Gynecological Malignant Tumors Research Articles

Difficulties in diagnosis of small intestine diseases

The article analyzes the problem of clinic and diagnosis of chronic small intestinal obstruction. Two women who had been undergoing longterm radiation therapy for gynecologic malignant neoplasms were observed. Endoscopic methods of investigation proved to be uninformative. The diagnosis was verified by radiological examination, and the localization of the process was specified. In one patient chronic small intestinal obstruction was provoked by a foreign body.

Relationship between loneliness and post-traumatic growth in patients with gynecologic malignancies: the mediating role of self-disclosure and psychological resilience

BackgroundTo explore the relationship between loneliness and post-traumatic growth, with a focus on the mediating role of psychological resilience and self-disclosure.MethodsThis study was a cross-sectional survey using the Loneliness Scale for Cancer Patients, the Distress Expression Index Scale (for measuring self-disclosure), the Psychological Resilience Scale, and the Posttraumatic Growth Scale on 215 inpatients with gynecologic malignancies at a tertiary care hospital in Guangzhou. Subsequently, Correlation, regression, and mediation analyses were performed using SPSS to test the relationships between the variables.ResultsThe results showed that loneliness was negatively correlated with posttraumatic growth (r = -0.261, P < 0.001), self-disclosure was positively correlated with posttraumatic growth (r = 0.360, P < 0.001), and psychological resilience was positively correlated with posttraumatic growth (r = 0.475, P < 0.001); loneliness was correlated with self-disclosure (r = -0.194, P < 0.01), loneliness was negatively correlated with psychological resilience (r = -0.287, P < 0.001), self-disclosure was correlated with psychological resilience (r = 0.287, P < 0.001); loneliness was significantly correlated with self-disclosure (r = -0.314, P < 0.001); loneliness was not a direct predictor of posttraumatic growth (β = -0.108, t = 1.734, P > 0.05), but could influence posttraumatic growth through the mediated effect of self-disclosure and psychological resilience, where the total indirect effect of self-disclosure and psychological resilience was − 0.155 (95% CI: -0.236, -0.081, P < 0.001).ConclusionsThe mechanism of loneliness on post-traumatic growth in patients with gynecologic malignancies is mainly through the indirect effect of self-disclosure and the indirect impact of psychological resilience. Great attention should be paid to patients’ loneliness, to find factors promoting patients’ self-disclosure, to improve the level of patients’ psychological resilience, and promote post-traumatic growth of gynecologic malignant tumors.

UBE2T is a diagnostic and prognostic biomarker for endometrial cancer.

Endometrial cancer (UCEC) is one of the most common malignant tumors in gynecology, and early diagnosis is crucial for its treatment. Currently, there is a lack of early screening tests specific to UCEC, and treatment advances are limited. It is crucial to identify more sensitive biomarkers for screening, diagnosis, and predicting UCEC. Previous studies have shown that UBE2T is involved in the development of various tumors such as breast cancer and liver cancer, but research on the role of UBE2T in UCEC is limited. Using data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and UALCAN databases, we analyzed the differential expression of UBE2T mRNA and protein in endometrial cancer (UCEC), along with its clinical relevance. A total of 113 clinical samples were collected, and immunohistochemistry and Western blot analysis were employed to validate bioinformatics analysis results. Volcano plots were generated using UBE2T and its differentially expressed genes, and a protein-protein interaction (PPI) network was constructed. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), gene set enrichment analysis (GSEA), and immune infiltration analysis were used to predict the functional role of UBE2T in UCEC progression. Correlation between UBE2T expression and patient survival was analyzed using TCGA data, and Kaplan-Meier survival curves were plotted. UBE2T is significantly overexpressed in UCEC and correlates with poor prognosis. Its overexpression is closely associated with mitosis, cell cycle regulation, and histological grade in UCEC patients. UBE2T is highly expressed in UCEC and suppresses anti-tumor immune responses in UCEC patients. It serves as a key participant in UCEC progression, associated with a range of adverse outcomes, and holds potential as a clinical diagnostic and prognostic biomarker.

