Open AccessMorphological analysis of in situ hybridization signals in cervical intraepithelial neoplasia containing human papillomavirus type 16 or 18: Relationship with histological grade and DNA content
Author(s) -
Lizard Gérard,
Roignot Patrick,
BrunetLecomte Patrick,
Chardonnet Yvette
Publication year - 1998
Publication title -
cytometry
Language(s) - English
Resource type - Journals
eISSN - 1097-0320
pISSN - 0196-4763
DOI - 10.1002/(sici)1097-0320(19980815)34:4<180::aid-cyto2>3.0.co;2-k
Subject(s) - in situ hybridization , biology , pathology , malignancy , cervical intraepithelial neoplasia , in situ , lesion , human papillomavirus , squamous intraepithelial lesion , ploidy , flow cytometry , cytometry , intraepithelial neoplasia , dna , papillomaviridae , carcinoma in situ , microbiology and biotechnology , carcinoma , cancer , cervical cancer , medicine , gene , genetics , chemistry , prostate , gene expression , organic chemistry
Among 345 lesions histologically defined as cervical intraepithelial neoplasia (CIN) examined by in situ hybridization (ISH) for the presence of DNA from human papillomavirus (HPV) types 6/11, 16, 18, 31, 33, and 51, a group of 69 lesions (41 low grade and 28 high grade) containing HPV 16 or 18 was further charac terized with the following criteria: DNA ploidy and morphological patterns of ISH spots, i.e., punctate or diffuse throughout the nuclei corresponding to integrated or episomal state of HPV DNA, respectively. The highest percentage of aneuploid lesions, the highest diploid index values, and the highest proportion of CIN with punctate ISH signals were associated with high‐grade lesions. In addition, punctate ISH signals were also most frequently found in aneuploid CIN. These results underline that punctate ISH signals considered as integrated HPV DNA were preferentially associated with aneuploid and high‐grade lesions, and lead to suggest that this later criteria could be used to predict the evolution of a lesion towards malignancy. Cytometry (Comm. Clin. Cytometry) 34:180–186, 1998. © 1998 Wiley‐Liss, Inc.