Herpesvirus-like DNA sequences detected in endemic, classic, iatrogenic and epidemic Kaposi's sarcoma (KS) biopsies

Buonaguro, Franco M.; Tornesello, Maria Lina; Beth‐Giraldo, Elke; Hatzakis, A; Müeller, Nancy; Downing, Robert; Biryamwaho, Bennon; Sempala, Silvester D. R.; Giraldo, Gaetano

doi:10.1002/(sici)1097-0215(19960103)65:1<25::aid-ijc5>3.0.co;2-3

Cited by 120 publications

(57 citation statements)

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“…All DNA samples were evaluated for nucleic acid degradation by PCR amplification with specific oligoprimers targeting a fragment of the exon 7 within the TP53 gene, 46 and for DNA quantity by spectrophotometric measurements. These tests provided 43 samples out of 45 (95.5%) suitable for subsequent amplifications.…”

Section: Pcr Amplificationsmentioning

confidence: 99%

Human papillomavirus genotypes and HPV16 variants in penile carcinoma

Tornesello

Duraturo

Losito

et al. 2007

Intl Journal of Cancer

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The causative role of human papillomaviruses (HPV) and HPV16 variants has been extensively studied in uterine cervix dysplastic lesions and invasive carcinoma; few such studies, however, have been performed in penile tumors. We have investigated HPV genotype and HPV16 variant distribution on 41 penile cancer biopsies from Italian patients. Cases were extracted from the respective pathology departments databases of National Cancer Institutes in Naples and Milan. HPV sequences were detected by PCR and characterized by direct sequence analysis. Infections with certain types of human papillomaviruses (HPV) have been strongly and consistently associated with the development of cervical intraepithelial neoplasia (CIN) and cervical cancer worldwide. 1-5 The more than 40 HPV genotypes infecting the genital mucosa can be divided into 3 groups: 'high-riskÕ or 'carcinogenicÕ types (16,18,31,33,35,39,45,51,52,56, 58, 59) associated with a high relative risk of cervical cancer; 'low riskÕ viruses (6,11,40,42,43,44,54, 61, 70, 72, 81, 89) associated with benign epithelial proliferations in the genital area, but not associated with invasive cervical cancer; and a group of 6 types (26,53, 66, 68, 73, 82) that is classified as 'probably carcinogenicÕ since there is limited data associating these HPV types with cervical cancer. 6,7 Additionally, carcinogenic HPVs are involved in the development of a subset of other carcinomas arising from mucosal squamous epithelial cells including penile carcinoma. 8 Penile cancer is a relatively rare disease in Europe and United States with incidence rates varying from 0.5 to 1.5 per 100,000 men. In other parts of the world and particularly in developing countries, however, it is a common male cancer with an incidence of 2 to 5 per 100,000 men, constituting for example, 12-22% of all male cancers in countries like Brazil, Uganda and Puerto Rico, which are also communities with high rates of cervical neoplasia. 9 Epidemiological studies have indicated that HPVs are sexually transmitted pathogens infecting the male and female squamous epithelium of the anogenital tract with similar prevalence rates (28%) in symptom-less university students. 10 Moreover, sub-clinical penile lesions (flat penile lesions) are frequently found in male sexual partners of women with CIN, with HPV infection rates of 73% and genotype concordance of 36% within the couples. 11 The prevalence of HPV-related high-grade penile intraepithelial neoplasia, however, is very low suggesting that penile tissue is less prone to maintain persistent infection and to undergo neoplastic transformation. As for the cervical cancer pathogenesis, several additional risk factors have been reported, in conjunction with HPV infection, for the development of invasive penile cancer: (i) exogenous cofactors (lack of circumcision in childhood, phimosis, smoking, trauma), 12,13 (ii) host cofactors (genetic factors, immune response) 14,15 and (iii) viral cofactors (infection by specific types, viral load, viral integration status).The frequency of ...

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Section: Pcr Amplificationsmentioning

confidence: 99%

Human papillomavirus genotypes and HPV16 variants in penile carcinoma

Tornesello

Duraturo

Losito

et al. 2007

Intl Journal of Cancer

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“…Viral DNA sequences can be detected in classical and endemic forms of KS, as well as transplant-related and AIDS-associated KS Dupin et al, 1995;Huang et al, 1995;Memar et al, 1995;Moore and Chang, 1995;Rady et al, 1995;Buonaguro et al, 1996;Kedda et al, 1996;Alkan et al, 1997). There is a strong association between the presence of the virus and the development of KS.…”

Section: Association Of Hhv-8 With Ksmentioning

confidence: 99%

The role of Kaposi's sarcoma-associated herpesvirus/human herpesvirus-8 regulator of transcription activation (RTA) in control of gene expression

2003

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The mechanisms that control the replication state, latency versus lytic, of human herpesviruses have been under intense investigations. Here we summarize some of the recent findings that help define such mechanisms for Kaposi's sarcoma-associated herpesvirus/human herpesvirus type 8 (KSHV/HHV-8). For HHV-8, the viral regulator of transcription activation (RTA) is a key mediator of the switch from latency to lytic gene expression in infected cells. RTA is necessary and sufficient to drive HHV-8 lytic replication and the production of viral progeny. The RTA is an immediateearly gene product, it is the initial activator of expression of a multitude of viral and cellular genes that have been implicated in the replication of HHV-8 and pathogenesis of KS. Interactions of RTA with a number of viral promoters, and with a number of transcription factors or transcriptional co-activators are highlighted. Modulation of transactivation, through alternate RTA-protein, or RTA-promoter interactions, is hypothesisized to participate in the selective tissue tropism and differential pathogenesis observed in KS.

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“…Kaposi's sarcoma (KS) is a multifocal vascular neoplasm (Ziegler et al, 1988), but the nature of the proliferating cells, and whether the lesions represent an exuberant hyperplasia or a true malignancy are still disputed (Buonaguro et al, 1995). The association with HHV8 infection in all forms of the disease (Babal and Pect, 2003) is consistent with a common pathologic process, but certain clinical-epidemiological aspects differentiate the course, the prognosis, and treatment of each form.…”

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confidence: 99%