Human Papillomavirus-16 Is the Predominant Type Etiologically Involved in Penile Squamous Cell Carcinoma

Heideman, Daniëlle A.M.; Waterboer, Tim; Pawlita, Michael; Diemen, Pien Delis-van; Nindl, Ingo; Leijte, Joost A.P.; Bonfrèr, Johannes M.G.; Horenblas, Simon; Meijer, Chris J.L.M.; Snijders, Peter J.F.

doi:10.1200/jco.2007.12.3182

Cited by 148 publications

(121 citation statements)

References 30 publications

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“…HPV has been associated with 50%-70% of cases of squamous penile cancer across multiple series, but these studies amalgamate early, and patients with late-stage PSCC who likely have distinct clinicopathologic features and biology [9][10][11][12][13][14]. Broader molecular studies of penile carcinoma have been performed in a limited series of patients, but interpretation is again confounded by heterogeneity of the stage of disease and diagnostic methodologies used [15,16].…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Genomic Profiling of Advanced Penile Carcinoma Suggests a High Frequency of Clinically Relevant Genomic Alterations

Ali¹,

Pal

Wang³

et al. 2015

The Oncologist

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Background. Advanced penile squamous cell carcinoma (PSCC) is associated with poor survival due to the aggressiveness of the disease and lack of effective systemic therapies. Comprehensive genomic profiling (CGP) was performed to identify clinically relevant genomic alterations (CRGAs). Materials and Methods. DNA was extracted from 40 mm of formalin-fixed, paraffin-embedded sections in patients with advanced PSCC. CGP was performed on hybridizationcaptured, adaptor ligation-based libraries to a mean coverage depth of 6923 for 3,769 exons of 236 cancerrelated genes plus 47 introns from 19 genes frequently rearranged in cancer. CRGAs were defined as genomic alterations (GAs) linked to targeted therapies on the market or under evaluation in mechanism-driven clinical trials.

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Section: Introductionmentioning

confidence: 99%

Comprehensive Genomic Profiling of Advanced Penile Carcinoma Suggests a High Frequency of Clinically Relevant Genomic Alterations

Ali¹,

Pal

Wang³

et al. 2015

The Oncologist

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confidence: 99%

“…Cancers of the anus, vulva and vagina occur more frequently than expected following cervical intraepithelial neoplasia III or invasive cervical cancer, suggesting a strong common aetiological factor (Evans et al, 2003). HPV infection may also play a role in a subset of penile squamous cell carcinomas (Iwasawa et al, 1993;Rubin et al, 2001; Daling et al, 2005;Heideman et al, 2007;Tornesello et al, 2008).Increasing trends in anal cancer have been reported, possibly due to changes in sexual practices (Daling et al, 1987;Scholefield et al, 1990;Frisch et al, 1993Frisch et al, , 1997. If this were the case, a strong generational effect would be expected in the incidence trends of anogenital cancers.…”

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confidence: 99%

An analysis of temporal and generational trends in the incidence of anal and other HPV-related cancers in Southeast England

2009

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Patients diagnosed in 1960 -2004 with cancer of the cervix, anus, vulva, vagina or penis were identified from the Thames Cancer Registry database, and age-standardised period (temporal) incidence rates calculated by direct standardisation. Age-cohort modelling techniques were used to estimate age-specific incidence rates in the earlier and later cohorts, enabling the calculation of agestandardised cohort (generational) rates. Incidence of anal cancer increased for both men and women over the period studied, mainly in those born from 1940 onwards. Similar generational patterns were seen for cancers of the vulva and vagina, but those for penile cancer were different. For cervix cancer, the steep downward trend in cohort rates due to screening levelled off in women born from 1940 onwards. Our findings are compatible with the hypothesis that changes in sexual practices were a major contributor to the increases of these cancers. Programmes of vaccination against HPV, aimed at reducing the burden of cervical cancer, may also help to reduce the incidence of cancer at other anogenital sites. (Daling and Sherman, 1992;Frisch et al, 1997;Daling et al, 2004; Bjørge et al, 2002), vulva and vagina (Madeleine et al, 1997; Daling et al, 2002;Goffin et al, 2006;Madsen et al, 2008). Cancers of the anus, vulva and vagina occur more frequently than expected following cervical intraepithelial neoplasia III or invasive cervical cancer, suggesting a strong common aetiological factor (Evans et al, 2003). HPV infection may also play a role in a subset of penile squamous cell carcinomas (Iwasawa et al, 1993;Rubin et al, 2001; Daling et al, 2005;Heideman et al, 2007;Tornesello et al, 2008).Increasing trends in anal cancer have been reported, possibly due to changes in sexual practices (Daling et al, 1987;Scholefield et al, 1990;Frisch et al, 1993Frisch et al, , 1997. If this were the case, a strong generational effect would be expected in the incidence trends of anogenital cancers. We have explored this hypothesis by plotting age-standardised period (temporal) and cohort (generational) rates for cancer sites linked to HPV infection. (World Health Organization, 1976), and were retrospectively recoded to the ICD-10 classification in the case of tumours diagnosed before its introduction in the early 1990s. Examination of proportional frequency plots revealed no coding discrepancies or inconsistencies over the period of the study. Age at diagnosis was categorised into 5-year groups (0 -4, 5-9, y, 80 -84, 85 þ ), and period of diagnosis into 5-year periods (1960 -1964, 1965 -1969, y, 2000 -2004). Nominal birth cohort groups (1875, 1880, y, 2000) were then calculated by subtracting the midpoint of the age group from the midpoint of the period. For each site, an age-standardised incidence rate for each calendar period was calculated by direct standardisation, using the European standard population. As the earlier and later birth cohorts were missing data from the younger and older age groups, respectively, a Poisson regression age-cohort m...