Construction of self-driving anti-αFR CAR-engineered NK cells based on IFN-γ and TNF-α synergistically induced high expression of CXCL10

IntroductionOvarian cancer is the most malignant gynecological tumor. Previous studies have demonstrated that chimeric antigen receptor (CAR)-engineered NK-92 cells targeting folate receptor α (αFR) (NK-92-αFR-CAR) can specifically kill αFR-positive ovarian cancer cells. However, the migration barrier restricts antitumor effects of CAR-engineered cells. ObjectivesTo elucidate the mechanism by which NK-92-αFR-CAR cells induce the secretion of chemokine CXCL10 during killing ovarian cancer cells. It is speculated that NK-92-αFR-CAR-CXCR3A can target αFR and have chemotaxis of CXCL10, and they may have stronger killing effect of ovarian cancer. MethodsStudy the mechanism of CXCL10 expression strongly induced by TNF-α and IFN-γ combined stimulation in ovarian cancer cells. Construct the fourth generation of NK-92-αFR-CAR-CXCR3A cells, which were co-expressed CXCR3A and αFR-CAR. Evaluate the killing and migration effects of NK-92-αFR-CAR-CXCR3A in vitro and in vivo. ResultsRNA sequencing (RNA-seq) first revealed that the expression level of the chemokine CXCL10 was most significantly increased in ovarian cancer cells co-cultured with NK-92-αFR-CAR. Secondly, cytokine stimulation experiments confirmed that IFN-γ and TNF-α secreted by NK-92-αFR-CAR synergistically induced high CXCL10 expression in ovarian cancer cells. Further signaling pathway experiments showed that IFN-γ and TNF-α enhanced the activation level of the IFN-γ-IFNGR-JAK1/2-STAT1-CXCL10 signaling axis. Cytotoxicity experiments showed that NK-92-αFR-CAR-CXCR3A cells could not only efficiently kill αFR-positive ovarian cancer cells in vitro but also secrete IFN-γ and TNF-α. Higher migration than that of NK-92-αFR-CAR was detected in NK-92-αFR-CAR-CXCR3A using transwell assay. NK-92-αFR-CAR-CXCR3A effectively killed tumor cells in different mouse xenograft models of ovarian cancer and increased infiltration into tumor tissue. ConclusionThis study confirmed that IFN-γ and TNF-α secreted by αFR-CAR-engineered NK cells can synergistically induce high expression of CXCL10 in ovarian cancer cells and constructed self-driving αFR-CAR-engineered NK cells that can break through migration barriers based on CXCL10, which may provide a new therapeutic weapon for ovarian cancer.

Identification of RTP4 facilitating ovarian cancer by bioinformatics analysis and experimental validation.

Ovarian cancer (OV) is the most malignant gynecological tumor in women, with poor prognosis and high mortality rate. This study aims to identify hub genes in OV and explore the role of Receptor transporter 4 (RTP4) in OV progression. Common differentially expressed genes (DEGs) were screened from two microarray datasets. GO and KEGG enrichment analysis were performed. Protein-protein interaction (PPI) network was constructed by STING. Kaplan-Meier plotter was used to analyze prognosis. The effect of target gene on immune infiltration was analyzed by TIMER. The proliferation, migration, and invasion of OV cells were measured by CCK-8, wound healing assay, and trans-well assay, respectively. A total of 293 common DEGs were selected from GSE12470 and GSE16709 datasets. Hub genes, EPCAM, KIFC1, RTP4, TAGLN, and ZFP36 were selected by PPI network. Kaplan-Meier plotter demonstrated that high expression of RTP4 was related to low overall survival in OV patients. The TIMER result showed that high expression of RTP4 promoted immune infiltration of CD8+ T cells, B cells, neutrophils, and dendritic cells in OV. Moreover, silencing RTP4 significantly inhibited the proliferation, migration, and invasion of OV cells. RTP4 was associated with the poor prognosis in OV. In summary, silencing RTP4 inhibited the proliferation, migration, and invasion of OV cells, having the potential to be a novel therapeutic target for OV.

