No abstract

The aim of this study was to assess trends in the age-specific incidence of vulvar cancer in 13 high-income countries satisfying a priori conditions regarding the availability of cancer registry data over a 20-year period; these were Canada, the United States, nine European countries, Australia and Japan. Five-yearly incidence and population at risk were obtained from the International Agency for Research on Cancer's Cancer Incidence in Five Continents for the years 1988-1992 (Volume 7) to 2003-2007 (Volume 10). The 5-yearly average percent change (AvPC) over the period and standardised rate ratios (SRRs) for 2003-2007 versus 1988-1992 were used to assess changes in the age-standardised incidence rates of vulvar cancer for all ages, and for <60 years and 60+ years. During the study period, the 5-yearly AvPC across the 13 countries increased by 4.6% (p = 0.005) in women of all ages, and 11.6% (p = 0.02) in those <60 years. No change was observed in women aged 60+ years (5-yearly AvPC = 0.1%, p = 0.94). The SRR for 2003-2007 versus 1988-1992 was significantly elevated in women <60 years of age (SRR = 1.38, 95% CI: 1.30-1.46), but not in women of 60+ years (SRR = 1.01, 95% CI: 0.97-1.05). The increase in incidence in women <60 years of age drove a significant increase in the overall SRR in women of all ages (SRR = 1.14, 95% CI: 1.11-1.18). Some differences in the specific findings at the individual country level were observed. The findings are consistent with changing sexual behaviours and increasing levels of exposure to human papillomavirus (HPV) in cohorts born around/after about 1950, but younger cohorts offered HPV vaccination are likely to receive some protection against developing vulvar cancer in the future.

Since the early 1980s, vulvar cancer incidence has increased by more than 80% in women younger than 60 years in Australia, but there has been no increased incidence in older women. These findings are consistent with the possibility of increased exposure to the human papillomavirus in cohorts born after 1950. By contrast, age-standardized vulvar cancer mortality rates have been stable in younger women, but have declined in older women.

Findings from this study indicated that the majority of women experienced little to no long-term disruption to sexuality and body image following conservative treatment for early-stage vulvar cancer. Intimacy and relationship status were more closely linked to women's sexual satisfaction than physical arousal. Factors contributing to women experiencing negative emotions were radical vulvar excision, multiple vulvar procedures and/or the development of lymphoedema.

Objective. To investigate the prognostic significance of HPV status in vulvar squamous cell carcinomas (VSCC) and to determine whether preoperative determination of p16 or p53 status would have clinical relevance. Methods. Patients treated for VSCC at a tertiary hospital in Sydney, Australia, from 2002 to 2014, were retrospectively evaluated (n = 119). Histological specimens were stained for p53 and p16 expression, and HPV status was determined by PCR detection of HPV DNA. Results. HPV DNA was detected in 19%, p16 expression in 53%, and p53 expression in 37% of patients. Kaplan–Meier survival estimates indicated that p16/HPV-positive patients had superior five-year disease-free survival (76% versus 42%, resp., p=0.004) and disease-specific survival (DSS) (89% versus 75% resp., p=0.05) than p53-positive patients. In univariate analysis, nodal metastases (p<0.001), tumor size >4 cm (p=0.03), and perineural invasion (p=0.05) were associated with an increased risk of disease progression and p16 expression with a decreased risk (p=0.03). In multivariable analysis, only nodal metastases remained independent for risk of disease progression (p=0.01). For DSS, lymph node metastases (p<0.001) and tumor size (p=0.008) remained independently prognostic. Conclusion. The p16/HPV and p53 status of VSCC allows separation of patients into two distinct clinicopathological groups, although 10% of patients fall into a third group which is HPV, p16, and p53 negative. p16 status was not independently prognostic in multivariable analysis. Treatment decisions should continue to be based on clinical indicators rather than p16 or p53 status.