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Department of Medicine, Section Endocrinology, Erasmus University Medical Center, Rotterdam, the Netherlands
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Princess Maxima Center for Pediatric Oncology, Utrecht, the Netherlands
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Rotterdam Thyroid Center, Erasmus University Medical Center, Rotterdam, the Netherlands
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Rotterdam Thyroid Center, Erasmus University Medical Center, Rotterdam, the Netherlands
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Department of Medicine, Section Endocrinology, Erasmus University Medical Center, Rotterdam, the Netherlands
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use objective methods to collect data on secondary malignant neoplasms. Although several studies reported a protective effect of gonadotoxic therapies and premature ovarian insufficiency on radiation-induced breast cancer ( Travis et al . 2003
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Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece
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association of clock genes and endocrine neoplasms. Methods To identify studies and determine eligibility a systematic search was conducted in the PubMed, MEDLINE and Cochrane databases. The search terms included the following: ‘clock genes
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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Department of Obstetrics and Gynecology, New Taipei Municipal Tu Cheng Hospital, New Taipei City, Taiwan
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Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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Department of Anatomic Pathology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
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). Collectively, these data suggest that a hypoxia-derived gene signature can be a relevant hallmark in SCT-NOS. Tumorigenic signals in this rare ovarian neoplasm may therefore act through multiple parallel pathways to activate the transcription factor HIF1α and
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Ovarian cancer accounts for 5% of all cancer deaths in Western countries and is the most frequent cause of gynaecologic cancer mortality. The incidence varies with age between 1% and 14% with a peak rate in the eighth decade, and in the majority of cases, the disease has already spread beyond the pelvic cavity at time of diagnosis. Although in the last decades the introduction of cisplatin-based chemotherapy resulted in an improvement of patient survival, the percentage of recurrent disease is high even in those patients who achieve a complete response to chemotherapy, so that more than 80% of patients with advanced stage of disease die within 5 years (Copeland & Gershenson 1986). At present the prognostic characterisation of ovarian cancer patients, based on clinico-pathological parameters, such as stage, histology, grade and residual tumour after surgery, seems to be inadequate, since patients with similar clinico- pathological characteristics often experienced different clinical outcome. Therefore, the identification of biological factors related to tumour aggressiveness could be relevant in order to identify patients with different prognosis and chance to respond to chemotherapy, thus allowing the selection, at time of initial diagnosis, of high risk patients needing more aggressive therapy or alternative treatment, and a closer follow-up. Among the biological parameters proposed as possible prognostic factors in ovarian cancer much attention has been focused on endocrine factors and especially on steroid hormones and their receptors. Although several epidemiological and in vitro evidences have demonstrated that, similarly to breast and endometrial cancer, ovarian cancer cell biology could be influenced by the biochemical pathways promoted by the interaction of estrogens and progesterone with their specific receptors (ER, PR) conflicting data have been reported about the possible clinical role of ER and PR in this neoplasm. This review is aimed: a) to summarise the informations about the influence of steroid hormones and their receptors in the biology of ovarian cancer in in vitro models as well as in primary tumours;b) to investigate the association of steroid hormone receptor expression with the clinico-pathological parameters and the clinical outcome in ovarian cancer patients.c) to report the data of the literature about the rationale and the results of endocrine therapy in ovarian cancer.
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Introduction Neuroendocrine tumors (NETs) are a heterogeneous group of neoplasms that predominantly arise from neuroendocrine cells of the embryonic gut and are subdivided into foregut, midgut and hindgut NETs ( Hofland et al. 2020 ). NET
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National Cancer Institute, Women's Malignancies Branch, Department of Gynecologic Oncology, National Institutes of Health, 10 Center Drive, Building 10, 12N226, Bethesda, Maryland 20892-1906, USA
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Introduction Ovarian cancer is the fifth leading cause of cancer-related deaths among women and the gynecologic malignancy with the highest mortality rate in the USA ( http://seer.cancer.gov/statfacts/html/ovary.html ; accessed May 2015). Diagnosis
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gonadotropin and activin receptor messenger ribonucleic acid in human ovarian epithelial neoplasms. Clinical Cancer Research 6 2764 –2770. Miyazaki M , Nagy A, Schally AV, Lamharzi N, Halmos G, Szepeshazi K, Groot K & Armatis P
Cancer and Population Studies Group, School of Population Health, Queensland Institute of Medical Research, Brisbane, 4029, Australia
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Cancer and Population Studies Group, School of Population Health, Queensland Institute of Medical Research, Brisbane, 4029, Australia
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Introduction In 1998, Risch (1998) put forward a hypothesis for the pathogenesis of ovarian cancer relating to the role of androgens in stimulating epithelial cell proliferation. Although widely discussed in the aetiologic literature, there is a
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. Minegishi T , Kameda T, Hirakawa T, Abe K, Tano M & Ibuki Y 2000 Expression of gonadotropin and activin receptor messenger ribonucleic acid in human ovarian epithelial neoplasms. Clinical Cancer Research 6 2764 –2770
Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
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Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
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Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
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Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Obstetrics and Gynecology, Graduate Institute of Clinical Medicine, Department of Anesthesiology, Department of Obstetrics and Gynecology, Genomics Research Center, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei, Taiwan
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PB Saboorian MH Ashfaq R Toyooka KO Toyooka S Minna JD Gazdar AF Schorge JO 2005 Promoter hypermethylation profile of ovarian epithelial neoplasms . Clinical Cancer Research 11 5365 – 5369 . ( doi:10.1158/1078-0432.CCR-04