Silencing PDCD4 Mediates Transcription Factor EB Overexpression Promoting Proliferation, Migration, and Invasion of Cervical Cancer Hela Cells

Cervical cancer is a common gynecologic malignant tumor, the occurrence and development of which are related to multiple genetic and environmental factors. Recent studies have shown that Programmed Cell Death 4 (PDCD4) plays a crucial role in cervical cancer, and that silencing PDCD4 mediates Transcription Factor EB (TFEB) overexpression, promoting cell proliferation, migration, and invasion in this disease. This study utilized the Hela cell line as a cervical cancer model to investigate the changes in TFEB expression levels and the proliferation, migration, invasion, and EMT processes of cervical cancer cells through the silencing of PDCD4. Real-time quantitative PCR and Western blot were employed to assess the expression levels of PDCD4 and TFEB, while CCK-8, scratch assay, Transwell invasion assay, and Western blot were used to evaluate changes in cell proliferation, migration, invasion capabilities, and EMT processes. The experimental results demonstrated that silencing PDCD4 significantly increased the expression level of TFEB. Simultaneously, silencing PDCD4 also significantly accelerated the proliferation rate of Hela cells, enhanced the cells’ migration, invasion capabilities, and promoted the EMT processes. Further experimental results showed that silencing TFEB could partially reverse the promoting effects of PDCD4 silencing on cell proliferation, migration, and invasion. In cervical cancer, silencing PDCD4 can lead to TFEB overexpression, thereby promoting the proliferation, migration, and invasion of Hela cells. These findings provide crucial clues for the in-depth study of molecular mechanisms in cervical cancer and indicate that the PDCD4-TFEB pathway could potentially serve as a target for the treatment and prevention of this disease.

Prognostic Factors in Uterine Sarcoma Based on the Tumor Size Stratification: A Retrospective Study.

Uterine sarcoma is a rare malignant gynecological tumor with a poor prognosis. Many studies have identified the clinical stage as an important prognostic factor; however, the heterogeneity of patient distribution in the International Federation of Gynecology and Obstetrics (FIGO) stage has reportedly required further revision. Therefore, this study retrospectively investigated the factors related to the prognosis of uterine sarcoma, with particular attention to tumor size, which can be evaluated preoperatively. Clinical data were extracted from the medical records of patients with uterine sarcoma treated between January 2010 and January 2023. Kaplan-Meier survival curves were plotted according to clinical factors such as histological type, clinical stage, chemotherapy, and tumor size. Factors that were significant in the univariate analysis were subjected to the multivariate analysis using Cox proportional hazards regression. Thirty-four patients with uterine sarcoma, comprising 24 (70.5%), five (14.7%), three (8.8%), and two (5.9%) with leiomyosarcoma, undifferentiated sarcoma, high-grade endometrial stromal sarcoma, and low-grade endometrial stromal sarcoma, respectively, were included. Based on the FIGO stage, 15 (44.1%), six (17.6%), three (8.8%), and 10 patients had stage I, II, III, and IV disease, respectively, at the time of diagnosis. All patients underwent surgery as initial treatment; 15 received postoperative chemotherapy. Among the 32 patients with uterine leiomyosarcoma, undifferentiated sarcoma, or high-grade endometrial stromal sarcoma, overall survival differed significantly in the univariate analysis based on disease stage (I + II vs. III + IV) and tumor size (≤10 vs. >10 cm). However, only tumor size was an independent prognostic factor in the multivariate analysis. Tumor size (≤10 vs. >10 cm) may possibly have a prognostic impact on uterine sarcoma.

ABT‑737 increases cisplatin sensitivity through the ROS‑ASK1‑JNK MAPK signaling axis in human ovarian cancer cisplatin‑resistant A2780/DDP cells.

