Failure to detect human papillomavirus in Kaposi's sarcoma.
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Aged↗
Biomedical subjects
K V Shah
Publications and source records attributed to K V Shah.
Investigation of colon cancers for human papillomavirus genomic sequences by polymerase chain reaction.
Two previous studies have reported the presence of human papillomavirus (HPV) genomic sequences in colorectal cancers. We examined DNAs from 50 colorectal tumors for HPV sequences by polymerase chain reaction (PCR), using HPV consensus L1 primers for amplification. The PCR products were screened with a generic HPV probe consisting of amplimers of HPV-16 and HPV-18. All tumor DNAs were negative for HPV sequences. These results call into the question the reported association of colorectal cancers with HPVs.
Colonic Neoplasms↗
Antibodies to HPV-16 E6 and E7 proteins as markers for HPV-16-associated invasive cervical cancer.
Transforming proteins E6 and E7 of human papillomaviruses (HPVs) are consistently expressed in HPV-associated cervical cancers. In ELISA with four HPV-16 E6-E7 peptides, patients with HPV-16-associated invasive cervical cancer (group 1) had a greater seroreactivity than all other groups, which included patients with HPV-16-associated cervical intraepithelial neoplasia, invasive cervical cancer patients without HPVs, and unaffected controls. A larger proportion of group 1 sera, as compared to sera of all other groups, was reactive with at least one peptide (49% vs 17-27%), and with two or more peptides (22% vs 0-6%). A clear difference between group 1 and all other groups was also found for high ELISA absorbance values to at least one peptide (22% vs 0-8%). This high seroreactivity of group 1 sera was confirmed by a radioimmunoprecipitation assay with in vitro transcribed and translated HPV-16 E7 protein. Sera from 50% of group 1 but only 3% of controls were reactive in this test. Antibodies to HPV-16 E6 and E7 proteins appear to be virus-specific and disease state-specific markers of HPV-associated cervical cancer.
Amino Acid Sequence↗
Antibody response to human papillomavirus (HPV) type 11 in children with juvenile-onset recurrent respiratory papillomatosis (RRP).
We previously established, using an ELISA, the presence of specific antibodies directed at human papillomavirus (HPV) type 11 virions in the sera of patients with condylomata acuminata, mostly a disease of young adults that, like recurrent respiratory papillomatosis (RRP), is caused by two closely related HPVs, types 6 and 11. The present study was done to investigate if children with RRP can make viral-specific antibodies to an infection that is acquired at birth. Using the same ELISA, we studied the sera of 32 children with biopsy-documented juvenile-onset RRP and compared them to the sera of 31 control children. The median (and interquartile range) of the OD values in the controls and the cases was 0.078 (0.003, 0.101) and 0.230 (0.063, 0.725), respectively, a statistically significant difference (P = 0.001). Among the cases, there was no difference in seroreactivity between children with HPV-11-induced RRP and those with HPV-6-induced RRP (P = 0.31). Since HPV-11 viral particles do bind to the ELISA plate and remain intact and accessible to antibodies, we conclude that children with RRP, like adults with condylomata acuminata, develop antibodies directed at HPV-11 virions.
Antibodies, Viral↗
Detection of human serum antibodies that neutralize infectious human papillomavirus type 11 virions.
A selection of human sera were tested for the presence of antibodies that neutralized infectious human papillomavirus (HPV) type 11. Neutralizing antibodies were detected by prevention of HPV-11-induced condylomatous transformation of human foreskin chips transplanted subrenally into athymic mice. Test sera were obtained from 21 female patients with genital condylomas and eight patients with laryngeal papillomas. Control patients consisted of 57 adult random blood donors and five asymptomatic children. ELISAs demonstrated that all sera from patients with genital papillomas were strongly reactive to disrupted papillomavirus (PV) antigens of HPV-11, bovine PV type 1 and cottontail rabbit PV, but only two were weakly reactive to intact HPV-11. None of the eight sera from the laryngeal papilloma bearers reacted significantly to disrupted PV antigens, but four of the eight showed strong specific responses to intact HPV-11 only. The majority of the sera that were reactive to intact HPV-11 by ELISA neutralized HPV-11 infectivity in the athymic mouse xenograft system. The data indicated that ELISA reactivity to intact HPV-11 virions was a good predictor for the presence of HPV-11 neutralizing antibodies.
