Perceptions and implications for cervical screening and self-collection: A qualitative exploration of never and under-screened Queensland women.

BACKGROUND: Over 70% of cervical cancers are detected in women not currently screening. Queensland Health wanted to better understand the drivers of screening to inform our planning and capitalise on self-collection as an option to reach under-screened women. In 2020 Queensland Health commissioned qualitative research to explore barriers and enablers to cervical screening with never-screened and under-screened women in Queensland (with under-screeners defined as having last screened more than 4 years ago and being more than 2 years overdue). Additionally, the research explored the acceptability of self-collection amongst this cohort. METHODS: A mixed methods qualitative approach of online focus groups and in-depth interviews was employed. Online focus groups were conducted with under-screeners. In-depth telephone interviews were conducted with never-screeners due to the anticipated personal nature of their reasons for not screening. RESULTS: A total of 51 Queensland women aged 30 to 50 years participated in the research. CONCLUSIONS: Queensland women cited several negative experiences and aspects of the current program, as well as barriers in their social and personal lives that limited screening intention and behaviour. Barriers and enablers to cervical screening identified in this research have been classified into four categories: structural, knowledge and attitudinal, social, and personal. The research identified more factors associated with nonparticipation than participation. However, the research did uncover a range of potential enablers to encourage screening, some of which related to the program design. SO WHAT?: The concept of self-collection was broadly well accepted by research participants, particularly by never-screeners. Recommendations resulting from this research include communications, systems, and eligibility changes, particularly regarding the availability and benefits of self-collection.

Temporal and area-level variation in prevalence of high-grade histologically confirmed cervical abnormalities among Indigenous and non-Indigenous women, Queensland, Australia, 2008-2017.

OBJECTIVE: Despite Australia's National Cervical Screening Program, Indigenous women have a disproportionately high burden of cervical cancer. We describe temporal and area-level patterns in prevalence of histologically conformed high-grade cervical abnormalities (hHGA) among cytologically screened women by Indigenous status. METHODS: This was a population-based study of 2,132,925 women, aged 20-69, who underwent cervical screening between 2008 and 2017, in Queensland, Australia. Of these, 47,136 were identified as Indigenous from linked hospital records. Overall patterns in hHGA prevalence by Indigenous status were quantified using prevalence rate ratios (PrRR) from negative binomial models. Bayesian spatial models were used to obtain smoothed prevalence estimates of hHGA across 528 small areas compared to the state average. Results are presented as maps and graphs showing the associated uncertainty of the estimates. RESULTS: Overall, screened Indigenous women had significantly higher hHGA prevalence than non-Indigenous women. However, the magnitude of the difference reduced over time (p < 0.001). Adjusted for age and area-level variables, Indigenous women had 36% higher hHGA prevalence (PrRR 1.36, 95% confidence interval [1.21-1.52]) than non-Indigenous women between 2013 and 2017. The overall effect of age decreased over time (p = 0.021). Although there was evidence of moderate spatial variation in 10-year prevalence estimates for both groups of women, the high levels of uncertainty for many estimates, particularly for Indigenous women, limited our ability to draw definitive conclusions about the spatial patterns. CONCLUSIONS: While the temporal reduction in Indigenous: non-Indigenous differential in hHGA prevalence is encouraging, further research into the key drivers of the continuing higher risk among Indigenous women is warranted.

Spatial and temporal variations in cervical cancer screening participation among indigenous and non-indigenous women, Queensland, Australia, 2008-2017.

BACKGROUND: Cervical cancer incidence and mortality have declined in Australia since the implementation of a national cervical screening program in 1991, however, disparities in both measures between Indigenous and non-Indigenous women remain. We describe spatial and temporal changes in Pap test participation rates by Indigenous status for Queensland (Australia). Analyses were done in the context of renewed screening program in December 2017. METHODS: Population-based study 2,132,925 Queensland female residents, aged 20-69 years who underwent cervical screening from 2008 to December 2017; 47,136 were identified as Indigenous through linkage to hospital records. Bayesian spatial models were used to generate smoothed estimates of participation across 528 small areas during 2008-2012 and 2013-2017 compared to the overall state average (2008-2017). Results are presented as thematic maps and graphs showing the associated uncertainty of the estimates. RESULTS: Overall screening participation decreased over time for both Indigenous and non-Indigenous women. Strong spatial patterns were evident in five-year participation for both groups. Indigenous women had significantly lower participation than the Queensland average for ≥ 88 % of areas during both reporting periods whereas corresponding estimates were lower than average for <30 % of areas among non-Indigenous women. Disparities by Indigenous status persisted over time and remained across broader geographical groups of accessibility and area disadvantage. CONCLUSIONS: Cervical cancer burden in Australia can only be reduced through concentrated efforts on identifying and addressing key drivers of the continuing disparities in screening participation. Achieving equitable screening participation for all women especially Indigenous women requires community engagement and localised interventions.

A conserved distal segment of the mouse CSF-1 receptor promoter is required for maximal expression of a reporter gene in macrophages and osteoclasts of transgenic mice.

Csf1r mRNA in adult mice is expressed in cells of the macrophage lineage, and during development, it is also expressed from a separate promoter in placental trophoblast cells. This mouse trophoblast promoter sequence is conserved across species, but human trophoblasts actually initiate transcription from a separate promoter 20 kb upstream, which is not conserved in rodents. A 7.2-kb fragment of the mouse Csf1r genomic DNA, including the 3.5-kb promoter, the first coding exon and downstream intron, is sufficient to direct reproducible position- and copy number-independent expression of an EGFP reporter in vitro and in vivo. In this study, we have examined the consequence of removal of the 150-bp fragment encompassing the conserved trophoblast promoter region in the context of the 7.2-kb promoter on reporter gene expression in transgenic mice. The deletion ablated expression in the placenta but also abolished expression in multinucleated OCL and reduced expression in macrophages. RT-PCR analyses of Csf1r mRNA revealed that mouse OCL use another promoter within this region, distinct from that used in placental trophoblasts, to generate an alternative 5'UTR.

Expression of Gal4-dependent transgenes in cells of the mononuclear phagocyte system labeled with enhanced cyan fluorescent protein using Csf1r-Gal4VP16/UAS-ECFP double-transgenic mice.

We generated double-transgenic mice carrying cointegrated tissue-specific Gal4 and Gal4 reporter transgenes to direct transgene overexpression in the mononuclear phagocyte system (MPS). A modified promoter of the Csf1r (c-fms) gene, containing a deletion of the trophoblast-specific promoter, was used to drive the expression of Gal4VP16 transcriptional activator specifically in macrophages. This module was cointegrated with a fluorescent reporter, enhanced cyan fluorescent protein (ECFP), driven by a Gal4-dependent promoter. ECFP fluorescence was first detected in forming blood islands of the yolk sac at 8 dpc, then in macrophages in the yolk sac and the embryo proper. In adult mice ECFP was detected primarily in monocytes, tissue macrophages, microglia, and dendritic cells, including Langerhans cells of the skin. Crossing of these mice to transgenics containing tagged protein under control of a Gal4-dependent promoter directed expression of that protein in mononuclear phagocytes of double-transgenic animals. The new mouse line provides a useful tool for overexpression of transgenes in cells of the myeloid lineage, while simultaneously labeling them by ECFP expression.