Background: Human papilloma virus infection and tobacco smoking are the major risk factors for cervical cancer. There are limited studies searching other risk factors for cervical cancer and the results are not consistent. This study investigated the relations between cervical cancer and possible risk factors, including secondhand cigarette smoke exposure, diabetes, body mass index (BMI), and work schedule. Methods: In this cross-sectional study, 29,557 women completed a cervical cancer questionnaire and were selected using 2010–2018 data from the Korea National Health and Nutrition Examination Survey. Details in secondhand smoke exposure, diabetes, BMI, and work schedule were assessed with participants’ health interviews and health-related surveys. Results: Two hundred sixty-two women (0.89%) in the sample were diagnosed with cervical cancer. Domestic secondhand smoke exposure, diabetes, and high BMI significantly increased cervical cancer risk. Respective odds ratios and 95% confidence intervals were: 1.547 (1.042–2.297), 2.156 (1.535–3.027), and 1.036 (1.006–1.067). Weekly work hours, and work schedule were not significantly related to cervical cancer incidence. Conclusion: Among Korean women, passive exposure to cigarette smoke at home, diabetes, and high BMI increase risk for cervical cancer.

The adhesion molecule Nectin-4 is a new potential therapeutic target for different types of cancer; however, little is known about its diagnosis significance in endometrial cancer (EC). We found that Nectin-4 expression was significantly higher in EC tissues than in nonadjacent normal tissue. The area under the receiver operating characteristic curve value of 0.922 indicated good diagnostic accuracy for Nectin-4 expression in EC. Furthermore, Nectin-4 expression was associated with DNA mismatch repair (MMR) protein deficiency. Notably, the high Nectin-4 expression group of patients with MSH2/6-deficient EC had shorter progression-free survival than that of the low Nectin-4 expression group. The number of lymphovascular space invasion-positive patients in groups with MMR deficiency and high Nectin-4 expression was also increased compared with that in the low Nectin-4 expression group. Bioinformatics analysis revealed that alteration in Nectin-4 and MMR genes is associated with Nectin-4 expression in EC. To the best of our knowledge, this is the first study to show that Nectin-4 expression may be a potential biomarker for EC diagnosis and that high Nectin-4 expression in MMR-deficient patients with EC can predict short progression-free survival, thus providing clues to identify patients for adjuvant therapy.

Shin YJ, et al. Obstet Gynecol Sci. 2017 Jul;60(4):362-368. https://doi.org/10.5468/ogs.2017.60.4.362

We used data from the 2011-2014 Korean National Health and Nutrition Examination Surveys (KNHANES) to investigate whether the age at menopause is related to alcohol consumption in South Korean women. This was a cross-sectional study of the data for 940 women who became menopausal within the 3 years preceding the KNHANES. The numbers of nondrinkers, mild to moderate drinkers, and heavy drinkers in this group were 345 (34.7%), 573 (62.2%), and 22 (3%). Body mass index (BMI), smoking, and exercise were adjusted in model 1 and age was additionally adjusted in model 2. The mean ages at menopause were 51.6 ± 0.2, 50.8 ± 0.1, and 50.4 ± 0.5 years (p = 0.0025) in model 1 and 51.7 ± 0.2, 51.1 ± 0.1, and 50.1 ± 0.5 years (p = 0.0018) in model 2 for nondrinkers, mild to moderate drinkers, and heavy drinkers, respectively. BMI, smoking, exercise, educational level, income, duration of menopause, age at menarche, age at first delivery, and gravidity were adjusted in model 3, and the respective mean ages at menopause were 51.3 ± 0.2, 50.7 ± 0.2, and 50.1 ± 0.8 years (p = 0.0402). The population was classified into groups using the Alcohol Use Disorders Identification Test (AUDIT) scores of <5 (n = 778), <10 (n = 108), and ≥10 score (n = 54). The mean ages at menopause according to AUDIT score were 51.3 ± 0.1, 50.5 ± 0.3, and 50.4 ± 0.4 years (p = 0.0222, model 1), 51.4 ± 0.1, 50.8 ± 0.3, and 50.8 ± 0.3 years (p = 0.0261, model 2), and 51.1 ± 0.1, 50.6 ± 0.4, and 49.5 ± 0.6 years (p = 0.0241, model 3) respectively. In Korean women, alcohol consumption was associated with younger age at menopause. A higher AUDIT score was also related to younger age at menopause.

The present study aimed to analyze the compensatory signaling pathways induced by forkhead domain inhibitor‑6 (FDI‑6), which is a forkhead box protein M1 (FOXM1) inhibitor, in ovarian cancer cells and evaluate the effectiveness of simultaneous inhibition of FOXM1 and the compensatory signaling pathway in decreasing the survival of ovarian cancer cells. The present study identified the proteins involved in the compensatory mechanism activated by FDI‑6 in HeyA8 ovarian cancer cells using western blot analysis and a reverse‑phase protein array. In addition, a cell viability assay was performed to determine the effects of FDI‑6 and the compensatory signaling pathway on cancer cell viability. All experiments were performed in three‑dimensional cell cultures. The present study observed that FDI‑6 stimulated the upregulation of N‑Ras, phosphoprotein kinase Cδ (p‑PKCδ) (S664) and HER3 in HeyA8 cells. Tipifarnib as an N‑Ras inhibitor, rottlerin as a p‑PKCδ (S664) inhibitor and sapitinib as a HER3 inhibitor were selected. The combination of FDI‑6 with tipifarnib attenuated the upregulation of N‑Ras induced by FDI‑6 and the combination of FDI‑6 with sapitinib also attenuated HER3 downstream signaling pathway in HeyA8 cells, as shown by on western blot analysis. Rottlerin downregulated p‑PKCδ (S664) by inhibiting the activity of a Src‑related tyrosine kinase that transfers a phosphate group to PKCδ. Compared with FDI‑6 alone, the addition of tipifarnib or rottlerin to FDI‑6 was significantly more effective in reducing the growth of HeyA8 cells. However, the combination of FDI‑6 and sapitinib did not induce a significant decrease in survival of HeyA8 cells. In conclusion, the addition of tipifarnib or rottlerin to inhibit N‑Ras or p‑PKCδ (S664), respectively, inhibited the compensatory signaling pathway response induced by FDI‑6 in HeyA8 cells. These inhibitors increased the efficacy of FDI‑6, which inhibits FOXM1, in reducing ovarian cancer cell viability.