Population-wide human papillomavirus vaccination has transformed the epidemiology of cervical cancer and accelerated the interest in risk-adapted screening approaches that tailor screening intervals, methods, and triage pathways to an individual's vaccination status and underlying risk. Although modeling studies suggest that vaccinated cohorts may require fewer lifetime screenings and later screening initiation, implementation science provides frameworks, methods, and strategies to guide the translation of these approaches into practice. However, real-world implementation is complex and constrained by incomplete linkages with immunization records, evolving evidence on cross-protection, and persistent inequities in screening participation. By focusing on multilevel contextual determinants that span patients, clinicians, organizations, and policy environments, implementation science can guide the design, testing, and optimization of strategies such as clinical decision support tools, tailored communication, and clinical workflow redesign that are required to translate emerging evidence into practice. We highlight examples from pragmatic and hybrid effectiveness-implementation trials demonstrating how approaches such as self-sampling, participatory co-design, peer advocacy models, and multicomponent strategies improve screening reach, acceptability, and fidelity. As risk-adapted screening becomes the next frontier in cervical cancer prevention, embedding implementation science early can prevent future translational bottlenecks, support equity, and ensure that health systems are prepared to adopt and sustain evidence-based recommendations once epidemiological data mature while guiding a research agenda for implementation of risk-adapted screening worldwide.

As vaccination coverage expands, the epidemiology of human papillomavirus (HPV) infection and related disease is shifting. The declining prevalence of infections by the most high-risk HPV types, for example, HPV16 and HPV18, reduces the positive predictive value of screening tests for cervical precancer and cancer and challenges the balance between benefits and harms of current standard-of-care screening intervals. This evolving context raises an important policy question: Can and should cervical cancer screening eventually be reduced or even stopped in fully HPV-vaccinated populations?

The substantial changes of human papillomavirus (HPV) type distribution and reductions of cervical precancer and cancer incidence in vaccinated populations, which are entering screening programs now, require reassessment of screening and triage approaches to maintain the balance of benefits and harms of cervical cancer screening. The reduction of precancer and cancer in vaccinated populations affects the risk indicated by most screening and triage tests. Among HPV-positive women, the type distribution changes in vaccinated women to less carcinogenic types that are less likely to progress to precancer, and that cause precancers that are less likely to invade. Conversely, HPV vaccines do not affect the natural history of existing HPV infections. Although infections with vaccine-targeted types are rare in vaccinated populations, their risk of precancer and cancer is not reduced. Host biomarkers that are more closely linked to the carcinogenic process are more likely to perform well in vaccinated individuals compared with biomarkers that mostly reflect HPV infections. We summarize data on HPV screening and triage tests, including cytology, dual stain, and methylation tests, either directly evaluated in vaccinated populations or in HPV genotype strata to estimate their performance in vaccinated populations. Combinations of limited or extended genotyping HPV tests with triage biomarkers can provide meaningful risk stratification for both unvaccinated and vaccinated populations.

There is substantial evidence examining effectiveness of human papillomavirus vaccines in populations using registry linkages. These studies initially mapped early outcomes, but in recent years have focused on harder endpoints, confirming that the vaccines have the anticipated effect against infection, lesions, and ultimately invasive cervical cancer. It is generally accepted that when vaccinated cohorts enter screening programs, adjustments to screening strategies are needed to maintain the balance of benefits and harms and achieve optimal resource use. The purpose of this chapter is to examine the practical considerations for implementing tailored screening in the context of increasingly vaccinated populations, with particular emphasis on data sources and their application in routine practice. We present real-world examples of linking vaccination and screening registries to enable screening strategies informed by individual human papillomavirus vaccination status. We also outline the common challenges encountered when establishing such linkages and offer practical suggestions for overcoming them.

As decisions are made worldwide about the best way to adapt cervical screening to cohorts and individuals who have been offered human papillomavirus (HPV) vaccination, we consider the issues this raises for communication. This article reviews the relevant literature on knowledge and awareness of HPV, lessons we can learn from emerging evidence on attitudes to risk-adapted cancer screening, and what the psychological literature tells us about the complex relationships between risk perceptions and behavior. We highlight the need to ensure communication strategies do not create or widen social inequalities. We conclude that there is a strong need for public education about the relationship between HPV, vaccination, screening, and cancer outcomes, an imperative for timely and transparent communication about the rationale for any proposed changes, a need to involve health-care professionals in supporting women to understand the changes, and a strong case for ongoing research and evaluation as changes are implemented.

