Objectives This study aimed to investigate the changes in the incidence and mortality trends of ovarian cancer (OC), cervical cancer (CC) and uterine cancer (UC) in the Fujian Province, southeastern China. Design Provincial, population-based, retrospective observational study. Setting Fujian province, southeastern China between 2011-2020. Participants From 2011 to 2020, 6178 new cases and 2037 deaths caused by 3 gynaecological cancers were eligible for analysis. Primary and secondary outcome measures The primary outcome measures were the incidence and mortality rates, including the age-standardised incidence rate (ASIR) and age-standardised mortality rate (ASMR), of three gynaecological cancers. The secondary outcome measure was the prevalence (average annual per cent changes (AAPC)). Results The incidence of all three gynaecological cancers increased from 2011 to 2020. CC had the slowest upward trend, with an AAPC of 2.54% over the period. However, it had the highest ASIR among the 3 cancers in 2020 (10.41/100 000). UC showed a rapid increase, with an AAPC of 15.15% from 2016 to 2020. While the mortality rate of UC remained stable, both CC and OC also exhibited rising trends, with the CC having the highest ASMR (3.05/100 000) in 2020. The ASMR for CC increased rapidly, with the highest AAPC of 5.51%. Conversely, changes in the ASMR for UC were not statistically significant (p=0.601). Moreover, high incidence rates were more common among perimenopausal women and older participants in the respective cancer groups where the increased mortality was observed. Conclusions Gynaecological cancer burden remains a public health issue in Fujian Province, with an increasing incidence. Improving the healthcare system and promoting a healthy lifestyle should be highlighted to reduce the cancer burden.

Aims:This study aimed to identify the prognostic value of tumor invasion distance (TID) based on MRI findings in cervical-cancer (CC) patients treated with radiotherapy (RT). Methods: A total of 218 CC patients diagnosed at Fujian Cancer Hospital from December 2018 to December 2019 were included in the study. Cox regression analyses were conducted to identify independent prognostic factors for overall survival (OS), including low 1/3 vaginal involvement, a longer TID, and RT without chemotherapy. These factors were subsequently used to construct a nomogram for individualized risk prediction. Kaplan–Meier survival analysis was employed to evaluate survival outcomes and establish a risk stratification system. The performance of the new stratification was assessed using the linear trend χ² test, Akaike information criterion, and Harrell’s concordance index. Results: A longer TID was associated with worse 3-year OS (p < 0.001, HR: 3.42, 95% CI: 1.67–7.00). A longer TID, lower 1/3 vaginal involvement, and concurrent chemotherapy were independent prognostic survival factors for CC patients. Compared with the 2018 FIGO staging system, the new risk stratification system provided better monotonicity with a higher linear trend χ² value (28.03 vs. 9.35), better discriminatory ability with smaller Akaike information criterion (312 vs. 331), and a greater Harrell C statistic (0.74 vs. 0.65) for predicting 3-year OS. Conclusions: This was the first study to demonstrate the prognostic value of TID in CC patients who received RT. The new risk stratification system based on TID could complement the 2018 FIGO staging system in identifying high-risk patients for more intense treatment and care. Further prospective research with larger samples is warranted to confirm the significance of TID for CC patients treated with RT.

Most ovarian cancer (OC) tumors are P53-mutant with some mutant P53 proteins possesses an oncogenic activity in OC development. Glycogen synthase kinase 3β (GSK3β), an enzyme closely relates to OC development was found to regulate P53 abundance in several cancer cells, however, whether GSK3β regulates P53 protein expression in OC is unknown. We initially aimed to address this issue, which led to identify a novel signaling axis involved in DNA damage repair in OC cell lines. We found GSK3β reversely regulated P53 signaling across ovarian OC cell lines. Inhibition of GSK3β impeded the homogenous recombination (HR) signaling pathway for DNA damage repair thus caused DNA damage, which was responsible for the raised P53 expression in the HR-proficient OC cells. The raised P53, whether mutated or not, attenuated DNA damage caused by GSK3β inhibition. We further confirmed PLK1/Aurora A axis was governed by GSK3β. Inhibition of GSK3β activated PLK1 via Aurora A in ovarian cancer cells and activation of PLK1 related to DNA damage repair. Double inhibition of GSK3β and PLK1 had a synergistic effect on inducing DNA damage and cell apoptosis in OC cells, which stands as a promising therapeutic strategy for OC.