Search

Additional file 2: CHEERS 2022 and HPV-FRAME checklists.

Additional file 1: Supplementary Information. This file provides additional information on model description, parameterization and calibration, settings on cervical screening and HPV vaccination used in the study, extra data for performing the cost-effectiveness analysis, and the supplementary results on sensitivity analyses. Table S1. The distribution of individuals by the level of sexual activity and age group. Table S2. Age distribution and mortality rate in Hong Kong. Table S3. Posterior distributions of inferred parameters. Table S4. Test performance parameters of cytology and HPV test. Table S5. Cost-effectiveness of guidelines-based screening strategies for unvaccinated cohorts. Table S6. ICERs of the most cost-effective screening strategy by vaccine uptake and duration of vaccine protection for unvaccinated cohorts. Table S7. Cost-effectiveness of screening strategies by annual discount rates for unvaccinated cohorts. Table S8. Sensitivity analysis on the estimated costs and health outcomes for unvaccinated cohorts by screen uptake. Table S9. Cost-effectiveness of guidelines-based screening strategies for vaccinated cohorts. Table S10. ICERs of the most cost-effective screening strategy by vaccine uptake and duration of vaccine protection for vaccinated cohorts. Table S11. Cost-effectiveness of screening strategies by annual discount rates for vaccinated cohorts. Table S12. Cost-effectiveness of screening strategies for vaccinated cohorts, with the assumption of faster HPV clearance rate and waning rate of natural immunity in males. Table S13. Sensitivity analysis of the estimated cost and health outcomes of screening strategies for vaccinated cohorts by screening uptake. Table S14. One-way sensitivity analysis on the cost-effectiveness of variants of strategy HPV + Genotyping for vaccinated cohorts. Table S15. Cost-effectiveness of variants of strategy HPV + Genotyping for vaccinated cohorts. Fig. S1. Schematic of the natural history model for high-risk HPV infection and cervical cancer. Fig. S2. Comparison of empirical data and the fitted model. Fig. S3. Trace plots and the posterior distributions of fitted parameters. Fig. S4. Schematic of evaluated cervical screening algorithms. Fig. S5. One-way sensitivity analysis of ICER for unvaccinated cohorts. Fig. S6. One-way sensitivity analysis of ICER for vaccinated cohorts.

Additional file 3: Supplementary Figure S1. MiR-141 is an exosomal miRNA derived from ovarian cancer cells. Supplementary Figure S2. MiR-141 induces stromal fibroblasts to have CAF-like properties. Supplementary Figure S3. GROα is the major proinflammatory chemokine in miR-141- expressing stroma. Supplementary Figure S4. YAP1 of Hippo signaling is the direct target of miR-141. Supplementary Figure S5. Conditional knockout (cKO) of Yap1 in stroma promotes tumor dissemination. Supplementary Figure S6. Depletion of CXCR1/2 impairs the oncogenic potential of OvCa cells induced by GROα.-enriched CM.

Additional file 2: Supplementary Table S2. The transcriptional binding sites of TEAD1 in GROα promoters.

Additional file 1: Supplementary Table S1. Oligo sequences of plasmid cloning and qPCR.

Additional file 7: Fig. S3. Heatmap visualization of DNA methylation levels in the PI3K-AKT, RAS, MAPK, and WNT signaling pathways and Kaplan–Meier estimates of OS using the methylation signature of genes.

Additional file 9: Fig. S5. (A) Table summarizing the IC50 values of a 48-h treatment with cisplatin, azacytidine, decitabine, and thioguanine in the six ovarian cancer cell lines using the XTT assay. IC50 values were determined at the drug concentration leading to a 50% viability reduction compared to the control. (B) Annexin V-PI staining of A2780cp and A2780s cells after a 48-h treatment with different concentrations of cisplatin, azacytidine, decitabine, and thioguanine by flow cytometry. Data analysis was performed with CytExpert software. (C) Population of apoptotic cells in each treatment condition from Annexin V-PI staining. The apoptotic cell population was represented by the cell population in the lower right quadrant (early apoptotic) and upper right quadrant (late apoptotic). (D) Cell cycle analysis of A2780cp and A2780s cells after 48 h of treatment with different concentrations of cisplatin, azacytidine, decitabine, and thioguanine by flow cytometry. Data analysis was performed with Modfit LT software. (E) Distribution of cells in different phases of the cell cycle in each treatment condition. Populations of cells distributed in G0/G1, S, G2/M and SubG1 phases are presented in different colored peaks.

Additional file 5: Fig. S1. Kaplan–Meier estimate of OS using methylation signature genes (CLDN16, LZTFL1, FARS2, SGMS2, ABHD2, RNF144A, and HPS4).

Additional file 6: Fig. S2. Boxplot visualization of comparison of the DNA methylation level of tumor grading. EOC samples were marked by tumor stage, tumor subtype, recurrence, and survival status.

Additional file 8: Fig. S4. Gene ontology (GO) enrichment analysis of the overall functional relevance of genes associated with DMPs using the clusterProfiler package in R.