosen as the object of this investigation because the p53 tumor suppressor gene, located on 17p, has been implicated in the development of many vulvar SCCs, 21-28 chromosome 17 polysomy is frequent in some forms of SCC, 9,11,29 -31 loss of chromosome 17 can be found in cervical and cutaneous SCCs, 32,33 and a susceptibility locus for oncogenic HPV infection has been identified on 17qter.…”

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confidence: 99%

Chromosome 17 Aneusomy Detected by Fluorescence in Situ Hybridization in Vulvar Squamous Cell Carcinomas and Synchronous Vulvar Skin

Carlson¹,

Healy²,

Tran³

et al. 2000

The American Journal of Pathology

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Vulvar squamous cell carcinoma (SCC) affects a spectrum of women with granulomatous vulvar diseases, human papillomavirus (HPV) infections, and chronic inflammatory vulvar dermatoses. To determine whether there is evidence of chromosomal instability occurring in synchronous skin surrounding vulvar SCCs, we investigated abnormalities in chromosome 17 copy number. Samples of SCC, vulvar intraepithelial neoplasia (VIN), and surrounding vulvar skin were obtained from all vulvar excisions performed for squamous neoplasia at Albany Medical College from 1996 to 1997. Histological categorization, fluorescent in situ hybridization (FISH) for the alpha satellite region of chromosome 17, DNA content by image analysis, and Ki-67 labeling were evaluated. Controls of normal vulvar skin not associated with cancer were used for comparison. One hundred ten specimens were obtained from 33 patients with either SCC or VIN 3 and consisted of 49 neoplastic, 52 nonneoplastic, and 9 histologically normal vulvar skin samples. The majority of SCCs (88%) and a minority (18%) of VIN 3 excisions were associated with lichen sclerosus. Normal vulvar skin controls did not exhibit chromosome 17 polysomy (cells with more than four FISH signals), whereas 56% of normal vulvar skin associated with cancer did. Moreover, the frequency of polysomy significantly increased as the histological classification progressed from normal to inflammatory to neoplastic lesions. The largest mean value and variance for chromosome 17 copy number was identified in SCCs (2.4 +/- 1.0) with intermediate values identified, in decreasing order, for SCC in situ (2.1 +/- 1.0), VIN 2 (2.1 +/- 0.8), lichen sclerosus (2.0 +/- 0.5), lichen simplex chronicus (1.9 +/- 0.4), and normal skin associated with SCC (1.8 +/- 0.4) compared with control vulvar skin (1.5 +/- 0. 05). Concordance of chromosome 17 aneusomy between cancers and synchronous skin lesions was found in 48% of patients. Loss of chromosome 17 was identified 5% of all samples and was significantly associated with women with SCC in situ (HPV-related). Both DNA content and Ki-67 labeling positively and significantly correlated with mean chromosome 17 copy number (r = 0.1, P: = 0.007). A high degree of genetic instability (aneuploidy) occurs in the skin surrounding vulvar carcinomas. As these events could be detected in histologically normal skin and inflammatory lesions (lichen sclerosus), chromosomal abnormalities may be a driving force in the early stages of carcinogenesis. Differences in chromosomal patterns (loss or gain) support the concept of at least two pathways in vulvar carcinogenesis.

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confidence: 99%

Chromosome 17 Aneusomy Detected by Fluorescence in Situ Hybridization in Vulvar Squamous Cell Carcinomas and Synchronous Vulvar Skin

Carlson¹,

Healy²,

Tran³

et al. 2000

The American Journal of Pathology

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Genomic aberration patterns and expression profiles of squamous cell carcinomas of the vulva

Micci

Panagopoulos

Haugom

et al. 2013

Genes Chromosomes & Cancer

161

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Little is known about the genomic abnormalities of squamous cell carcinomas (SCC) of the vulva and how they correlate with gene expression. We determined the genomic and expression profiles of 15 such SCC using karyotyping, DNA ploidy analysis, arrayCGH, and expression arrays. Four of the five cases with clonal chromosomal aberrations found by G-banding showed highly abnormal karyotypes with multiple rearrangements. The imbalances scored by arrayCGH mapped to different chromosomes with losses being more common than gains. Frequent losses were scored from 3p and 8p whereas gains were frequent from 3q and 8q (loss of 8p with concomitant gain of 8q mostly occurred via 8q isochromosome formation). This is the first study of vulvar tumors using arrayCGH, and some frequent imbalances could be defined precisely. Of particular note were the sometimes large, sometimes small deletions of 3p and 9p which had minute areas in 3p14 and 9p23 as minimal commonly deleted regions. FHIT (3p14) and PTPRD (9p23) are the only genes here. They were both lost in seven cases, including homozygous losses of PTPRD in four tumors. Using qPCR we could demonstrate deregulation of the FHIT gene in tumor cells. Hence, this gene is likely to play a pathogenetic role in vulvar SCC tumorigenesis. Expression array analyses also identified a number of other genes whose expression profile was altered. Notable among the downregulated genes were MAL (in 2q11), KRT4 (in 12q13), and OLFM4 (in 13q14), whereas upregulated genes included SPRR2G (in 1q21.3) and S100A7A (in 1q21.3).

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Cytogenetic abnormalities in a squamous cell carcinoma of the penis

Xiao

Feng

Shi

et al. 1992

Cancer Genetics and Cytogenetics

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Chromosome changes in a squamous cell carcinoma of the vagina

Cited by 6 publications

References 8 publications

Chromosome 17 Aneusomy Detected by Fluorescence in Situ Hybridization in Vulvar Squamous Cell Carcinomas and Synchronous Vulvar Skin

Chromosome 17 Aneusomy Detected by Fluorescence in Situ Hybridization in Vulvar Squamous Cell Carcinomas and Synchronous Vulvar Skin

Genomic aberration patterns and expression profiles of squamous cell carcinomas of the vulva

Cytogenetic abnormalities in a squamous cell carcinoma of the penis

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