Ovarian cancer is a gynecological malignant tumor with the highest mortality rate, and chemotherapy resistance seriously affects patient therapeutic outcomes. It has been shown that the high expression of anti‑apoptotic proteins Bcl‑2 and Bcl‑xL is closely related to ovarian cancer chemotherapy resistance. Therefore, reducing Bcl‑2 and Bcl‑xL expression levels may be essential for reversing drug resistance in ovarian cancer. ABT‑737 is a BH3‑only protein mimetic, which can effectively inhibit the expression of the anti‑apoptotic proteins Bcl‑xL and Bcl‑2. Although it has been shown that ABT‑737 can increase the sensitivity of ovarian cancer cells to cisplatin, the specific molecular mechanism remains unclear and requires further investigation. In the present study, the results revealed that ABT‑737 can significantly increase the activation levels of JNK and ASK1 induced by cisplatin in A2780/DDP cells, which are cisplatin‑resistant ovarian cancer cells. Inhibition of the JNK and ASK1 pathway could significantly reduce cisplatin cytotoxicity increased by ABT‑737 in A2780/DDP cells, while inhibiting the ASK1 pathway could reduce JNK activation. In addition, it was further determined that ABT‑737 could increase reactive oxygen species (ROS) levels in A2780/DDP cells induced by cisplatin. Furthermore, the inhibition of ROS could significantly reduce JNK and ASK1 activation and ABT‑737‑mediated increased cisplatin cytotoxicity in A2780/DDP cells. Overall, the current data identified that activation of the ROS‑ASK1‑JNK signaling axis plays an essential role in the ability of ABT‑737 to increase cisplatin sensitivity in A2780/DDP cells. Therefore, upregulation the ROS‑ASK1‑JNK signaling axis is a potentially novel molecular mechanism by which ABT‑737 can enhance cisplatin sensitivity of ovarian cancer cells. In addition, the present research can also provide new therapeutic strategies and new therapeutic targets for patients with cisplatin‑resistant ovarian cancer with high Bcl‑2/Bcl‑xL expression patterns.

Progress of Clinical Research on Treatment of Lower Limb Lymphedema after Cervical Cancer Surgery

Cervical cancer is one of the most common gynecological malignant tumors, the early stage often without obvious symptoms and signs, with the development of lesions, clinical will appear to vaginal bleeding and vaginal drainage of the main symptoms, and according to the cancer focus of the scope of frequent urination urgent, constipation, lower limb swelling pain and a series of secondary symptoms. Not only that, according to the survey research shows that China's cervical cancer mortality accounted for the fourth of the total cancer mortality, accounting for the second female cancer, and the average age of cervical cancer patients in China to 40~50 years old. Surgical treatment, radiotherapy, chemotherapy, targeted therapy and immunotherapy are important methods for the treatment of cervical cancer. Complications may also occur during treatment, such as urinary tract infections, urinary retention, deep vein thrombosis and lymphedema of the lower extremities. Among them, lower extremity lymphedema is the most common and tricky, according to a foreign study found that the incidence of lower extremity lymphedema in patients with cervical cancer is as high as 47%, the main clinical manifestations of swelling, heavy, stinging, numbness, coarsedness and hardening, serious joint dysfunction, difficulty in activity, and even more, can cause erysipelas and cellulitis. Because it is incurable for a long time, the quality of life of patients is seriously reduced. In recent years, for the treatment of lower limb lymphedema after cervical cancer surgery, there are no safe and effective drugs in modern clinical medicine. Despite various treatment methods, its efficacy is still controversial. Therefore, most patients with lymphedema cannot receive effective treatment. Traditional Chinese medicine believes that the disease is mainly characterized by "mixed good and evil, deficiency and deficiency", so the treatment advocates the principle of "attack and tonification, specimen treatment", and its treatment methods are diverse and effective. This article discusses the treatment methods of lower limb lymphedema after cervical cancer surgery, and concludes that the combined treatment of traditional Chinese and Western medicine is effective.

Decoding the immune landscape: a comprehensive analysis of immune-associated biomarkers in cervical carcinoma and their implications for immunotherapy strategies.