Adult↗
Ureteric-anal canal fistula secondary to ureteric calculus.
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Adolescent↗
Human papillomavirus in sinonasal papillomas and squamous cell carcinoma.
The diagnostic and prognostic relevance of human papillomavirus (HPV) types 6, 11, 16, and 18 in squamous papilloma, inverted papilloma, and squamous carcinoma of the sinonasal epithelium was examined using the polymerase chain reaction (PCR) technique. Four (15%) of 26 squamous papillomas, 7 (24%) of 29 inverted papillomas, and 1 (4%) of 24 squamous carcinomas were positive for HPV when examined using the PCR amplification technique. Human papillomavirus 6 was present in 5 specimens (3 squamous and 2 inverted papillomas); HPV-11 was present in 6 specimens (1 squamous and 5 inverted papillomas); and HPV-18 was present in 1 of 24 squamous carcinomas. HPV-16 was not identified in any specimen. The proportion of tissue samples showing HPV presence, and the association of HPV types 6 and 11 with benign lesions and HPV-18 with malignant lesions, are both in accord with findings from prior investigations. Two major questions regarding nasal papilloma are the probability for lesion recurrence after surgical excision and the risk for malignant transformation. There is no unanimity of opinion regarding the prognostic value of histopathologic dysplasia to forecast these outcomes. HPV is etiologically related to a subset of sinonasal papillomas and squamous carcinoma, and those with benign and malignant clinical course are separable on basis of HPV type. Because of the paucity of these nasal lesions, a multi-institutional prospective collaborative study is the ideal way to address these questions.
Carcinoma, Squamous Cell↗
Biology of genital tract human papillomaviruses.
A large number of HPV types infect humans. They infect squamous epithelia of the skin and mucous membranes. Infections are widespread in sexually active populations. Some HPV types have oncogenic potential. Infections with HPV-16, HPV-18, and some additional types are risk factors for cervical cancer. The HPV-6 and HPV-11 types are responsible for most of the genital condylomas and nearly all respiratory papillomas. The immunologic responses to HPVs are not well understood.
Female↗
A morphologic, pathologic, and virologic study of anogenital warts in men.
BACKGROUND AND DESIGN: Infection with human papillomavirus (HPV) in the anogenital region is associated with benign papillomas (condyloma acuminatum), subtle verrucous changes, subclinical infection, and malignant lesions. Although both men and women are affected, much of the investigation has been directed toward women in the study of cervical and vulvar carcinoma. The current investigation focuses on HPV infection in men. This study was undertaken to correlate the clinical spectrum of disease in our population of male patients with histopathologic features, immunoperoxidase staining for viral capsid antigen, and viral typing. Genital lesions from 26 patients were examined and tested prospectively over a 1-year period. RESULTS: The 26 lesions examined demonstrated variable morphologic features with regard to location, size, surface characteristics, and color. Histopathologic features were consistent with the diagnosis of venereal warts, but not necessarily diagnostic. Three of five standard histopathologic criteria were present in only 71% of the specimens. Despite the morphologic variability and the indeterminant histopathologic findings, 20 of 23 lesions positive for the genital tract HPV types tested contained HPV types 6 and/or 11. CONCLUSIONS: We conclude that the morphologic appearance of anogenital warts does not necessarily correlate with HPV type. Histopathologic study is helpful in excluding other diagnoses but may be indeterminant in the diagnosis of venereal warts. All men with anogenital warts should be counseled, treated, and undergo follow-up regardless of HPV type.
Adolescent↗
Human papillomavirus and the pathogenesis of vulvar carcinoma.
