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1. Harvey PW, Everett DJ: The adrenal cortex and steroidogenesis as cellular and molecular targets for toxicity: critical omissions from regulatory endocrine disrupter screening strategies for human health? J Appl Toxicol; 2003 Mar-Apr;23(2):81-7
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  • [Title] The adrenal cortex and steroidogenesis as cellular and molecular targets for toxicity: critical omissions from regulatory endocrine disrupter screening strategies for human health?
  • Current testing strategies to assess the endocrine disrupting properties of chemicals have omitted examination of the adrenal gland and do not adequately cover the process of steroidogenesis.
  • Steroidogenesis is critical for adrenocortical function as well as that of the testes and ovaries, and presents multiple molecular targets for toxicity, ranging from general effects on all steroidogenic tissues (e.g. via StAR protein or CYP11A1 cholesterol side-chain cleavage) through to specific targets affecting only adrenocortical function (e.g.
  • Numerous chemicals of environmental relevance are now being shown to affect adrenocortical function both in vivo in aquatic species and in vitro in human cell lines, and given the vital role of the adrenal gland to human health and development, there is a strong case for including dedicated assessment techniques in screening batteries for endocrine-disrupting chemicals, not least to assist in general data interpretation (e.g. whether adrenal hypertrophy is due to stress or to a more sinister adrenocortical insufficiency).
  • Cell lines such as H295R (derived from a human adrenocortical adenocarcinoma) currently exist that will allow assessment of cortisol production and most of the major enzymes and functional proteins in the steroidogenic pathway (e.g.
  • Adequate assessment of adrenocortical function, as with any component of the integrated endocrine system, probably also will require the development of specific in vivo methodology to include effects on hypothalamo-pituitary function.
  • Finally, although there is currently no direct evidence that environmental exposure to endocrine-disrupting (oestrogenic) chemicals has actually caused adverse human health effects, lessons have been learned on their potential from the diethylstilboestrol case.
  • [MeSH-major] Adrenal Cortex / drug effects. Cytochrome P-450 Enzyme System / drug effects. Endocrine System / drug effects. Pesticides / toxicity. Steroids / biosynthesis. Toxicity Tests / methods
  • [MeSH-minor] Animals. Fishes. Humans. Hydrocortisone / biosynthesis. Hydrocortisone / deficiency. Molecular Structure. Oxidoreductases / drug effects

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  • (PMID = 12666151.001).
  • [ISSN] 0260-437X
  • [Journal-full-title] Journal of applied toxicology : JAT
  • [ISO-abbreviation] J Appl Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Pesticides; 0 / Steroids; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.- / Oxidoreductases; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 58
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2. Nakano S, Shomura H, Akabane H, Inagaki M, Yanagida N: [Two cases of gastric endocrine cell carcinoma]. Gan To Kagaku Ryoho; 2010 Nov;37(12):2505-7
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  • [Title] [Two cases of gastric endocrine cell carcinoma].
  • Gastric endocrine cell carcinoma is rare and associated with a poor prognosis.
  • The first case was a man in his sixties with gastric endocrine cell carcinoma, of which a clinical finding was T2N1M0H1 (Stage IV).
  • But the tumor was re-grown and the patient died twenty months after diagnosis.
  • The second case was a man in his seventies with gastric endocrine cell carcinoma, of which a clinical finding was T3N1M0H0P0, Stage IIIa, underwent total gastrectomy.
  • [MeSH-major] Endocrine Gland Neoplasms / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / therapy. Aged. Antineoplastic Agents / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Cisplatin / administration & dosage. Drug Combinations. Humans. Male. Middle Aged. Oxonic Acid / administration & dosage. Tegafur / administration & dosage

