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      Quercetin and cancer: new insights into its therapeutic effects on ovarian cancer cells

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          Abstract

          Ovarian cancer is known as a serious malignancy that affects women’s reproductive tract and can considerably threat their health. A wide range of molecular mechanisms and genetic modifications have been involved in ovarian cancer pathogenesis making it difficult to develop effective therapeutic platforms. Hence, discovery and developing new therapeutic approaches are required. Medicinal plants, as a new source of drugs, could potentially be used alone or in combination with other medicines in the treatment of various cancers such as ovarian cancer. Among various natural compounds, quercetin has shown great anti-cancer and anti-inflammatory properties. In vitro and in vivo experiments have revealed that quercetin possesses a cytotoxic impact on ovarian cancer cells. Despite obtaining good results both in vitro and in vivo, few clinical studies have assessed the anti-cancer effects of quercetin particularly in the ovarian cancer. Therefore, it seems that further clinical studies may introduce quercetin as therapeutic agent alone or in combination with other chemotherapy drugs to the clinical setting. Here, we not only summarize the anti-cancer effects of quercetin but also highlight the therapeutic effects of quercetin in the ovarian cancer.

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          Most cited references118

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          Biodegradable luminescent porous silicon nanoparticles for in vivo applications.

          Nanomaterials that can circulate in the body hold great potential to diagnose and treat disease. For such applications, it is important that the nanomaterials be harmlessly eliminated from the body in a reasonable period of time after they carry out their diagnostic or therapeutic function. Despite efforts to improve their targeting efficiency, significant quantities of systemically administered nanomaterials are cleared by the mononuclear phagocytic system before finding their targets, increasing the likelihood of unintended acute or chronic toxicity. However, there has been little effort to engineer the self-destruction of errant nanoparticles into non-toxic, systemically eliminated products. Here, we present luminescent porous silicon nanoparticles (LPSiNPs) that can carry a drug payload and of which the intrinsic near-infrared photoluminescence enables monitoring of both accumulation and degradation in vivo. Furthermore, in contrast to most optically active nanomaterials (carbon nanotubes, gold nanoparticles and quantum dots), LPSiNPs self-destruct in a mouse model into renally cleared components in a relatively short period of time with no evidence of toxicity. As a preliminary in vivo application, we demonstrate tumour imaging using dextran-coated LPSiNPs (D-LPSiNPs). These results demonstrate a new type of multifunctional nanostructure with a low-toxicity degradation pathway for in vivo applications.
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            Asymmetric and symmetric stem-cell divisions in development and cancer.

            Much has been made of the idea that asymmetric cell division is a defining characteristic of stem cells that enables them to simultaneously perpetuate themselves (self-renew) and generate differentiated progeny. Yet many stem cells can divide symmetrically, particularly when they are expanding in number during development or after injury. Thus, asymmetric division is not necessary for stem-cell identity but rather is a tool that stem cells can use to maintain appropriate numbers of progeny. The facultative use of symmetric or asymmetric divisions by stem cells may be a key adaptation that is crucial for adult regenerative capacity.
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              KRAS mutations as an independent prognostic factor in patients with advanced colorectal cancer treated with cetuximab.

              Cetuximab is efficient in advanced colorectal cancer (CRC). We previously showed that KRAS mutations were associated with resistance to cetuximab in 30 CRC patients. The aim of this study was to validate, in an independent larger series of 89 patients, the prognostic value of KRAS mutations on response to cetuximab and survival. Eighty-nine metastatic CRC patients treated with cetuximab after treatment failure with irinotecan-based chemotherapy were analyzed for KRAS mutation by allelic discrimination on tumor DNA. The association between KRAS mutations and tumor response, skin toxicity, progression-free survival (PFS) and overall survival (OS) was analyzed. A KRAS mutation was present in 27% of the patients and was associated with resistance to cetuximab (0% v 40% of responders among the 24 mutated and 65 nonmutated patients, respectively; P < .001) and a poorer survival (median PFS: 10.1 v 31.4 weeks in patients without mutation; P = .0001; median OS: 10.1 v 14.3 months in patients without mutation; P = .026). When we pooled these 89 patients with patients from our previous study, the multivariate analysis showed that KRAS status was an independent prognostic factor associated with OS and PFS, whereas skin toxicity was only associated with OS. In a combined analysis, median OS times of patients with two, one, or no favorable prognostic factors (severe skin toxicity and no KRAS mutation) was of 15.6, 10.7, and 5.6 months, respectively. These results confirm the high prognostic value of KRAS mutations on response to cetuximab and survival in metastatic CRC patients treated with cetuximab.
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                Author and article information

                Contributors
                asma.vafadar76@gmail.com
                shabanizahra1369@gmail.com
                ahmad.movahed14@gmail.com
                farzaneh.fallahi1376@gmail.com
                Mona.taghavi98u@gmail.com
                Ghasemi.y76y@gmail.com
                Maryam.akbari87u@yahoo.com
                md.shafiee@yahoo.com
                Ghadimi.sarah@gmail.com
                San.moraadi@gmail.com
                ebirazi2015@gmail.com
                Dashtaki63@gmail.com
                h.mirzaei2002@gmail.com , Mirzaei-h@kaums.ac.ir
                Journal
                Cell Biosci
                Cell Biosci
                Cell & Bioscience
                BioMed Central (London )
                2045-3701
                10 March 2020
                10 March 2020
                2020
                : 10
                : 32
                Affiliations
                [1 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Department of Medical Biotechnology, School of Advanced Medical Sciences and Technologies, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [2 ]GRID grid.412266.5, ISNI 0000 0001 1781 3962, Department of Nanotechnology, Faculty of Biological Sciences, , Tarbiat Modares University, ; Tehran, Iran
                [3 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Pharmaceutical Sciences Research Center, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [4 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Student Research Committee, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [5 ]GRID grid.444768.d, ISNI 0000 0004 0612 1049, Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, , Kashan University of Medical Sciences, ; Kashan, I.R. of Iran
                [6 ]GRID grid.411623.3, ISNI 0000 0001 2227 0923, Department of Gynecology and Obstetrics, Ramsar Campus, , Mazandaran University of Medical Sciences, ; Sari, Iran
                [7 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Department of Pharmaceutical Biotechnology, School of Pharmacy and Pharmaceutical Sciences Research Center, , Shiraz University of Medical Sciences, ; Shiraz, Iran
                [8 ]GRID grid.444768.d, ISNI 0000 0004 0612 1049, Department of Surgery, , Kashan University of Medical Sciences, ; Kashan, Iran
                [9 ]GRID grid.417184.f, ISNI 0000 0001 0661 1177, Division of General Internal Medicine, , Toronto General Hospital, ; Toronto, ON Canada
                [10 ]The Advocate Center for Clinical Research, Ayatollah Yasrebi Hospital, Kashan, Iran
                Article
                397
                10.1186/s13578-020-00397-0
                7063794
                31911829
                73e745ab-7a6f-4cdc-95eb-ac77037e6c2f
                © The Author(s) 2020

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 10 November 2019
                : 29 February 2020
                Categories
                Review
                Custom metadata
                © The Author(s) 2020

                Cell biology
                quercetin,ovarian cancer,therapy
                Cell biology
                quercetin, ovarian cancer, therapy

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