The pathogenesis of vulvar and cervical cancer are thought to be similar and to be related to a sexually transmitted agent, which, in recent years, has been demonstrated to be human papillomavirus. These two neoplasms differ dramatically in age distribution and relationship to precursor lesions, making a common etiology unlikely. The apparent discrepancies can be explained by a hypothesis that implicates human papillomavirus as an etiologic factor for the majority of cervical carcinomas but for only a small proportion of vulvar carcinomas. Most vulvar carcinomas occur in older women and are not related to human papillomavirus, whereas a subset of vulvar carcinomas occur in young women and are related to this virus. Characterization of two distinct types of vulvar carcinoma may clarify associated risk factors and may have important implications in the clinical management of this disease.
Adolescent↗
Human papillomaviruses and other biological markers in cervical cancer.
The presence of HPV DNA in the genital tract and the genotype of the infecting HPV are now widely employed as biochemical markers in epidemiological studies of cervical cancer. Additional HPV markers could be utilized in future investigations. The amount of HPV DNA is likely to be higher in case specimens than in control specimens; viral genome would be integrated frequently in cases but almost never in controls; and early region transcripts may be relatively more abundant in cases than in controls. When valid serological markers for past HPV infection become available (very likely, antibodies to HPV capsid proteins), they will be useful to estimate lifetime exposure to HPVs. Serological markers for HPV-associated neoplasia (very likely, antibodies to early proteins) may prove useful for surveillance and have prognostic value. A serological marker capable of detecting past herpes simplex virus 2 infection would permit an analysis of the role of this virus in cervical cancer, either as an independent risk factor or in interaction with HPVs. Other possible biomarkers include activation of oncogenes and inactivation of tumour-suppressor genes, assays for serum micronutrients, and analysis of leukocytes for HLA antigens; these should provide insights into the sequence of events that lead to cervical cancer and help to explain the geographic distribution of the disease.
Biomarkers↗
Possible etiologic heterogeneity of vulvar intraepithelial neoplasia. A correlation of pathologic characteristics with human papillomavirus detection by in situ hybridization and polymerase chain reaction.
A correlated histopathologic and molecular virologic study of 30 cases of vulvar intraepithelial neoplasia Grade 3 (VIN 3) and six associated invasive vulvar carcinomas was performed. Paraffin sections were examined for human papillomavirus (HPV) types 6, 11, 16, and 18 by in situ hybridization for viral transcripts and by polymerase chain reaction (PCR) for amplification of HPV and of the beta-globin gene. Vulvar intraepithelial neoplasia Grade 3 was histologically subclassified into warty (bowenoid) (20 cases) and basaloid (undifferentiated) (ten cases) types. Warty VIN characteristically was composed of squamous cells displaying abnormal proliferation and maturation and an undulating or spiked surface creating a "condylomatous" appearance whereas basaloid VIN had a smooth surface and was composed of undifferentiated basaloid cells resembling carcinoma in situ of the cervix. Human papillomavirus-16 was the only type detected in 16 of 30 VIN 3 and in five of six invasive carcinomas. The HPV-positive women were younger than HPV-negative women (mean age at diagnosis, 49 versus 60 years), their lesions more frequently demonstrated koilocytotic atypia (94% versus 43%), and they were more likely to have warty compared with basaloid VIN lesions (65% versus 30%). These findings suggest that there are at least two different types of VIN which have differing clinical, pathologic, and viral profiles.
Adult↗
Detection of human papillomavirus genotypes in cervical neoplasia from Korean women using polymerase chain reaction.
The histopathologic features of cervical dysplasia (20 cases) and cervical carcinoma (15 cases) in Korean women were correlated with the presence of human papillomaviruses (HPVs) as determined by polymerase chain reaction technology on paraffin-processed specimens. A segment of the E6 open reading frame of several HPV types (HPV 6, 11, 16, 18, 31, 33, and 35) was amplified using primers which were synthesized to contain 50% G + C, in order to give optimum annealing for the amplification of HPVs. All specimens were also tested for amplification of the cellular beta-globin gene. HPV was found in 19 (54%) cases. The HPV types were HPV 6 in 1 case (3%), HPV 16 in 15 cases (43%), HPV 18 in 2 cases (6%), and HPV 33 in 3 cases (9%). HPV was identified in 16 of 25 (64%) beta-globin-positive and 3 of 10 (30%) beta-globin-negative tissues. HPV types 11, 31, and 35 were not detected in any of the specimens. HPV 6, 18, and 33 were detected only in preneoplastic lesions, and co-infection with these three viruses was observed in one case of severe dysplasia. HPV type 16 was found in 8 (40%) premalignant lesions and in 7 (47%) invasive carcinomas. These data indicate that HPVs are found along the entire spectrum of cervical neoplasia. HPV 16 was the predominant virus in invasive cancer of the cervix.
