For the American Cancer Society (ACS), the time for primary human papillomavirus (HPV) screening implementation has unequivocally arrived for the United States, but it will require broad knowledge ...mobilization and addressing logistical barriers to engage the public and health providers. The ACS is using its convener role and marshalling its considerable educational and knowledge dissemination resources to advance primary HPV screening in the United States and to share best practices from countries that have done the same through the ACS Primary HPV Screening Initiative.
Summary Background The extent of cross-protection is a key element in the choice of human papillomavirus (HPV) vaccine to use in vaccination programmes. We compared the cross-protective efficacy of ...the bivalent vaccine (HPV 16 and 18; Cervarix, GlaxoSmithKline Biologicals, Rixensart, Belgium) and quadrivalent vaccine (HPV 6, 11, 16, and 18; Gardasil, Merck, Whitehouse Station, NJ, USA) against non-vaccine type HPVs. Methods We searched Medline and Embase databases, conference abstracts, and manufacturers' websites for randomised clinical trials assessing the efficacy of bivalent and quadrivalent vaccines against persistent infections (lasting ≥6 months) and cervical intraepithelial neoplasia (CIN) associated with the non-vaccine type HPVs (types 31, 33, 45, 52, and 58). We included studies of participants who were HPV DNA negative before vaccination for all HPV types assessed. We assessed heterogeneity in vaccine efficacy estimates between trials with I2 and χ2 statistics. Findings We identified two clinical trials (Females United to Unilaterally Reduce Endo/Ectocervical Disease FUTURE I and II) of the quadrivalent vaccine and three (Papilloma Trial Against Cancer In Young Adults PATRICIA, HPV007, and HPV-023) of the bivalent vaccine. Analysis of the most comparable populations (pooled FUTURE I/II data vs PATRICIA) suggested that cross-protective vaccine efficacy estimates against infections and lesions associated with HPV 31, 33, and 45 were usually higher for the bivalent vaccine than the quadrivalent vaccine. Vaccine efficacy in the bivalent trial was higher than it was in the quadrivalent trial against persistent infections with HPV 31 (77·1% 95% CI 67·2 to 84·4 for bivalent vaccine vs 46·2% 15·3 to 66·4 for quadrivalent vaccine; p=0·003) and HPV 45 (79·0% 61·3 to 89·4 vs 7·8% –67·0 to 49·3; p=0·0003), and against CIN grade 2 or worse associated with HPV 33 (82·3% 53·4 to 94·7 vs 24·0% –71·2 to 67·2; p=0·02) and HPV 45 (100% 41·7 to 100 vs −51·9% –1717·8 to 82·6; p=0·04). We noted substantial heterogeneity between vaccine efficacy in bivalent trials against persistent infections with HPV 31 ( I2 =69%, p=0·04) and HPV 45 ( I2 =70%, p=0·04), with apparent reductions in cross-protective efficacy with increased follow-up. Interpretation The bivalent vaccine seems more efficacious against non-vaccine HPV types 31, 33, and 45 than the quadrivalent vaccine, but the differences were not all significant and might be attributable to differences in trial design. Efficacy against persistent infections with types 31 and 45 seemed to decrease in bivalent trials with increased follow-up, suggesting a waning of cross-protection; more data are needed to establish duration of cross-protection. Funding Public Health Agency of Canada.
Clinical and subclinical human papillomavirus (HPV) infections are the most common sexually transmitted infections in the world, and most sexually-active individuals are likely to be exposed to HPV ...infection during their lifetimes. More than 40 genotypes of HPV infect the epithelial lining of the anogenital tract and other mucosal areas of the body; of these, 13–18 types are considered to be high-oncogenic risk HPV types (HR-HPV). Persistent infection with HR-HPVs is now unequivocally established as a necessary cause of cervical cancer and is likely to be responsible for a substantial proportion of other anogenital neoplasms and upper aero-digestive tract cancers. Low oncogenic risk HPV types (LR-HPV) are also responsible for considerable morbidity as the cause of genital warts. Youth and certain sexual characteristics are key risk factors for HPV acquisition and persistence of HPV infection, but other mediating factors include smoking, oral contraceptive (OC) use, other STIs (e.g. chlamydia, herpes simplex virus), chronic inflammation, immunosuppressive conditions including HIV infection, parity, dietary factors, and polymorphisms in the human leukocyte antigen system. Not surprisingly, these factors are also established or candidate cofactors identified in epidemiologic studies of cervical cancer. HPV transmissibility and molecular events in HPV-induced carcinogenesis have been the focus of recent multidisciplinary epidemiologic studies. This shift in research focus coincides with a shift in cancer prevention techniques towards immunization with HPV vaccines and HPV testing of precancerous lesions.
As a cancer epidemiologist focused on the science of cervical cancer prevention and control, the author journeyed to the home of his hero, Georgios Nikolaou Papanikolaou, whose pioneering ...contribution of the cervicovaginal cytology test (the Pap test) has saved countless female lives over generations throughout the world, laying the groundwork for one of the most beautiful stories in public health.
Abstract
In their accompanying article, Vänskä et al. (Am J Epidemiol. 2021;190(4):506–514) provide us with cohort lifetime risks of cervical cancer attributable to different types of human ...papillomavirus in Sweden. We argue that a standardized lifetime risk such as those calculated by Vänskä et al. might be a more appropriate public health target for cervical cancer elimination than age-standardized incidence rates. Age standardization to an arbitrary standard age distribution implies an implicit value choice regarding the weight of different age groups for which we find little moral justification. Conversely, a standardized lifetime risk uses standard life expectancy as a weight, corresponding to the likelihood that cervical cancer would impact a woman and prevent her from pursuing opportunities within a standard life span. Based on the data from Vänskä et al., a standardized lifetime risk of 129–250 cervical cancers per 100,000 women born could be an aspirational alternative public health target for cervical cancer elimination as a public health problem, complementary to the World Health Organization’s arbitrary draft target of 4 cervical cancers per 100,000 age-standardized woman-years.
The COVID-19 pandemic has affected cancer care worldwide. This study aimed to estimate the long-term impacts of cancer care disruptions on cancer mortality in Canada using a microsimulation model. ...The model simulates cancer incidence and survival using cancer incidence, stage at diagnosis and survival data from the Canadian Cancer Registry. We modeled reported declines in cancer diagnoses and treatments recorded in provincial administrative datasets in March 2020 to June 2021. Based on the literature, we assumed that diagnostic and treatment delays lead to a 6% higher rate of cancer death per 4-week delay. After June 2021, we assessed scenarios where cancer treatment capacity returned to prepandemic levels, or to 10% higher or lower than prepandemic levels. Results are the median predictions of 10 stochastic simulations. The model predicts that cancer care disruptions during the COVID-19 pandemic could lead to 21 247 (2.0%) more cancer deaths in Canada in 2020 to 2030, assuming treatment capacity is recovered to 2019 prepandemic levels in 2021. This represents 355 172 life years lost expected due to pandemic-related diagnostic and treatment delays. The largest number of expected excess cancer deaths was predicted for breast, lung and colorectal cancers, and in the provinces of Ontario, Québec and British Columbia. Diagnostic and treatment capacity in 2021 onward highly influenced the number of cancer deaths over the next decade. Cancer care disruptions during the COVID-19 pandemic could lead to significant life loss; however, most of these could be mitigated by increasing diagnostic and treatment capacity in the short-term to address the service backlog.
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