Cervical cancer, a prevalent gynecological malignant tumor, poses a significant threat to women's health and lives. Immune checkpoint inhibitor (ICI) therapy has emerged as a promising avenue for treating cervical cancer. For patients with persistent or recurrent metastatic cervical cancer, If the sequence of dead receptor ligand-1 (PD-L1) is positive, ICI show significant clinical efficacy. PD-L1 expression serves as a valuable biomarker for assessing ICI therapeutic efficacy. However, the complex tumor immune microenvironment (TIME), encompassing immune cell composition and tumor-infiltrating lymphocyte (TIL) status, also exerts a profound influence on tumor immunity and prognosis. Given the remarkable strides made by ICI treatments in improving the survival rates of cervical cancer patients, it becomes essential to identify a comprehensive biomarker that integrates various TIME aspects to enhance the effectiveness of ICI treatment. Therefore, the quest for biomarkers linked to multiple facets of TIME in cervical cancer is a vital pursuit. In this study, we have developed an Immune-Associated Gene Prognostic Index (IRGPI) with remarkable prognostic value specifically for cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). The Cancer Genome Atlas CESC dataset (n = 305) was meticulously analyzed to pinpoint key immune-related genes via weighted gene co-expression network analysis and differential gene expression assays. Subsequently, we employed Cox regression analysis to construct the IRGPI. Furthermore, the composition of immune cells and TIL status were examined using CIBERSORT and TIDE. Tumor expression of Epigen, LCN10, and P73 were determined with immunohistochemistry. The resulting IRGPI, composed of EPGN, LCN10, and TP73 genes, displayed a strong negative correlation with patient survival. The discovery was validated with a patient cohort from our hospital. The IRGPI not only predicts the composition of immune cell subtypes such as Macrophages M1, NK cells, Mast cells, Plasma cells, Neutrophils, Dendritic cells, T cells CD8, and T cells CD4 within CESC, but also indicates TIL exclusion, dysfunction, and PD-1 and PD-L1 expression. Therefore, the IRGPI emerges as a promising biomarker not only for prognostic assessment but also for characterizing multiple immune features in CESC. Additionally, our results underscored the significant associations between the IRGPI and immune cell composition, TIL exclusion, and dysfunction, along with PD-1 and PD-L1 expression in the TIME. Consequently, the IRGPI stands out as a biomarker intimately connected to both the survival and TIME status of CESC patients, offering potential insights into immunotherapy strategies for CESC.

Research progress on the genetic factors and treatment methods of gynecological malignant tumors

Research progress on the genetic factors and treatment methods of gynecological malignant tumors

A Pilot Study Based on the Correlation Between Whole Exome and Transcriptome Reveals Potent Variants in the Indian Population of Cervical Cancer.

Cervical malignancy (CC) is the 2nd most prevalent malignancy among females, leading to cancer mortality. Primary detection of CC tumors results in an improved prognosis. CC is a malignant gynecological tumor, with few treatment options. New diagnostic and therapeutic agents are required to expand patient survival and quality of life. If CC tumors can be found at an early stage, the prognosis is much brighter. New diagnostic and therapeutic agents are needed to increase patient survival and quality of life. In this work, we performed whole-exome sequencing utilizing V5 (Illumina platform) 10 samples, 5 control and 5 CC tumour tissue, and we compared the results with transcriptome studies. KMT2C variations were shown to be among the most vicious in this analysis. From an Indian viewpoint, we found a plethora of SNVs and mutations, including those with known, unknown, and possible effects on health. Based on our findings, we know that the KMT2C gene is on chr. Seven and in exon 8, all three recognized variants are missense, synonymous, coding synonymous, non-coding variants, and GnomAD MAF (- 0.05). The variation at position (7:152265091, T > A, SNV 62478356) in KMT2C is unique, potent, and pathogenic. The missense coding transcript CIQTNF maps to chromosome 7 and displays T > C SNV. In addition, we performed single strand conformational polymorphism analysis on 64 samples and further confirmed them using Sanger sequencing to understand and verify the mutations. KMT2C shows a log FC value of - 1.16. Understanding emerging harmful mutations from an Indian viewpoint is facilitated by our bioinformatics-based, extensive correlation studies of WES analysis. Potentially harmful and new mutations were found in our preliminary analysis; among these ten top mutated genes, KMT2C and CIQTNF were altered in ten cases of CC with an Indian phenotype.