Adult↗
HPV-16 viral transcripts in vulvar neoplasia: preliminary studies.
Specific human papillomavirus (HPV) types are strongly associated with intraepithelial neoplasia and invasive cancer of the cervix. In contrast, the role of HPVs in the pathogenesis of invasive carcinoma of the vulva is poorly understood. We have employed in situ hybridization for the detection of subgenomic transcripts in four vulvar specimens to elucidate the role of HPV type 16 in the development and progression of vulvar cancer. These analyses revealed that the transcripts of the E6-E7 region were more abundant than those of the L1-L2 region in vulvar neoplastic tissues. The transcripts from early and late region of HPV-16 continued to increase with the differentiation of the epithelial cells in both the warty and the basaloid types of vulvar precancerous lesions. This pattern persisted in invasive warty carcinoma but not in basaloid invasive carcinoma; the transcripts in basaloid carcinoma were distributed in an even and discrete pattern. In contrast to earlier studies, L1-L2-region transcripts, as well as viral capsid protein, were detected in focal areas of well-differentiated cells of invasive warty carcinoma. These findings suggest that expression of HPV-16 is regulated by the degree of cellular differentiation.
Carcinoma↗
Probable nonpapillomavirus etiology of squamous cell carcinoma of the vulva in older women: a clinicopathologic study using in situ hybridization and polymerase chain reaction.
A clinical, pathologic, and molecular virologic analysis of 30 cases of invasive squamous cell carcinoma of the vulva was undertaken to investigate the relationship of human papillomavirus (HPV) to this neoplasm. The presence of the virus was detected by the polymerase chain reaction and localized in the tumor and in the adjacent epithelium by in situ hybridization of paraffin sections of vulvectomy specimens. Specimens were examined for nucleic acid sequences of HPVs 6, 11, 16, and 18 were detected by in situ hybridization utilizing 35S-labeled antisense RNA probes and by polymerase chain reaction using HPV type-specific primers for a segment of the E6 gene followed by Southern hybridization of the amplified products. The cases were classified as typical squamous cell carcinoma, basaloid carcinoma, and warty carcinoma. Typical squamous cell carcinoma shows varying degrees of squamous maturation, whereas basaloid carcinoma is characterized by immature basal-type cells showing minimal or no squamous maturation. Warty carcinoma displays an exophytic condylomatous appearance. The squamous cells of this tumor are mature, and many show koilocytotic atypia characterized by a variable degree of nuclear atypia and cytoplasmic vacuolization. The adjacent epithelium was classified as squamous hyperplasia, lichen sclerosus, or vulvar intraepithelial neoplasia (VIN). VIN was subdivided into basaloid or warty VIN using similar criteria as for the invasive carcinomas. Overall, HPV 16 was detected in 11 cases and HPV 18 in two; none of the cases were positive for HPVs 6/11. HPV was detected in four (21%) of 19 squamous cell carcinomas, six (75%) of eight basaloid carcinomas, and three (100%) of three warty carcinomas. The adjacent epithelial lesions also showed a close correlation with the tumor type and presence of HPV. Fourteen (74%) squamous cell carcinomas had adjacent squamous hyperplasia; all of these squamous hyperplasias were negative for HPV. In contrast, seven (87%) of the basaloid carcinomas had adjacent basaloid-VIN and HPV 16 was detected within the VIN in three. Three warty carcinomas (100%) had adjacent warty VIN or basaloid VIN, and HPV was detected within VIN in two. The mean age of women with squamous cell carcinoma was 77 years, for women with basaloid carcinoma 54 years, and for those with warty carcinoma 47 years. The mean age of women with HPV-negative tumors was 77 years compared with 55 years for women with HPV-positive tumors (p less than 0.01). Thus, there appears to be a close correlation between the presence of HPV, specific subsets of invasive carcinoma and VIN, and age.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Detection of transcripts of human papillomaviruses 16 and 18 in cancer-derived cell lines and cervical biopsies by enzyme immunoassay for DNA-RNA hybrids following solution hybridization.
