Etiology of Squamous Cell Carcinoma of the Penis

Dillner, Joakim; G, von Krogh; Horenblas, Simon; Cj, Meijer

doi:10.1080/00365590050509913

Cited by 259 publications

(195 citation statements)

References 53 publications

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“…Among discordant sites that showed increased risks among spouses, sexual and smoking habits were the likely reason for the associations found in Table 1. Human papilloma virus (HPV) infection is the main etiological factor for cervical cancer and it is also strongly indicated in penile cancer (Dillner et al, 2000;Zur Hausen, 2000). The SIRs between these two cancers were the highest noted for the whole study, over 1.8.…”

Section: Discussionmentioning

confidence: 94%

Cancer risks among long-standing spouses

Hemminki

Jiang

2002

Br J Cancer

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We estimated risks for concordant and discordant cancers in spouses in order to quantify cancer risks from the shared environment. The study was restricted to spouses who had one or more children in common and who lived together for at least 15 years after the first child's birth. The nation-wide Family-Cancer Database was used as the source of family and cancer data. Standardised incidence ratios were calculated for concordant and discordant cancers in spouses after 50 years of age. Among the 18 cancer sites considered, only three sites, stomach, lung and bladder, showed concordant increases of cancer among spouses, standardised incidence ratios ranging only from 1.19 to 1.38. Additionally, gastric and pancreatic cancer were associated among spouses, as did many cancers which were related to tobacco smoking or human papilloma virus infection. By contrast, standardised incidence ratios of colon, rectal, renal and skin cancers showed no increases among spouses. Shared lifestyle among family members seems to explain only a small proportion of familial cancer susceptibility. Because lifestyles are likely to differ more between parents and offspring than between spouses, familial cancer risks between parents and offspring are even more likely to be due to heritable than environmental effects. (Doll and Peto, 1981; IARC, 1990;Lichtenstein et al, 2000;Peto, 2001). During the past decade it has become increasingly clear that overweight and lack of physical activity convey a risk of cancer, which may account for 5% of all cancers in Europe (Bergstrom et al, 2001; IARC, 2002). Moreover, the risks at the population level caused by various infections have become better understood, and the known infections have been estimated to account for 15% of cancer worldwide, though less in Europe (Pisani et al, 1997;Zur Hausen, 1999). In spite of the enormous research effort on diet and cancer, the proportion of cancer attributable to diet or to any specific dietary component remains speculative. It has been estimated that at least 50%, and probably as much as 70% of cancer deaths are unavoidable among non-smokers mainly because their aetiology remains unknown (Peto, 2001).Decades long cohabitation by spouses should tend to result in many habits and carcinogenic exposures being similar. Interest in disease among spouses earlier focused on sexually transmitted diseases and the effects of passive smoking (IARC, 1995;Hackshaw, 1998;Hemminki et al, 2000a;Hemminki and Dong, 2000a). Besides assessing life-style factors and cancer risks, they can point to the environmental contribution to the familial aggregation of cancer, and they thus help to apportion heritable effects (Hemminki et al, 2001a,d). The studies from the Swedish Family-Cancer Database have shown limited spouse concordance, affecting mainly the sites of known environmental carcinogens (Hemminki and Dong, 2000b;Hemminki et al, 2001a). However, in the previous studies the length of cohabitation between the spouses was not considered, nor were any adjustments for socio-economi...

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Section: Discussionmentioning

confidence: 94%

Cancer risks among long-standing spouses

Hemminki

Jiang

2002

Br J Cancer

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“…Only a few studies are reported on penile cancer and the role of HPV; a review is given by Griffiths and Mellon (1999) and later by Dillner et al (2000). The prevalence of subclinical or latent penile HPV infections among young, sexually active and healthy individuals is reported between 20 and 50%, while the incidence of penile carcinoma is relatively low (Van Doornum et al, 1994;Wikström et al, 2000).…”

Section: Penile Carcinomamentioning

confidence: 99%

“…Presence of HPV DNA in carcinomas of the penis is observed in a proportion of the specimens analysed (Grussendorf-Cronen, 1997;Tornesello et al, 1997;Dianzani et al, 1998;Levi et al, 1998;Poblet et al, 1999;Dillner et al, 2000;Rubin et al, 2001). Some serological studies relative to HPV infection in individuals with penile carcinoma were carried out in relatively small groups of patients (Wideroff et al, 1996b;Strickler et al, 1998;Carter et al, 2001).…”

mentioning

confidence: 99%

Reactivity to human papillomavirus type 16 L1 virus-like particles in sera from patients with genital cancer and patients with carcinomas at five different extragenital sites

et al. 2003

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A retrospective seroepidemiologic study was performed to examine the association between human papillomaviruses (HPV) 16 infection and carcinomas of the oropharynx, the oesophagus, penis and vagina. Sera were selected from the serum bank from the Antoni van Leeuwenhoek Hospital (Netherlands Cancer Institute) and the Slotervaart Hospital in Amsterdam, the Netherlands. Presence of HPV 16 specific antibody was assessed using HPV 16 L1 capsids. Sera positive for HPV 16 capsid antibody were further tested for antibody against HPV 16 E7 peptides. Prevalence of antibody against HPV 16 L1 capsids among both the negative control group without cancer and the negative control group with gastric cancer was 18%, while seroprevalence among the control group of patients with HPV-associated cervical squamous cell carcinoma was 47% (Po0.001). Among the patients with penile squamous cell carcinoma seroprevalence was 38% (Po0.001), among patients with oropharyngeal carcinoma 33% (P ¼ 0.04) and among patients with oesophageal squamous cell carcinoma 14% (P ¼ 0.7). The serological evidence for association between HPV 16 infection and both oropharyngeal carcinoma and penile carcinoma was established. The conclusion that no association was found between the presence of antibody against HPV 16 L1 capsids and oesophageal squamous cell carcinoma was in accordance with results of other studies carried out in the Netherlands using HPV DNA technology. In the subjects with HPV 16 L1 capsid antibody, no association was found between the antibody against HPV 16 E7 and clinical outcome.

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“…Males deserve access to a vaccine that can prevent the majority of cases of genital warts, especially considering that males often suffer longer duration of genital warts and incur greater treatment costs than females [49]. Furthermore, HPV is responsible for a wide range of cancers including 70-100 percent of penile intraepithelial neoplasia and 40-50 percent of all invasive penile cancers [50]. In recognition of these factors, the FDA approved Gardasil for the prevention of genital warts [51], anal cancer, and associated precancerous lesions in males in 2010 [36], The prophylactic prevention of HPV infection is clearly warranted regardless of sex, and the vaccination of males is regarded as a costeffective approach to reduce rates of HPV infection [52].…”

Section: Maximizing Vaccine Efficacymentioning

confidence: 99%