Mesencephalic astrocyte-derived neurotrophic factor inhibits cervical cancer progression via regulating macrophage phenotype.

Cervical cancer is a common gynecologic malignant tumor, but the critical factors affecting cervical cancer progression are still not well demonstrated. Mesencephalic astrocyte-derived neurotrophic factor (MANF) has been widely recognized as an anti-inflammatory factor to regulate macrophage polarization. In this study, the effect and mechanism of MANF on cervical cancer were preliminarily explored. Kaplan-Meier curve was used to show the overall survival time of the involved cervical cancer patients with high and low MANF expression in cervical cancer tissues. MANF was highly expressed in peritumoral tissues of cervical carcinoma by using immunohistochemistry and western blot. MANF mRNA level was detected by using qRT-PCR. Dual-labeled immunofluorescence showed MANF was mainly expressed in macrophages of cervical peritumoral tissues. Moreover, MANF-silenced macrophages promoted HeLa and SiHa cells survival, migration, invasion and EMT via NF-κB signaling activation. The results of tumor formation in nude mice indicated MANF-silenced macrophages promoted cervical tumor formation in vivo. Our study reveals an inhibitory role of MANF in cervical cancer progression, indicating MANF as a new and valuable therapeutic target for cervical cancer treatment.

Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer

Ovarian cancer is one of the most common gynecological malignant tumors with insidious onset, strong invasiveness, and poor prognosis. Metabolic alteration, particularly aerobic glycolysis, which is tightly regulated by transcription factors, is associated with the malignant behavior of OC. We screened FOXK2 in this study as a key transcription factor that regulates glycolysis in OC. FOXK2 is overly expressed in OC, and poor prognosis is predicted by overexpression. FOXK2 promotes OC cell proliferation both in vitro and in vivo and cell migration in vitro. Further studies showed that PDK2 directly binds to the forkhead-associated (FHA) domain of FOXK2 to phosphorylate FOXK2 at Thr13 and Ser30, thereby enhancing the transcriptional activity of FOXK2. FOXK2 transcriptionally regulates the expression of PDK2, thus forming positive feedback to sustain glycolysis in OC cells.

Study on the Profiles of Sleep Disorders, Associated Factors, and Pathways Among Gynecological Cancer Patients - A Latent Profile Analysis.

Gynecological cancer generally refers to malignant tumors in gynecology, commonly including cervical cancer, endometrial cancer, and ovarian cancer. Patients with gynecological cancer often suffer from sleep disorders after clinical treatment. Except for serious sleep disorders, female characteristics, family roles, and feudal beliefs make their self-stigma at a medium to high level, leading to huge pressure. This study aims to identify potential categories of sleep disorders, and analyze the relationship between self-stigma, perceived stress, and sleep disorders. A cross-sectional study was conducted in 2021-2022. Two hundred and two patients' data were collected from ShengJing Hospital Affiliated to China Medical University in Liaoning, Shenyang by using paper questionnaires for face-to-face surveys. The survey tools included the Pittsburgh Sleep Quality Index (PSQI), the Perceived Stress Scale (PSS), and the Social Impact Scale (SIS). Potential profile analysis (LPA), multiple logistic regression analysis, and structural equation modeling (SEM) were performed by Mplus 8.3, SPSS 26.0, and Amos 24.0 statistical tools, respectively. Three latent patterns of sleep disorders were found: "Good Sleep group (42.5%)", "Sleep Deficiency group (32.4%)", and "Sleep Disturbance group (25.1%)". Patients with high perceived stress were more likely to report a moderate (OR=1.142, 95% CI: 1.061-1.230) or high (OR=1.455, 95% CI: 1.291-1.640) level of sleep disorders. Self-stigma did not have a direct effect on sleep disorders (0.055, P>0.05), but it could have indirect effect on sleep disorders through perceived stress (0.172, P<0.01). The perceptions of sleep disorders among gynecological cancer patients varies and exhibits individual differences. Gynecological cancer patients who feels alienated or discriminated may cause high pressure. This internal pressure can exacerbate sleep disorders.

