Epithelial ovarian cancer (EOC) is considered the deadliest gynecological disease and is normally diagnosed at late stages, at which point metastasis has already occurred. Throughout disease progression, EOC will encounter various ecosystems and the communication between cancer cells and these microenvironments will promote the survival and dissemination of EOC. The primary tumor is thought to develop within the ovaries or the fallopian tubes, both of which provide a microenvironment with high risk of causing DNA damage and enhanced proliferation. EOC disseminates by direct extension from the primary tumors, as single cells or multicellular aggregates. Under the influence of cellular and non-cellular factors, EOC spheroids use the natural flow of peritoneal fluid to reach distant organs within the peritoneal cavity. These cells can then implant and seed distant organs or tissues, which develop rapidly into secondary tumor nodules. The peritoneal tissue and the omentum are two common sites of EOC metastasis, providing a microenvironment that supports EOC invasion and survival. Current treatment for EOC involves debulking surgery followed by platinum-taxane combination chemotherapy; however, most patients will relapse with a chemoresistant disease with tumors developed within the peritoneum. Therefore, understanding the role of the unique microenvironments that promote EOC transcoelomic dissemination is important in improving patient outcomes from this disease. In this review article, we address the process of ovarian cancer cellular fate at the site of its origin in the secretory cells of the fallopian tube or in the ovarian surface epithelial cells, their detachment process, how the cells survive in the peritoneal fluid avoiding cell death triggers, and how cancer- associated cells help them in the process. Finally, we report the mechanisms used by the ovarian cancer cells to adhere and migrate through the mesothelial monolayer lining the peritoneum. We also discuss the involvement of the transcoelomic ecosystem on the development of chemoresistance of EOC.
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http://dx.doi.org/10.3389/fendo.2022.886533 | DOI Listing |
J Ovarian Res
January 2025
Department of Medical Genetics, National Taiwan University Hospital, 19F, No. 8, Chung-Shan South Road, Taipei City, Taiwan.
Background: The homologous recombination deficiency (HRD) test is an important tool for identifying patients with epithelial ovarian cancer (EOC) benefit from the treatment with poly(adenosine diphosphate-ribose) polymerase inhibitor (PARPi). Using whole exome sequencing (WES)-based platform can provide information of gene mutations and HRD score; however, the clinical value of WES-based HRD test was less validated in EOC.
Methods: We enrolled 40 patients with EOC in the training cohort and 23 in the validation cohort.
J Ovarian Res
January 2025
Department of Health Education, Nanjing Municipal Center for Disease Control and Prevention, No.3, Zizhulin Road, Nanjing, Jiangsu Province, 210003, China.
Background: PARP inhibitors (PARPis) have shown promising effectiveness for ovarian cancer. This network meta-analysis (PROSPERO registration number CRD42024503390) comprehensively evaluated the effectiveness and safety of PARPis in platinum-sensitive recurrent ovarian cancer (PSROC).
Methods: Articles published before January 6, 2024 were obtained from electronic databases.
J Transl Med
January 2025
Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, Shenyang, China.
Background: The evidence on the relationship of dietary antioxidant nutrients with the survival of ovarian cancer (OC) remains scarce.
Objective: This study aimed to investigate these associations in a prospective cohort of Chinese patients with OC.
Methods: In this prospective cohort study, patients with epithelial OC completed a food frequency questionnaire at diagnosis and 12 months post-diagnosis, and were followed from 2015 to 2023.
JMIRx Med
January 2025
Department of Biochemistry and Medical Genetics, Cancer Center, University of Illinois Chicago, 900 s Ashland, Chicago, IL, 60617, United States, 1 8479124216.
Background: The causes of breast cancer are poorly understood. A potential risk factor is Epstein-Barr virus (EBV), a lifelong infection nearly everyone acquires. EBV-transformed human mammary cells accelerate breast cancer when transplanted into immunosuppressed mice, but the virus can disappear as malignant cells reproduce.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
Centre for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), School of Computing, University of Leeds, Leeds, UK.
Histopathology foundation models show great promise across many tasks, but analyses have been limited by arbitrary hyperparameters. We report the most rigorous single-task validation study to date, specifically in the context of ovarian carcinoma morphological subtyping. Attention-based multiple instance learning classifiers were compared using three ImageNet-pretrained encoders and fourteen foundation models, each trained with 1864 whole slide images and validated through hold-out testing and two external validations (the Transcanadian Study and OCEAN Challenge).
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