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  • (PMID = 21224621.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; 7673326042 / irinotecan; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin
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3. Fröhlich E, Machicao F, Wahl R: Action of thiazolidinediones on differentiation, proliferation and apoptosis of normal and transformed thyrocytes in culture. Endocr Relat Cancer; 2005 Jun;12(2):291-303
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  • Differentiating drugs may be able to re-sensitize thyroid carcinomas to radioiodine therapy.
  • Substituted thiazolidinediones (TZDs) belong to the group of oral anti-diabetic drugs that also possess anti-proliferative and pro-apoptotic effects and, potentially, differentiating effects on several cancer cell lines.
  • Differentiation was investigated by measuring 125I uptake and the expression of sodium-iodide symporter and thyroglobulin proteins.
  • [MeSH-major] Adenocarcinoma, Follicular / metabolism. Apoptosis. Radiation-Sensitizing Agents / pharmacology. Thiazolidinediones / pharmacology. Thyroid Gland / drug effects. Thyroid Neoplasms / metabolism
  • [MeSH-minor] Animals. Annexin A5 / analysis. Cell Differentiation / drug effects. Cell Line, Transformed. Cell Proliferation / drug effects. Chromans / pharmacology. PPAR gamma / genetics. RNA, Messenger / analysis. RNA, Messenger / metabolism. Retinoid X Receptor alpha / genetics. Swine. Symporters / metabolism. Thyroglobulin / metabolism

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  • [ErratumIn] Endocr Relat Cancer. 2005 Sep;12(3):681
  • (PMID = 15947104.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Chromans; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Radiation-Sensitizing Agents; 0 / Retinoid X Receptor alpha; 0 / Symporters; 0 / Thiazolidinediones; 0 / sodium-iodide symporter; 05V02F2KDG / rosiglitazone; 9010-34-8 / Thyroglobulin; I66ZZ0ZN0E / troglitazone; X4OV71U42S / pioglitazone
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4. Sarlis NJ, Gourgiotis L: Molecular elements of apoptosis-regulating pathways in follicular thyroid cells: mining for novel therapeutic targets in the treatment of thyroid carcinoma. Curr Drug Targets Immune Endocr Metabol Disord; 2004 Sep;4(3):187-98
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  • The cell death machinery includes cell surface receptors, adaptor molecules, proteolytic enzymes, such as caspases, and a variety of mitochondrial proteins, which interact with each other in a complex fashion.
  • For such patients with clinically aggressive ThyrCa, novel therapeutic agents are urgently needed.
  • In this review, we outline the main molecular targets that play a role in apoptosis in ThyrCa cells, and discuss various options for promoting apoptosis, either by pharmacologic or gene transfer therapeutic interventions.
  • [MeSH-major] Adenocarcinoma, Follicular / drug therapy. Adenocarcinoma, Follicular / pathology. Apoptosis / physiology. Drug Delivery Systems / methods. Signal Transduction / drug effects. Thyroid Neoplasms / drug therapy. Thyroid Neoplasms / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Humans. Thyroid Gland / drug effects. Thyroid Gland / metabolism. Thyroid Gland / pathology

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  • (PMID = 15379722.001).
  • [ISSN] 1568-0088
  • [Journal-full-title] Current drug targets. Immune, endocrine and metabolic disorders
  • [ISO-abbreviation] Curr. Drug Targets Immune Endocr. Metabol. Disord.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 162
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5. Prins GS, Birch L, Tang WY, Ho SM: Developmental estrogen exposures predispose to prostate carcinogenesis with aging. Reprod Toxicol; 2007 Apr-May;23(3):374-82
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  • Using the neonatal rodent as an animal model, it has been shown that early exposure to high doses of estradiol results in an increased incidence of prostatic lesions with aging which include hyperplasia, inflammatory cell infiltration and prostatic intraepithelial neoplasia or PIN, believed to be the precursor lesion for prostatic adenocarcinoma.
  • Furthermore, recent studies performed with low-dose estradiol exposures during development as well as exposures to environmentally relevant doses of the endocrine disruptor bisphenol A show increased susceptibility to PIN lesions with aging following additional adult exposure to estradiol.
  • Gene methylation analysis revealed a potential epigenetic basis for the estrogen imprinting of the prostate gland.
  • Taken together, our results suggest that a full range of estrogenic exposures during the postnatal critical period - from environmentally relevant bisphenol A exposure to low-dose and pharmacologic estradiol exposures - results in an increased incidence and susceptibility to neoplastic transformation of the prostate gland in the aging male which may provide a fetal basis for this adult disease.

