COVID-19-associated lncRNAs as predictors of survival in uterine corpus endometrial carcinoma: A prognostic model.

Patients with uterine corpus endometrial carcinoma (UCEC) may be susceptible to the coronavirus disease-2019 (COVID-19). Long non-coding RNAs take on a critical significance in UCEC occurrence, development, and prognosis. Accordingly, this study aimed to develop a novel model related to COVID-19-related lncRNAs for optimizing the prognosis of endometrial carcinoma.

The Expression of Pyroptosis-Related Gene May Influence the Occurrence, Development, and Prognosis of Uterine Corpus Endometrial Carcinoma.

Background: Increasing evidence has demonstrated that pyroptosis exerts key roles in the occurrence, development, and prognosis of uterine corpus endometrial carcinoma (UCEC). However, the mechanism of pyroptosis and its predictive value for prognosis remain largely unknown.

Methods: UCEC data were acquired from The Cancer Genome Atlas (TCGA) database.

Aurora B prevents aneuploidy via MAD2 during the first mitotic cleavage in oxidatively damaged embryos.

Objectives: A high rate of chromosome aneuploidy is exhibited in in vitro fertilization (IVF)-derived embryos. Our previous experiments suggested that reactive oxygen species (ROS) can activate Mad2, a key protein in the spindle assembly checkpoint (SAC), and delay the first mitotic, providing time to prevent the formation of embryonic aneuploidy. We aimed to determine whether mitotic kinase Aurora B was involved in the SAC function to prevent aneuploidy in IVF-derived embryos.

CHK1-CENP B/MAD2 is associated with mild oxidative damage-induced sex chromosome aneuploidy of male mouse embryos during in vitro fertilization.

A high incidence of aneuploidy is observed in vitro fertilization (IVF)-derived embryos, but the formation and repair mechanisms are unknown. Here, we investigated the effects of slightly increased reactive oxygen species (ROS) produced by in vitro culture conditions on embryo aneuploidy and the roles of the spindle assembly checkpoint (SAC) protein, mitotic arrest-deficient 2 (MAD2), and the DNA damage response (DDR) protein, checkpoint kinase 1 (CHK1), in aneuploidy repair. By assessing chromosome abnormalities via DAPI staining, karyotype analysis and next-generation sequencing technology, we demonstrated that mild oxidative damage mainly increased the risk of sex chromosome aneuploidy in male mouse embryos (41,XXY,+X and 41,XYY,+Y) through chromosome mis-segregation during the first mitosis.

Association between ERCC2 rs13181 polymorphism and ovarian cancer risk: an updated meta-analysis with 4024 subjects.

Background: Genetic variants in the excision repair cross-complimentary group 2 (ERCC2) gene may affect individual susceptibility to cancer by modulating the capability of DNA damage repair. However, the current studies concerning the association of ERCC2 rs13181 polymorphism with ovarian cancer risk provided inconsistent evidence.

Methods: This study was to quantitatively summarize the evidence from the individual studies electronically retrieved by a meta-analysis.