Ploidy in human papillomavirus positive and negative vulvar squamous cell carcinomas and adjacent skin lesions

J. Scurry, J. Hung, L. Flowers, P. Kneafsay, A. Gazdar

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Original languageEnglish
Pages (from-to)187-193
Number of pages7
JournalInternational Journal of Gynecological Cancer
Volume9
Issue number3
DOIs
StatePublished - 1999
Externally publishedYes

Fingerprint

Ploidies
Squamous Cell Carcinoma
Skin
Lichen Sclerosus et Atrophicus
Carcinoma
Hyperplasia
Aneuploidy
Epithelial Cells
Neoplasms
DNA
Cervical Intraepithelial Neoplasia
Carcinoma in Situ
Population

ASJC Scopus subject areas

  • Cancer Research
  • Obstetrics and Gynecology
  • Oncology

Cite this

Ploidy in human papillomavirus positive and negative vulvar squamous cell carcinomas and adjacent skin lesions. / Scurry, J.; Hung, J.; Flowers, L.; Kneafsay, P.; Gazdar, A.

In: International Journal of Gynecological Cancer, Vol. 9, No. 3, 1999, p. 187-193.

Research output: Contribution to journalArticle

Scurry, J. ; Hung, J. ; Flowers, L. ; Kneafsay, P. ; Gazdar, A. / Ploidy in human papillomavirus positive and negative vulvar squamous cell carcinomas and adjacent skin lesions. In: International Journal of Gynecological Cancer. 1999 ; Vol. 9, No. 3. pp. 187-193.
@article{d667240289fc4c769d4f10360905da37,
title = "Ploidy in human papillomavirus positive and negative vulvar squamous cell carcinomas and adjacent skin lesions",
abstract = "To better characterize the two clinicopathologic types of squamous cell carcinoma, human papillomavirus (HPV) positive and negative, and their adjacent skin changes, we performed cytomorphometric analysis on 12 HPV- positive squamous cell carcinomas and adjacent vulvar intraepithelial neoplasia and 22 HPV-negative squamous cell carcinomas and adjacent squamous cell hyperplasia and lichen sclerosis. Our results were that 83{\%} (10 of 12) HPV-positive carcinomas and 78{\%} (7 of 9) adjacent vulvar intraepithelial neoplasia were aneuploid, compared with 59{\%} (13 of 22) HPV-negative carcinomas, 6{\%} (1 of 16) squamous cell hyperplasias and 0{\%} (0 of 20) lichen scleroses. Seventy-five percent (9 of 12) HPV carcinomas and 78{\%} (7 of 9) vulvar intraepithelial neoplasias showed two aneuploid peaks, but no HPV- negative carcinoma or nonneoplastic epithelial lesion showed multiple aneuploid peaks. Fifty percent of squamous cell hyperplasias (8 of 16) and lichen scleroses (10 of 20) adjacent to HPV-negative carcinomas were hypodiploid. The mean DNA indices were: 1.70 for the dominant tumor cell population of HPV-positive carcinoma, 1.64 for the dominant population of vulvar intraepithelial neoplasia, 1.41 for HPV-negative carcinoma, 0.85 for squamous cell hyperplasia and 0.83 for lichen sclerosis. In conclusion, the higher rate of aneuploidy, higher mean DNA index, and presence of multiploid peaks in HPV-positive carcinomas and adjacent vulvar intraepithelial neoplasias compared with the lower rate of aneuploidy, lower mean DNA index, absence of multiploid peaks of HPV-negative carcinomas and tendency to hypodiploidy in squamous cell hyperplasia and lichen sclerosis support the hypothesis that there are two clinicopathologic types of vulvar carcinoma, with different pathogenetic mechanisms. The similarities in ploidy findings between vulvar HPV-positive carcinomas and vulvar intraepithelial neoplasia and those previously published for cervical carcinoma and cervical intraepithelial neoplasia support the view that these two cancers are analogous and have similar pathogenetic mechanisms. The frequent finding of hypodiploidy in squamous cell hyperplasia and lichen sclerosis next to HPV- negative carcinomas requires further investigation of the molecular pathogenesis of this cancer type.",
keywords = "Cytomorphometry, Human papillomavirus, Neoplasm, Ploidy, Squamous cell carcinoma, Vulva",
author = "J. Scurry and J. Hung and L. Flowers and P. Kneafsay and A. Gazdar",
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T1 - Ploidy in human papillomavirus positive and negative vulvar squamous cell carcinomas and adjacent skin lesions

AU - Scurry, J.

AU - Hung, J.

AU - Flowers, L.

AU - Kneafsay, P.

AU - Gazdar, A.