Screening has been instrumental in reducing the global burden of cervical cancer over the past several decades. However, the landscape of prevention and early detection is rapidly evolving, driven by widespread human papillomavirus (HPV) vaccination, advances in molecular diagnostics, and a growing emphasis on personalized medicine, which collectively call for a reassessment of traditional screening paradigms to align with the new risk landscape. In settings with a high prevalence of cervical precancerous lesions, where cytology and HPV testing yield a substantial proportion of true positives, frequent screening intervals are justified. Conversely, in vaccinated populations where the incidence of precancerous lesions is becoming substantially reduced, screening, irrespective of test modality, produces more false positives, leading to unnecessary diagnostic procedures and their consequent reproductive health risks and psychological distress. In HPV-based screening, reduced positive predictive value (PPV) in vaccinated populations reflects the lower oncogenic potential of nonvaccine HPV types that predominate postvaccination. Although these infections are detectable, they are less likely to progress to high-grade precancer or cancer, thereby lowering PPVs. In cytology-based screening, PPV declines for 2 reasons. First, as vaccine-targeted high-risk infections are eliminated, lower-risk infections account for a greater share of cytologic abnormalities. Second, as true precancerous lesions decline, nonspecific cytologic abnormalities, unrelated to HPV, become more prominent, increasing false positives and further reducing PPV. This commentary, drawing on prior work from our group, examines the complex interplay among disease prevalence, individual risk profiles, test performance, and screening program design and argues for a transition toward risk-based screening strategies that reflect changing epidemiological patterns and align with contemporary public health priorities. It further argues for adaptive, evidence-informed policies that incorporate molecular tools such as HPV genotyping and methylation assays to optimize prevention and early detection in the postvaccination era.

The success of prophylactic human papillomavirus (HPV) vaccination in reducing disease burden came with an epidemiological concern: HPV type replacement, the potential compensatory increase of nonvaccine targeted HPV types following the elimination of HPV16 and 18. Postvaccination surveillance across several countries suggests some signs of increase in the nonvaccine targeted HPV types, which may be explainable because of type replacement. However, should HPV type replacement be occurring, it is unlikely to generate disease replacement because of the significantly lower oncogenic potential of nonvaccine targeted HPV types. The modernization of screening to align with this new risk profile is necessary. Personalized screening protocols based on individual risk profiles informed by primary HPV testing with extended genotyping and future molecular triage to accurately risk-stratify HPV types are necessary in the postvaccination era.

Public engagement has the potential to make research more impactful, and it has increased in recent years in cancer research. Yet, there is limited understanding of how this process of bringing lived experience into research works, and of what leads to tokenistic and non-tokenistic engagement.

To explore public engagement in cancer research in the United States from the perspective of both lived-experience experts and researchers.

A qualitative study consisting of interviews with 15 lived-experience experts engaged in cancer research and 15 cancer researchers. Data were analysed using reflexive thematic analysis.

Findings are captured in four themes shared by both participant groups and mapped onto Jürgen Habermas's theory of communicative action, which helped explain the engagement process. First, public engagement was invaluable to research, but also personally and professionally. Second, underlying foundations and principles underpinned the non-tokenistic engagement process. Third, engagement led to the creation of a partnership between cancer researchers and lived-experience experts. Fourth, engagement was about creating and enriching culture within a research institution and in the community.

The study provided a better understanding of public engagement in cancer research. Habermas's communicative action theory offered an analytical framework to elicit the importance of mutual understanding in developing common ground between lived-experience experts and researchers. It highlighted that tensions between lived-experience experts and researchers, choosing not to act on feedback, and limited institutional support can lead to tokenistic engagement.

Four Community Advisory Board members contributed to this study from design through dissemination. They co-developed topic guides, co-analysed data, co-wrote this paper and are named as co-authors.

Previous studies suggested links between obesity, glucose regulation, and autoimmune diseases, but the associations of weight and glucose levels with myasthenia gravis (MG) remain uncertain. We examined these associations and a potential indirect pathway through glucose levels.

We investigated the associations of weight and glucose levels with MG risk using Mendelian randomization (MR) and a retrospective case-control study.

We conducted two-sample MR analyses using genome-wide association study summary statistics from European populations. The clinical component retrospectively included patients with MG and healthy controls and used propensity-score matching and logistic regression.

The MR analyses suggested associations among genetically predicted weight, glucose levels, and MG risk. They also yielded a small indirect estimate through glucose levels that was opposite in direction to the direct and total effects. This opposing-direction indirect estimate was sensitive to the inferential method and was not observed in the retrospective case-control analysis. In the clinical analysis, MG cases had higher weight and lower glucose levels than controls, and both variables were associated with MG status.

Two-sample MR suggested that genetically predicted higher weight was associated with higher odds of MG, whereas genetically predicted higher glucose levels were associated with lower odds of MG. The retrospective case-control analysis showed directionally similar associations for measured weight and fasting glucose, but the indirect pathway suggested by MR was not observed in the clinical analysis.

Synchronous clear cell renal cell carcinoma (ccRCC) and papillary renal cell carcinoma (pRCC) within the same kidney are uncommon, and distinguishing a true collision tumor from a composite neoplasm with shared clonal origin requires molecular confirmation. We report an 83-year-old woman who underwent radical nephrectomy for an incidentally detected left renal mass. Pathologic examination revealed two well-demarcated adjacent tumors (3.3 cm and 3.2 cm) with characteristic morphologic and immunophenotypic features of ccRCC and pRCC, both staged pT1a. Separate next-generation sequencing analyses demonstrated completely distinct molecular profiles: the pRCC harbored RHEB p.Y35C and TERT promoter mutations with TMB-High status, whereas the ccRCC contained truncating alterations in PBRM1, ARID1A, and TGFBR1. No shared somatic mutations were identified, confirming independent clonal origins and establishing this as a true collision tumor. This case illustrates the value of per-component molecular profiling for histologically discordant renal tumors.