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      The Role of Inflammation and Inflammatory Mediators in the Development, Progression, Metastasis, and Chemoresistance of Epithelial Ovarian Cancer

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          Abstract

          Inflammation plays a role in the initiation and development of many types of cancers, including epithelial ovarian cancer (EOC) and high grade serous ovarian cancer (HGSC), a type of EOC. There are connections between EOC and both peritoneal and ovulation-induced inflammation. Additionally, EOCs have an inflammatory component that contributes to their progression. At sites of inflammation, epithelial cells are exposed to increased levels of inflammatory mediators such as reactive oxygen species, cytokines, prostaglandins, and growth factors that contribute to increased cell division, and genetic and epigenetic changes. These exposure-induced changes promote excessive cell proliferation, increased survival, malignant transformation, and cancer development. Furthermore, the pro-inflammatory tumor microenvironment environment (TME) contributes to EOC metastasis and chemoresistance. In this review we will discuss the roles inflammation and inflammatory mediators play in the development, progression, metastasis, and chemoresistance of EOC.

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          Pathogenesis and pathophysiology of endometriosis.

          Richard O Burney, Linda C Giudice (2012)
          Originally described over three hundred years ago, endometriosis is classically defined by the presence of endometrial glands and stroma in extrauterine locations. Endometriosis is an inflammatory, estrogen-dependent condition associated with pelvic pain and infertility. This work reviews the disease process from theories regarding origin to the molecular basis for disease sequelae. A thorough understanding of the histopathogenesis and pathophysiology of endometriosis is essential to the development of novel diagnostic and treatment approaches for this debilitating condition. Copyright © 2012 American Society for Reproductive Medicine. All rights reserved.
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            AACR centennial series: the biology of cancer metastasis: historical perspective.

            James E Talmadge, Isaiah J Fidler (2010)
            Metastasis resistant to therapy is the major cause of death from cancer. Despite almost 200 years of study, the process of tumor metastasis remains controversial. Stephen Paget initially identified the role of host-tumor interactions on the basis of a review of autopsy records. His "seed and soil" hypothesis was substantiated a century later with experimental studies, and numerous reports have confirmed these seminal observations. An improved understanding of the metastatic process and the attributes of the cells selected by this process is critical for the treatment of patients with systemic disease. In many patients, metastasis has occurred by the time of diagnosis, so metastasis prevention may not be relevant. Treating systemic disease and identifying patients with early disease should be our goal. Revitalized research in the past three decades has focused on new discoveries in the biology of metastasis. Even though our understanding of molecular events that regulate metastasis has improved, the contributions and timing of molecular lesion(s) involved in metastasis pathogenesis remain unclear. Review of the history of pioneering observations and discussion of current controversies should increase understanding of the complex and multifactorial interactions between the host and selected tumor cells that contribute to fatal metastasis and should lead to the design of successful therapy. (c)2010 AACR.
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              Reactive oxygen species: role in the development of cancer and various chronic conditions

              Gulam Waris, Haseeb Ahsan (2006)
              Oxygen derived species such as superoxide radical, hydrogen peroxide, singlet oxygen and hydroxyl radical are well known to be cytotoxic and have been implicated in the etiology of a wide array of human diseases, including cancer. Various carcinogens may also partly exert their effect by generating reactive oxygen species (ROS) during their metabolism. Oxidative damage to cellular DNA can lead to mutations and may, therefore, play an important role in the initiation and progression of multistage carcinogenesis. The changes in DNA such as base modification, rearrangement of DNA sequence, miscoding of DNA lesion, gene duplication and the activation of oncogenes may be involved in the initiation of various cancers. Elevated levels of ROS and down regulation of ROS scavengers and antioxidant enzymes are associated with various human diseases including various cancers. ROS are also implicated in diabtes and neurodegenerative diseases. ROS influences central cellular processes such as proliferation a, apoptosis, senescence which are implicated in the development of cancer. Understanding the role of ROS as key mediators in signaling cascades may provide various opportunities for pharmacological intervention.
              Article 0 comments Cited 301 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancers (Basel)
                Journal ID (iso-abbrev): Cancers (Basel)
                Journal ID (publisher-id): cancers
                Title: Cancers
                Publisher: MDPI
                ISSN (Electronic): 2072-6694
                Publication date (Electronic): 30 July 2018
                Publication date Collection: August 2018
                Volume: 10
                Issue: 8
                Electronic Location Identifier: 251
                Affiliations
                [1 ]Medical Sciences, Indiana University School of Medicine, Bloomington, IN 47405, USA; ssavant@ 123456iu.edu
                [2 ]Cell, Molecular and Cancer Biology Graduate Program, Indiana University, Bloomington, IN 47405, USA; ssriramk@ 123456iu.edu
                [3 ]Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, IN 46202, USA
                Author notes
                [* ]Correspondence: hmohagan@ 123456indiana.edu ; Tel.: +1-812-855-3035
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-9750-5088
                Article
                Publisher ID: cancers-10-00251
                DOI: 10.3390/cancers10080251
                PMC ID: 6116184
                PubMed ID: 30061485
                SO-VID: 23dcb4b7-0d1d-481e-991f-64f8424bf850
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 14 June 2018
                Date accepted : 24 July 2018
                Categories
                Subject: Review

                Keywords: inflammation,epithelial ovarian cancer,cytokines,reactive oxygen species,growth factors
                Data availability:
                Keywords: inflammation, epithelial ovarian cancer, cytokines, reactive oxygen species, growth factors

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