Genital warts and cervical cancer. VI: The relationship between aneuploid and polyploid cervical lesions
Human papillomaviral infection is now widely implicated in the causation of cervical neoplasia. Genotype analysis provides the best guide to biologic outcome; most polyploid lesions regress and most aneuploid ones persist or progress. This prospective survey examined the relationships between cell p...
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| Veröffentlicht in: | American journal of obstetrics and gynecology 1984-09, Vol.150 (2), p.189-199 |
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| container_title | American journal of obstetrics and gynecology |
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| creator | REID, R YAO SHI FU HERSCHMAN, B. R CRUM, C. P BRAUN, L SHAH, K. V AGRONOW, S. J STANHOPE, C. R |
| description | Human papillomaviral infection is now widely implicated in the causation of cervical neoplasia. Genotype analysis provides the best guide to biologic outcome; most polyploid lesions regress and most aneuploid ones persist or progress. This prospective survey examined the relationships between cell ploidy and 24 objectively validated criteria of human papillomaviral infection or premalignant change in 52 biopsies from a dysplasia clinic. Histologic evidence of benign warty expression and human papillomaviral capsid antigen production decreased steadily as DNA content ranged from diploidy to polyploidy to aneuploidy. In contrast, premalignant change increased with progressive distortion of nuclear DNA content. No absolute discriminants were found between polyploidy and aneuploidy, as evidenced by the detection of human papillomaviral proteins in three of 21 aneuploid epithelia and the recognition of abnormal mitotic figures in five of 17 polyploid lesions. Polyploid and aneuploid lesions differed only in severity, and it appears that some polyploid epithelia may be transition forms between diploidy and aneuploidy. |
| doi_str_mv | 10.1016/S0002-9378(84)80015-0 |
| format | Article |
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VI: The relationship between aneuploid and polyploid cervical lesions</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>REID, R ; YAO SHI FU ; HERSCHMAN, B. R ; CRUM, C. P ; BRAUN, L ; SHAH, K. V ; AGRONOW, S. J ; STANHOPE, C. R</creator><creatorcontrib>REID, R ; YAO SHI FU ; HERSCHMAN, B. R ; CRUM, C. P ; BRAUN, L ; SHAH, K. V ; AGRONOW, S. J ; STANHOPE, C. R</creatorcontrib><description>Human papillomaviral infection is now widely implicated in the causation of cervical neoplasia. Genotype analysis provides the best guide to biologic outcome; most polyploid lesions regress and most aneuploid ones persist or progress. This prospective survey examined the relationships between cell ploidy and 24 objectively validated criteria of human papillomaviral infection or premalignant change in 52 biopsies from a dysplasia clinic. Histologic evidence of benign warty expression and human papillomaviral capsid antigen production decreased steadily as DNA content ranged from diploidy to polyploidy to aneuploidy. In contrast, premalignant change increased with progressive distortion of nuclear DNA content. No absolute discriminants were found between polyploidy and aneuploidy, as evidenced by the detection of human papillomaviral proteins in three of 21 aneuploid epithelia and the recognition of abnormal mitotic figures in five of 17 polyploid lesions. 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Obstetrics ; Humans ; Immunoenzyme Techniques ; Medical sciences ; Mitosis ; Models, Biological ; Papillomaviridae - genetics ; Papillomaviridae - immunology ; Ploidies ; Precancerous Conditions - genetics ; Precancerous Conditions - pathology ; Tumor Virus Infections - genetics ; Tumor Virus Infections - pathology ; Tumors ; Uterine Cervical Diseases - genetics ; Uterine Cervical Diseases - pathology ; Uterine Cervical Dysplasia - genetics ; Uterine Cervical Dysplasia - pathology ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - pathology ; Warts - genetics ; Warts - pathology</subject><ispartof>American journal of obstetrics and gynecology, 1984-09, Vol.150 (2), p.189-199</ispartof><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9137082$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6089564$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>REID, R</creatorcontrib><creatorcontrib>YAO SHI FU</creatorcontrib><creatorcontrib>HERSCHMAN, B. 