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  • (PMID = 17123779.001).
  • [ISSN] 0890-6238
  • [Journal-full-title] Reproductive toxicology (Elmsford, N.Y.)
  • [ISO-abbreviation] Reprod. Toxicol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK040890; United States / NIEHS NIH HHS / ES / R21 ES012281; United States / NIEHS NIH HHS / ES / R01 ES015584; United States / NIEHS NIH HHS / ES / ES12281; United States / NIEHS NIH HHS / ES / P30 ES006096; United States / NIDDK NIH HHS / DK / DK40890
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogens
  • [Number-of-references] 90
  • [Other-IDs] NLM/ NIHMS23013; NLM/ PMC1927084
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6. Villeneuve DL, Ankley GT, Makynen EA, Blake LS, Greene KJ, Higley EB, Newsted JL, Giesy JP, Hecker M: Comparison of fathead minnow ovary explant and H295R cell-based steroidogenesis assays for identifying endocrine-active chemicals. Ecotoxicol Environ Saf; 2007 Sep;68(1):20-32
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  • [Title] Comparison of fathead minnow ovary explant and H295R cell-based steroidogenesis assays for identifying endocrine-active chemicals.
  • An in vitro steroidogenesis assay using H295R human adenocarcinoma cells has been suggested as a possible alternative to gonad explant assays for use as a Tier I screening assay to detect endocrine active chemicals capable of modulating steroid hormone synthesis.
  • Overall, however, results of this study suggest that both the H295R and fathead minnow ovary explant assays have utility for identifying endocrine-active chemicals in screening-type applications.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adrenal Gland Neoplasms / drug therapy. Cyprinidae. Estradiol / biosynthesis. Hormone Antagonists / toxicity. Ovary / drug effects. Testosterone / biosynthesis
  • [MeSH-minor] Animal Testing Alternatives. Animals. Biological Assay. Cell Line, Tumor. Dose-Response Relationship, Drug. Female. Humans. Organ Culture Techniques. Reproducibility of Results

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  • (PMID = 17449096.001).
  • [ISSN] 0147-6513
  • [Journal-full-title] Ecotoxicology and environmental safety
  • [ISO-abbreviation] Ecotoxicol. Environ. Saf.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormone Antagonists; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol
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7. Lange D, Sporny S, Sygut J, Kulig A, Jarzab M, Kula D, Jarzab B: [Histopathological diagnosis of thyroid cancer in a multicenter trial]. Endokrynol Pol; 2006 Jul-Aug;57(4):336-42
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  • [Title] [Histopathological diagnosis of thyroid cancer in a multicenter trial].
  • INTRODUCTION: In the front of the problems related to the differentiation between benign and malignant thyroid tumors we decided to perform a multicentre study in order to validate diagnoses of malignant thyroid tumors and assess the inter-observer variability.
  • The studies were sent from centres which agreed to participate in the project and than coded in the independent centre--Department of Nuclear Medicine and Endocrine Oncology.
  • The reference diagnosis was made by an agreement between four expert pathologists (D.L., S.S., J.S. and A.K.).
  • Concerning the diagnosis of cancer histotype, the difference between participants diagnosis and the reference one was even higher.
  • The best concordance was achieved in the diagnosis of papillary thyroid cancer, however, on the cost of cancer overdiagnosis by some participants.
  • CONCLUSION: The study documents a high inter-observer variability of thyroid cancer diagnosis and confirms the lesser accuracy of diagnosis of follicular cancer.
  • [MeSH-major] Adenocarcinoma, Follicular / pathology. Adenoma / pathology. Carcinoma, Papillary / pathology. Goiter, Nodular / pathology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Histological Techniques / methods. Histological Techniques / standards. Humans. Multicenter Studies as Topic / statistics & numerical data. Observer Variation. Thyroid Gland