mRNAs of human papillomaviruses (HPV) 16 and 18 were detected in cancer-derived cell lines and genital tract biopsy specimens by a novel hybridization assay. Biotinylated whole genomic HPV DNA probes were hybridized in solution to extracted total nucleic acids. Hybrids between the labeled probes and RNA transcripts were captured on a microplate coated with an antibiotin antibody. Bound hybrids were incubated with a beta-galactosidase-labeled monoclonal antibody to DNA-RNA hybrids and measured by the addition of a fluorogenic substrate. HPV 18 and HPV 16 mRNAs were detected in nucleic acids from 2.3 x 10(3) HeLa cells and 10(4) SiHa cells, respectively. The specificity of the assay for mRNA was demonstrated by the low reactivity of nucleic acids from SiHa cells after treatment with T1 RNase and by the selective reactivity of cellular nucleic acids which bound to an oligo(dT) column. With HPV 16 subgenomic probes, E6-E7 transcripts but not L1-L2 transcripts were detected in SiHa cells. Tests of 58 biopsy specimens from 31 patients showed that the detection of HPV 16 and HPV 18 transcripts in tissue specimens was feasible. Analysis of biopsy specimens with subgenomic probes revealed HPV 16 E6-E7 transcripts in all specimens that reacted with the whole genomic probe, while L1-L2 transcripts were found infrequently.
Cervix Uteri↗
Identification of human papillomaviruses in paraffin embedded cervical pathological tissues from Indian women by polymerase chain reaction.
The polymerase chain reaction (PCR) technology was used to identify human papillomaviruses (HPV) in 52 paraffin embedded cervical tissues from Indian women with chronic cervicitis, different grades of cervical dysplasia and invasive cervical carcinoma. The tissues were screened for amplification of the cellular beta-globin gene as well as of HPVs. Sets of primers designed to amplify a portion of the E6 gene of HPV 6, 11, 16, 18, 31, 33 and 35 were employed. HPV 6, 16 and 31 were identified in 58% of 33 beta-globin positive tissues as compared to 16% of 19 beta-globin negative tissues. HPV 11, 18, 33 and 35 were not identified in any of the specimens. Double infection of HPV 16 and 31 was observed in one case of carcinoma in situ and one case of invasive carcinoma. HPV-16 was the predominant virus in HPV positive cases of higher grades of cervical dysplasia (severe dysplasia and carcinoma in situ) and cervical cancer.
Carcinoma↗
Variability in beta-globin and HPV DNA amplification by PCR from fixed tissues.
Paraffin-embedded tissues from a variety of sources and treated with different fixatives were tested for beta-globin and HPV amplification by polymerase chain reaction (PCR). In tests of tissues collected in the previous 2 to 3 yr, excellent rates (87% to 93%) for beta-globin amplification were obtained for specimens fixed in buffered formalin, Bouin's, and Hartmann's solutions. In contrast, the rate of beta-globin amplification was low for tissues fixed in Hollande's solution (7%) and in Hartmann's solution with eosin (33%). The results of beta-globin amplification from archival tissues stored for variable time periods showed no decrease in the amplification rate with longer periods of storage. Human papillomaviruses (HPVs) were identified in 17% of globin negative and in 43% of globin positive tissues. HPV-16 amplification was more efficient when the targeted DNA sequence was small. Variability in amplification depends not only on the type of fixative used, but also on other ill-defined factors. Therefore, conditions for optimal amplification should be determined before undertaking studies of archival material.
Blotting, Southern↗