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      Comprehensive review on how platinum- and taxane-based chemotherapy of ovarian cancer affects biology of normal cells

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          Abstract

          One of the most neglected aspects of chemotherapy are changes, and possible consequences of these changes, that occur in normal somatic cells. In this review, we summarize effects of selected drugs used to treat ovarian cancer (platin derivatives—cisplatin and carboplatin; and taxanes—paclitaxel and docetaxel) on cellular metabolism, acquisition of reactive stroma features, cellular senescence, inflammatory reactions, apoptosis, autophagy, mitophagy, oxidative stress, DNA damage, and angiogenesis in various types of normal cells, including fibroblasts, epithelial cells, endothelial cells, and neurons. The activity of these drugs against the normal cells is presented from a broader perspective of their desirable anti-tumoral effects.

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          How Taxol/paclitaxel kills cancer cells

          Beth Weaver (2014)
          Taxol (generic name paclitaxel) is a microtubule-stabilizing drug that is approved by the Food and Drug Administration for the treatment of ovarian, breast, and lung cancer, as well as Kaposi's sarcoma. It is used off-label to treat gastroesophageal, endometrial, cervical, prostate, and head and neck cancers, in addition to sarcoma, lymphoma, and leukemia. Paclitaxel has long been recognized to induce mitotic arrest, which leads to cell death in a subset of the arrested population. However, recent evidence demonstrates that intratumoral concentrations of paclitaxel are too low to cause mitotic arrest and result in multipolar divisions instead. It is hoped that this insight can now be used to develop a biomarker to identify the ∼50% of patients that will benefit from paclitaxel therapy. Here I discuss the history of paclitaxel and our recently evolved understanding of its mechanism of action.
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            Recent progress in the diagnosis and treatment of ovarian cancer.

            Danijela Jelovac, Deborah Armstrong (2011)
            Epithelial ovarian cancer is the most lethal of the gynecologic malignancies, largely due to the advanced stage at diagnosis in most patients. Screening strategies using ultrasound and the cancer antigen (CA) 125 tumor marker are currently under study and may lower stage at diagnosis but have not yet been shown to improve survival. Women who have inherited a deleterious mutation in the BRCA1 or BRCA2 gene and those with the Lynch syndrome (hereditary nonpolyposis colorectal cancer) have the highest risk of developing ovarian cancer but account for only approximately 10% of those with the disease. Other less common and less well-defined genetic syndromes may increase the risk of ovarian cancer, but their contribution to genetic risk is small. A clear etiology for sporadic ovarian cancer has not been identified, but risk is affected by reproductive and hormonal factors. Surgery has a unique role in ovarian cancer, as it is used not only for diagnosis and staging but also therapeutically, even in patients with widely disseminated, advanced disease. Ovarian cancer is highly sensitive to chemotherapy drugs, particularly the platinum agents, and most patients will attain a remission with initial treatment. Recent advances in the delivery of chemotherapy using the intraperitoneal route have further improved survival after initial therapy. Although the majority of ovarian cancer patients will respond to initial chemotherapy, most will ultimately develop disease recurrence. Chemotherapy for recurrent disease includes platinum-based, multiagent regimens for women whose disease recurs more than 6 to 12 months after the completion of initial therapy and sequential single agents for those whose disease recurs earlier. New targeted biologic agents, particularly those involved with the vascular endothelial growth factor pathway and those targeting the poly (ADP-ribose) polymerase (PARP) enzyme, hold great promise for improving the outcome of ovarian cancer.
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              The Wnt signaling pathway in cancer.

              Yann Duchartre, Yong-Mi Kim, Michael Kahn (2016)
              The Wnt signaling pathway is critically involved in both the development and homeostasis of tissues via regulation of their endogenous stem cells. Aberrant Wnt signaling has been described as a key player in the initiation of and/or maintenance and development of many cancers, via affecting the behavior of Cancer Stem Cells (CSCs). CSCs are considered by most to be responsible for establishment of the tumor and also for disease relapse, as they possess inherent drug-resistance properties. The development of new therapeutic compounds targeting the Wnt signaling pathway promises new hope to eliminate CSCs and achieve cancer eradication. However, a major challenge resides in developing a strategy efficient enough to target the dysregulated Wnt pathway in CSCs, while being safe enough to not damage the normal somatic stem cell population required for tissue homeostasis and repair. Here we review recent therapeutic approaches to target the Wnt pathway and their clinical applications.
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                Author and article information

                Contributors
                Krzysztof Książek:
                ORCID: http://orcid.org/0000-0002-6066-5747
                +48 61 854-90-86 , kksiazek@ump.edu.pl
                Journal
                Journal ID (nlm-ta): Cell Mol Life Sci
                Journal ID (iso-abbrev): Cell. Mol. Life Sci
                Title: Cellular and Molecular Life Sciences
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 1420-682X
                ISSN (Electronic): 1420-9071
                Publication date (Electronic): 31 October 2018
                Publication date PMC-release: 31 October 2018
                Publication date (Print): 2019
                Volume: 76
                Issue: 4
                Pages: 681-697
                Affiliations
                ISNI 0000 0001 2205 0971, GRID grid.22254.33, Department of Hypertensiology, Angiology and Internal Medicine, , Poznań University of Medical Sciences, ; Długa 1/2 Str., 61-848 Poznań, Poland
                Author information
                http://orcid.org/0000-0002-6066-5747
                Article
                Publisher ID: 2954
                DOI: 10.1007/s00018-018-2954-1
                PMC ID: 6514066
                PubMed ID: 30382284
                SO-VID: 16cd2162-c818-4caa-9f50-42e40407c3be
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 21 January 2018
                Date revision received : 19 October 2018
                Date accepted : 22 October 2018
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100004281, Narodowe Centrum Nauki;
                Award ID: 2017/25/B/NZ3/00122
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100010438, Uniwersytet Medyczny im. Karola Marcinkowskiego w Poznaniu;
                Award ID: 502-14-02203310-10597
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Springer Nature Switzerland AG 2019

                ScienceOpen disciplines: Molecular biology
                Keywords: chemotherapy,ovarian cancer,platin analogs,side effects,taxanes
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: chemotherapy, ovarian cancer, platin analogs, side effects, taxanes

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