PY - 1999

Y1 - 1999

N2 - To better characterize the two clinicopathologic types of squamous cell carcinoma, human papillomavirus (HPV) positive and negative, and their adjacent skin changes, we performed cytomorphometric analysis on 12 HPV- positive squamous cell carcinomas and adjacent vulvar intraepithelial neoplasia and 22 HPV-negative squamous cell carcinomas and adjacent squamous cell hyperplasia and lichen sclerosis. Our results were that 83% (10 of 12) HPV-positive carcinomas and 78% (7 of 9) adjacent vulvar intraepithelial neoplasia were aneuploid, compared with 59% (13 of 22) HPV-negative carcinomas, 6% (1 of 16) squamous cell hyperplasias and 0% (0 of 20) lichen scleroses. Seventy-five percent (9 of 12) HPV carcinomas and 78% (7 of 9) vulvar intraepithelial neoplasias showed two aneuploid peaks, but no HPV- negative carcinoma or nonneoplastic epithelial lesion showed multiple aneuploid peaks. Fifty percent of squamous cell hyperplasias (8 of 16) and lichen scleroses (10 of 20) adjacent to HPV-negative carcinomas were hypodiploid. The mean DNA indices were: 1.70 for the dominant tumor cell population of HPV-positive carcinoma, 1.64 for the dominant population of vulvar intraepithelial neoplasia, 1.41 for HPV-negative carcinoma, 0.85 for squamous cell hyperplasia and 0.83 for lichen sclerosis. In conclusion, the higher rate of aneuploidy, higher mean DNA index, and presence of multiploid peaks in HPV-positive carcinomas and adjacent vulvar intraepithelial neoplasias compared with the lower rate of aneuploidy, lower mean DNA index, absence of multiploid peaks of HPV-negative carcinomas and tendency to hypodiploidy in squamous cell hyperplasia and lichen sclerosis support the hypothesis that there are two clinicopathologic types of vulvar carcinoma, with different pathogenetic mechanisms. The similarities in ploidy findings between vulvar HPV-positive carcinomas and vulvar intraepithelial neoplasia and those previously published for cervical carcinoma and cervical intraepithelial neoplasia support the view that these two cancers are analogous and have similar pathogenetic mechanisms. The frequent finding of hypodiploidy in squamous cell hyperplasia and lichen sclerosis next to HPV- negative carcinomas requires further investigation of the molecular pathogenesis of this cancer type.

AB - To better characterize the two clinicopathologic types of squamous cell carcinoma, human papillomavirus (HPV) positive and negative, and their adjacent skin changes, we performed cytomorphometric analysis on 12 HPV- positive squamous cell carcinomas and adjacent vulvar intraepithelial neoplasia and 22 HPV-negative squamous cell carcinomas and adjacent squamous cell hyperplasia and lichen sclerosis. Our results were that 83% (10 of 12) HPV-positive carcinomas and 78% (7 of 9) adjacent vulvar intraepithelial neoplasia were aneuploid, compared with 59% (13 of 22) HPV-negative carcinomas, 6% (1 of 16) squamous cell hyperplasias and 0% (0 of 20) lichen scleroses. Seventy-five percent (9 of 12) HPV carcinomas and 78% (7 of 9) vulvar intraepithelial neoplasias showed two aneuploid peaks, but no HPV- negative carcinoma or nonneoplastic epithelial lesion showed multiple aneuploid peaks. Fifty percent of squamous cell hyperplasias (8 of 16) and lichen scleroses (10 of 20) adjacent to HPV-negative carcinomas were hypodiploid. The mean DNA indices were: 1.70 for the dominant tumor cell population of HPV-positive carcinoma, 1.64 for the dominant population of vulvar intraepithelial neoplasia, 1.41 for HPV-negative carcinoma, 0.85 for squamous cell hyperplasia and 0.83 for lichen sclerosis. In conclusion, the higher rate of aneuploidy, higher mean DNA index, and presence of multiploid peaks in HPV-positive carcinomas and adjacent vulvar intraepithelial neoplasias compared with the lower rate of aneuploidy, lower mean DNA index, absence of multiploid peaks of HPV-negative carcinomas and tendency to hypodiploidy in squamous cell hyperplasia and lichen sclerosis support the hypothesis that there are two clinicopathologic types of vulvar carcinoma, with different pathogenetic mechanisms. The similarities in ploidy findings between vulvar HPV-positive carcinomas and vulvar intraepithelial neoplasia and those previously published for cervical carcinoma and cervical intraepithelial neoplasia support the view that these two cancers are analogous and have similar pathogenetic mechanisms. The frequent finding of hypodiploidy in squamous cell hyperplasia and lichen sclerosis next to HPV- negative carcinomas requires further investigation of the molecular pathogenesis of this cancer type.

KW - Cytomorphometry

KW - Human papillomavirus

KW - Neoplasm

KW - Ploidy

KW - Squamous cell carcinoma

KW - Vulva

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