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Histologic evidence of benign warty expression and human papillomaviral capsid antigen production decreased steadily as DNA content ranged from diploidy to polyploidy to aneuploidy. In contrast, premalignant change increased with progressive distortion of nuclear DNA content. No absolute discriminants were found between polyploidy and aneuploidy, as evidenced by the detection of human papillomaviral proteins in three of 21 aneuploid epithelia and the recognition of abnormal mitotic figures in five of 17 polyploid lesions. Polyploid and aneuploid lesions differed only in severity, and it appears that some polyploid epithelia may be transition forms between diploidy and aneuploidy.</description><subject>Animals</subject><subject>Antigens, Viral - analysis</subject><subject>Biological and medical sciences</subject><subject>Capsid - analysis</subject><subject>Carcinoma in Situ - genetics</subject><subject>Carcinoma in Situ - pathology</subject><subject>DNA, Neoplasm - analysis</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Medical sciences</subject><subject>Mitosis</subject><subject>Models, Biological</subject><subject>Papillomaviridae - genetics</subject><subject>Papillomaviridae - immunology</subject><subject>Ploidies</subject><subject>Precancerous Conditions - genetics</subject><subject>Precancerous Conditions - pathology</subject><subject>Tumor Virus Infections - genetics</subject><subject>Tumor Virus Infections - pathology</subject><subject>Tumors</subject><subject>Uterine Cervical Diseases - genetics</subject><subject>Uterine Cervical Diseases - pathology</subject><subject>Uterine Cervical Dysplasia - genetics</subject><subject>Uterine Cervical Dysplasia - pathology</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Uterine Cervical Neoplasms - pathology</subject><subject>Warts - genetics</subject><subject>Warts - pathology</subject><issn>0002-9378</issn><issn>1097-6868</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9LwzAUx4Moc07_BCEHET10JmmTJt5k6BwMPDi9lpc2ZZGsrU3r2H9v5squnt6vz_fx3heha0qmlFDx8E4IYZGKU3knk3tJCOUROUFjSlQaCSnkKRofkXN04f3XvmSKjdBIEKm4SMZoPTeV7cDhLbSdx1AVODftj81DK4cq5FP8uXjEq7XBrXHQ2brya9tgbbqtMVVQmL5xtS3-tE3tdofquMUZv9dcorMSnDdXQ5ygj5fn1ew1Wr7NF7OnZdRQSbuI0XBjyUvGQCRAgbJCMy10AUBKVZKEF6nSWikAJTQwqpQGkYPiXKSyEPEE3R72Nm393RvfZRvrc-NcOLTufSZpsCDh6l-QJozHMd2D1wPY640psqa1G2h32eBhmN8Mc_Dh4bINtll_xBSNUyJZ_As6QoHZ</recordid><startdate>19840915</startdate><enddate>19840915</enddate><creator>REID, R</creator><creator>YAO SHI FU</creator><creator>HERSCHMAN, B. 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Obstetrics</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Medical sciences</topic><topic>Mitosis</topic><topic>Models, Biological</topic><topic>Papillomaviridae - genetics</topic><topic>Papillomaviridae - immunology</topic><topic>Ploidies</topic><topic>Precancerous Conditions - genetics</topic><topic>Precancerous Conditions - pathology</topic><topic>Tumor Virus Infections - genetics</topic><topic>Tumor Virus Infections - pathology</topic><topic>Tumors</topic><topic>Uterine Cervical Diseases - genetics</topic><topic>Uterine Cervical Diseases - pathology</topic><topic>Uterine Cervical Dysplasia - genetics</topic><topic>Uterine Cervical Dysplasia - pathology</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - pathology</topic><topic>Warts - genetics</topic><topic>Warts - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>REID, R</creatorcontrib><creatorcontrib>YAO SHI FU</creatorcontrib><creatorcontrib>HERSCHMAN, B. 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| ispartof | American journal of obstetrics and gynecology, 1984-09, Vol.150 (2), p.189-199 |
| issn | 0002-9378 1097-6868 |
| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Antigens, Viral - analysis Biological and medical sciences Capsid - analysis Carcinoma in Situ - genetics Carcinoma in Situ - pathology DNA, Neoplasm - analysis Female Female genital diseases Gynecology. Andrology. Obstetrics Humans Immunoenzyme Techniques Medical sciences Mitosis Models, Biological Papillomaviridae - genetics Papillomaviridae - immunology Ploidies Precancerous Conditions - genetics Precancerous Conditions - pathology Tumor Virus Infections - genetics Tumor Virus Infections - pathology Tumors Uterine Cervical Diseases - genetics Uterine Cervical Diseases - pathology Uterine Cervical Dysplasia - genetics Uterine Cervical Dysplasia - pathology Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - pathology Warts - genetics Warts - pathology |
| title | Genital warts and cervical cancer. VI: The relationship between aneuploid and polyploid cervical lesions |
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