Machine learning models for prediction of postoperative venous thromboembolism in gynecological malignant tumor patients.

To identify risk factors that associated with the occurrence of venous thromboembolism (VTE) within 30 days after hysterectomy among gynecological malignant tumor patients, and to explore the value of machine learning (ML) models in VTE occurrence prediction. A total of 1087 patients between January 2019 and January 2022 with gynecological malignant tumors were included in this single-center retrospective study and were randomly divided into the training dataset (n = 870) and the test dataset (n = 217). Univariate logistic regression analysis was used to identify risk factors that associated with the occurrence of postoperative VTE in the training dataset. Machine learning models (including decision tree (DT) model and logistic regression (LR) model) to predict the occurrence of postoperative VTE were constructed and internally validated. The incidence of developing 30-day postoperative VTE was 6.0% (65/1087). Age, previous VTE, length of stay (LOS), tumor stage, operative time, surgical approach, lymphadenectomy (LND), intraoperative blood transfusion and gynecologic Caprini (G-Caprini) score were identified as risk factors for developing postoperative VTE in gynecological malignant tumor patients (p < 0.05). The AUCs of LR model and DT model for predicting VTE were 0.722 and 0.950, respectively. The ML models, especially the DT model, constructed in our study had excellent prediction value and shed light upon its further application in clinic practice.

Germ cell-specific gene 2 accelerates cell cycle in epithelial ovarian cancer by inhibiting GSK3α-p27 cascade

Epithelial ovarian cancer (EOC) is one of the most common malignant gynecological tumors with rapid growth potential and poor prognosis, however, the molecular mechanism underlying its outgrowth remained elusive. Germ cell-specific gene 2 (GSG2) was previously reported to be highly expressed in ovarian cancer and was essential for the growth of EOC. In this study, GSG2-knockdown cells and GSG2-overexpress cells were established through lentivirus-mediated transfection with Human ovarian cancer cells HO8910 and SKOV3. Knockdown of GSG2 inhibited cell proliferation and induced G2/M phase arrest in EOC. Interestingly, the expression of p27, a well-known regulator of the cell cycle showed a most significant increase after GSG2 knockdown. Further phosphorylation-protein array demonstrated the phosphorylation of GSK3αSer21 decreased in GSG2-knockdown cells to the most extent. Notably, inhibiting GSK3α activity effectively rescued GSG2 knockdown’s suppression on cell cycle as well as p27 expression in EOC. Our study substantiates that GSG2 is able to phosphorylate GSK3α at Ser21 and then leads to the reduction of p27 expression, resulting in cell cycle acceleration and cell proliferation promotion. Thus, GSG2 may have the potential to become a promising target in EOC.

Co-existence of Ovarian Teratomas With Other Gynecological Tumors.

This study aims to investigate the co-existence of ovarian teratomas with other benign or malignant gynecological tumors in women who underwent gynecological surgery. We retrospectively reviewed all women who underwent gynecological surgery over a 15-year period. Pre-operative, surgical, and histological records were obtained from women who presented with gynecological pathology, aiming to discover a possible link between ovarian teratomas and other gynecological tumors. Of the total patient sample, 288 (8.2%) had a mature teratoma, and 9 (0.3%) had an immature teratoma. The mean age was 38.0±13.3 years and 30.9±11.1 years, respectively. Women with mature teratoma showed a positive correlation with struma ovarii (SO, p=0.001). Moreover, we reported a positive linear relationship between struma ovarri and thecoma. Of the 288 women with a mature teratoma, 1 (0.3%) had co-existent endometrioid ovarian cancer, and 1 (0.3%) had borderline cancer. There were 14 women (4.9%) with a co-existent serous cystadenoma, 7 (2.4%) with a mucin cystadenoma, 1 (0.3%) with a thecoma, 4 (1.4%) with struma ovarii, 3 (1.0%) had Brenner cyst, 3 (1.0%) had ovarian fibroma, 2 had endometriosis (0.7%), and 8 (2.8%) had endometriomas. Of a total of nine women with immature teratomas, one (11.1%) had a serous cystadenoma. Ovarian teratomas may co-exist with other gynecological diseases. Our study reports various cases of the co-existence of several gynecological tumors with teratomas.

