Comparison of early-onset and later-onset cervical cancer clinical characteristics and trends in Eswatini.

A Systematic Review of Patient-Reported Outcomes on the Impact of Radiation Therapy on Sexual Health in Patients With Gynecologic Cancer.

RHBDD1 promotes cervical cancer progression by activating the EGFR/PI3K/AKT signaling pathway.

RNF2 facilitates the progression of cervical cancer through the degradation of LATS1.

Reprogramming NF-κB signaling in cervical cancer: Implications for immune microenvironment and therapeutic resistance.

Cervical cancer in foreign-born women living in Italy: A systematic review of population-based studies.

Investigation of the impact of image-guided radiotherapy selection on image registration results and non-coding RNAs for cervical cancer patients.

PIK3CA mutant cervical cancer is selectively suppressed by PI3Kα inhibition (Alpelisib/BYL-719 and Inavolisib/GDC-0077) and cooperates with HPV directed T cell therapy.

Healthcare infrastructure and cervical cancer screening in low-resource settings: A systematic review focused on Sub-Saharan Africa

Impact of switching from a quadrivalent to a nonavalent HPV vaccine on HPV infections and cervical cancer in Colombia: a mathematical modelling study.

RNA polymerase I inhibitor CX-5461 suppresses cervical cancer cell growth by inducing DNA damage and mitotic catastrophe and enhances cisplatin sensitivity.

People with HIV have a higher incidence and mortality from screenable cancers than the general population. Among women, the 4 most common cancers are breast, colorectal, lung, and cervical cancers. This study examined breast, colorectal, lung, and cervical cancer screening rates among Black women with HIV and disparities that exist by immigration status. With a sample of 604 women, we examined cancer screening rates for breast, colorectal, lung, and cervical cancers and examined the rates by country of origin. Generalized linear mixed models were used to examine potential factors affecting these rates and the odds of screening by country of origin: US-born women (USBW) and non-US-born women (NUSBW). Cancer screening rates were low for all cancer categories for both groups. A screening rate of 48.7% was estimated for breast cancer (NUSBW-35.9% versus USBW-50.4%), 6.3% for lung cancer, 25.5% for colorectal cancer, and 72.8% for cervical cancer. NUSBW had lower screening rates for all 4 cancers compared with USBW. Possible predictors for cancer screenings were years of living with HIV [odds ratios (OR) 1.11; 95% CI: 1.07 to 1.14] and no viral suppression (OR 0.34; 95% CI: 0.15 to 0.76). Black women with HIV and much more immigrant subgroups may face additional barriers to accessing required cancer screening services in addition to being disproportionately affected by HIV. This emphasizes the urgent need for tailored, culturally relevant outreach and education to enhance cancer screening.

Comprehensive analysis of mutational signatures and corresponding driver genes in cervical cancer from Xinjiang.

A nanoplatform for hypoxia-responsive co-delivery of an NQO1 enzyme-responsive pterostilbene prodrug and phenanthriplatin for multi-mechanistic cervical cancer therapy.

Trends and regional patterns of cervical cancer incidence by histological subtypes: A Chinese population-based analysis from cancer registry data.

Head-to-head Comparison of Fibroblast Activation Protein Inhibitors and 18F-fluorodeoxyglucose in Cervical Cancer: A Systematic Review and Meta-analysis.

Diagnostic utility of apparent diffusion coefficient values in cervical cancer staging: A retrospective study.

Nicotine exerts a substantial influence on cervical carcinogenesis by affecting the malignant progression of human papillomavirus (HPV)-18 positive and HPV-negative cervical cancer cells, as well as HPV-immortalized cervical epithelial cells. Further research is needed to fully elucidate the impact of nicotine on HPV-16 positive cervical cancer. This study investigated the molecular mechanisms of nicotine in HPV-16-positive cervical (SiHa) cells. First, we conducted cell counting kit-8, flow cytometry, wound healing, transwell assays to evaluate cellular proliferation, migration, and invasion capabilities. The data illustrated that nicotine-treated SiHa cells displayed stronger malignant transformation capability compared to the control (p < 0.05). Furthermore, western blot analysis was used to evaluate the expression changes of cellular proteins in SiHa cells. The results revealed that nicotine induces a significant upregulation of PI3K, AKT, phosphorylated AKT (Ser473) (p-AKT), the p-AKT/AKT ratio, and matrix metalloproteinase-2 (MMP-2), along with a marked increase in its secretion. Also, it was accompanied by the suppression of tumor suppressor p53 and decreased levels of p21 and Caspase-3, as well as the active form of Caspase-3 (cleaved Caspase-3), indicating suppression of apoptosis. Critically, the use of a PI3K inhibitor (LY294002) demonstrated that the nicotine-induced downregulation of p53 and upregulation of MMP-2, as well as the enhancement of cellular invasion are dependent on PI3K/AKT pathway activation. These findings conclusively demonstrate that nicotine promotes the malignant transformation of HPV-16 positive cervical cancer cells by altering the expressions of MMP-2, p53, Caspase-3, and p21 via the activation of the PI3K/AKT pathway. This highlights the therapeutic potential of targeting this pathway in cervical cancer treatment.

Genotype-specific Human Papillomavirus patterns and their implications across the cervical cancer spectrum: A cross-sectional study from Western India.

Diagnostic performance of urine-based versus cervical swab human papillomavirus testing among women in a high-burden region in Northeastern, India: A prospective cross-sectional study.