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“…30 This system allows the typing of both high-risk HPV (types 16,18,26,30,31,33,35,39,45, 51, 52, 56, 58, 59, 66, 68, 70,73, 82i and 82m) and low-risk HPV (6,11,34,40,42,43,44,54,55,57,61,64,71,72,81 and CP6108).…”

Section: Hpv Dna Detection and Typingmentioning

confidence: 99%

“…However, occasionally low-risk HPV types have been detected in malignant lesions, such as penile carcinomas. [16][17][18] Infection with high-risk HPV has been associated with malignant transformation, and causally related to cervical cancer 19,20 and a subset of squamous cell carcinomas in the head and neck and anogenital region different from the cervix. [21][22][23] Verrucous carcinoma has been associated with both low-risk (types 6 and 11) and high-risk (types 16 and 18) types of HPV.…”

mentioning

confidence: 99%

Comprehensive analysis of human papillomavirus prevalence and the potential role of low-risk types in verrucous carcinoma

et al. 2012

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The role of human papillomavirus (HPV) infections in the development of verrucous carcinoma, a welldifferentiated variant of squamous cell carcinoma with difficult differential diagnosis, is controversial in the literature. In this study, we analysed verrucous carcinoma from different origins for the presence and activity of a broad spectrum of HPV types, and carefully reviewed the histopathological features. A random series of 27 formalin-fixed, paraffin-embedded specimens of verrucous carcinoma was taken, representing the head and neck region (n ¼ 6), anogenital area (n ¼ 16) and extragenital skin region (n ¼ 5). After review of the histological slides, all samples were subjected to different polymerase chain reaction-based HPV detection techniques, together detecting a total of 83 HPV types, including both mucosal and cutaneous types. Histological revision was carefully performed. Lesions with keratinised papillae, blunt stromal invaginations and minimal cytological atypia were considered verrucous carcinoma. Condylomatous lesions with viral changes were defined as giant condyloma. Verrucous lesions that did not meet those criteria were classified as verrucous hyperplasia. Tumours with stromal infiltration were considered as invasive squamous cell carcinoma. Histological revision revealed that 13 out of 27 cases were verrucous carcinoma (one showing a double infection with HPV 35 and 45), 5 invasive squamous cell carcinomas, 5 verrucous hyperplasia (one with a double infection with HPV 4 and 8), 1 pseudoepitheliomatous hyperplasia and 3 giant condylomas. All three giant condylomas were low-risk HPV positive (HPV 6 and 11) and showed active mRNA transcription. None of the HPV-positive samples tested positive for diffuse p16 INK4A staining. In conclusion, our results do not support a causal role of HPV in the development of verrucous carcinoma. Testing for LR-HPV, particularly HPV 6 and 11, may help in the differential diagnosis of lesions suspicious of verrucous carcinoma as those testing positive for LR-HPV most likely represent giant condylomas.

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Human Papillomavirus-16 Is the Predominant Type Etiologically Involved in Penile Squamous Cell Carcinoma

Cited by 148 publications

References 30 publications

Comprehensive Genomic Profiling of Advanced Penile Carcinoma Suggests a High Frequency of Clinically Relevant Genomic Alterations

Comprehensive Genomic Profiling of Advanced Penile Carcinoma Suggests a High Frequency of Clinically Relevant Genomic Alterations

An analysis of temporal and generational trends in the incidence of anal and other HPV-related cancers in Southeast England

Comprehensive analysis of human papillomavirus prevalence and the potential role of low-risk types in verrucous carcinoma

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