Abstract 3640: RAB26 accelerates endometrial cancer cell progression by regulating the Hedgehog signaling pathway

Abstract As one of the most common gynecological malignant tumors, endometrial cancer (EC) is continuously being studied since its etiology is still not clear. RAB26, a member of the RAB family, has been shown to influence cell proliferation, metastasis and other malignant phenotypes in several cancers. However, whether and how RAB26 plays roles in EC remain unknown. Our previous study showed that RAB26 was related to the cell cycle-associated protein IK, which has been shown to contribute to carcinogenesis. Herein, we further explored the clinical significance and biological function of RAB26 in EC. Immunohistochemical staining of 615 endometrial tissue samples was conducted to explore whether RAB26 expression was related to the clinicopathological characteristics of EC. In vitro and in vivo experiments were used to evaluate the role of RAB26 in EC and investigate the underlying mechanism. RAB26 expression was higher in EC than in normal endometrium (NE), hyperplastic endometrium (HE) and atypical hyperplastic endometrium (AHE). High RAB26 expression was positively correlated with tumor histological grade (P=0.010), FIGO stage (P=0.042) and tumor size (P=0.003) in EC. RAB26 attenuation inhibited cell proliferation and metastasis but promoted cell apoptosis and caused G0/G1 arrest. After RAB26 attenuation, RNA sequencing data showed that the Hedgehog signaling (SHH) pathway was enriched. Further western blot results confirmed that the levels of SHH pathway proteins (SHH, PTCH1, smo and Gli1) decreased as RAB26 expression was attenuated. Moreover, an agonist of the SHH pathway, purmorphamine, blocked the inhibitory effect of RAB26 attenuation on EC progression. The results of an in vivo study also showed that RAB26 attenuation exerted a significant antitumor effect. Accordingly, RAB26 may act as an oncogenic protein to promote EC progression through the SHH pathway. RAB26 may be a potential target for the treatment of EC patients. Citation Format: Chao Gao, Yanyan Liu, Yanyan Han, Fengxia Xue, Yingmei Wang. RAB26 accelerates endometrial cancer cell progression by regulating the Hedgehog signaling pathway [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3640.

The impact of short-term multimodal prehabilitation on functional capacity in patients with gynecologic malignancies during the perioperative period: A prospective study

PurposeTo explore the effect of a short-term, hospital-based, multimodal preoperative prehabilitation intervention on perioperative functional ability of patients with gynecological malignant tumors. MethodsAccording to the order in which they underwent surgery, 97 patients were divided into the control group (48 cases) and the intervention group (49 cases). The control group was given routine preoperative guidance, whereas the intervention group was given short-term multimodal prehabilitation guidance on the basis of the control group intervention. The 6-min walk test was performed on the day of admission to the hospital, the day before surgery, and the 30th day after surgery. ResultsCompared with the control group, the intervention group had significantly better 6-min walk distance and superior physical and psychological status on the day before surgery and the 30th day after surgery (P < 0.001). For three consecutive days after surgery, the quality of recovery in the intervention group was significantly higher than that in the control group (P < 0.001), and the first ambulation time and exhaust time were achieved earlier in the intervention group than in the control group (P < 0.05). ConclusionThe preoperative intervention group showed improved preoperative exercise ability and reduced anxiety in patients with gynecological cancer. Furthermore, this intervention improved the overall health of patients and accelerated their postoperative recovery.