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  • (PMID = 17006833.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
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8. Mitsumori K, Shimo T, Onodera H, Takagi H, Yasuhara K, Tamura T, Aoki Y, Nagata O, Hirose M: Modifying effects of ethinylestradiol but not methoxychlor on N-ethyl-N-nitrosourea-induced uterine carcinogenesis in heterozygous p53-deficient CBA mice. Toxicol Sci; 2000 Nov;58(1):43-9
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  • It is unknown whether endocrine-disrupting chemicals (EDCs) with estrogenic activities have any modifying effects on uterine carcinogenesis.
  • To investigate the effects of ethinylestradiol (EE) and methoxychlor (MXC) on development of ENU-induced uterine tumors, female p53 (+/-) mice and their wild-type littermates [p53 (+/+) mice] received an intraperitoneal injection of 120 mg/kg body weight (bw) of ENU, followed, in Group 1, by no further treatment; in Group 2, by a diet containing 1 ppm EE; in Group 3, by a diet containing 5 ppm EE for 4 weeks and 2.5 ppm EE thereafter; and in Group 4, by a diet containing 2000 ppm MXC for 26 weeks.
  • Atypical hyperplasias (clear-cell type) of the endometrial gland in p53 (+/-) mice were seen at incidences of 0, 14, 60, and 0% in Groups 1, 2, 3, and 4, respectively, while their incidence in p53 (+/+) mice was 0, 7, 53, and 0%, respectively, with a significant difference between Groups 1 and 3 in both cases.
  • One p53 (+/-) mouse in Group 3 also had an adenocarcinoma consisting of clear cells, and the PCNA labeling indices of the clear-cell atypical hyperplasias, and this endometrial adenocarcinoma, were higher than those of glandular hyperplasias.
  • [MeSH-minor] Adenocarcinoma, Clear Cell / chemically induced. Adenocarcinoma, Clear Cell / genetics. Adenocarcinoma, Clear Cell / pathology. Animals. Body Weight / drug effects. Diet. Drug Synergism. Endometrial Hyperplasia / chemically induced. Endometrial Hyperplasia / pathology. Ethylnitrosourea / administration & dosage. Ethylnitrosourea / toxicity. Female. Immunoenzyme Techniques. Injections, Intraperitoneal. Mice. Mice, Inbred CBA. Mice, Knockout. Organ Size / drug effects. Proliferating Cell Nuclear Antigen / analysis. Uterus / chemistry. Uterus / drug effects. Uterus / pathology

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  • (PMID = 11053539.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Proliferating Cell Nuclear Antigen; 423D2T571U / Ethinyl Estradiol; P8M1T4190R / Ethylnitrosourea; RIA79UD69L / Methoxychlor
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9. Balcerzak W, Bednarz W, Domosławski P, Olewiński R, Kolesińska J, Kaminski Z, Dziarkowska K, Wieczorek P: [Preliminary approach towards construction of peptide libraries as potential tools for diagnosis of malignant thyroid tumors]. Endokrynol Pol; 2006 Jul-Aug;57(4):307-13
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  • [Title] [Preliminary approach towards construction of peptide libraries as potential tools for diagnosis of malignant thyroid tumors].
  • INTRODUCTION: Cancer of thyroid gland is the most common malignancy of the endocrine system.
  • The treatment improvement could be achieved by early diagnosis.
  • CONCLUSIONS: It is important to optimize construction of peptide libraries by using different staining agents hydrolyzed by proteases.
  • [MeSH-major] Adenocarcinoma, Follicular / pathology. Adenoma, Oxyphilic / pathology. Biomarkers, Tumor / analysis. Carcinoma, Papillary, Follicular / pathology. Peptide Library. Thyroid Neoplasms / pathology

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  • (PMID = 17006829.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3; 0 / Peptide Library; EC 1.11.1.8 / Iodide Peroxidase
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10. Sampath D, Winneker RC, Zhang Z: The angiogenic factor Cyr61 is induced by the progestin R5020 and is necessary for mammary adenocarcinoma cell growth. Endocrine; 2002 Jul;18(2):147-59
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  • [Title] The angiogenic factor Cyr61 is induced by the progestin R5020 and is necessary for mammary adenocarcinoma cell growth.
  • In this study, both Cyr61 mRNA and protein were induced by the progestin, R5020, in T47D mammary adenocarcinoma cells in a dose- and time-dependent fashion.
  • Cyr61 gene induction by R5020 was transcriptionally regulated by progesterone receptor (PR) as the antiprogestin, RU486, and actinomycin D blocked induction completely.
  • Moreover, Cyr61 was upregulated by epidermal growth factor (EGF) but not by R5020 in the PR-MDA-MB-431 mammary adenocarcinoma cell line, underscoring the necessity of PR.
  • Remarkably, increased Cyr61 protein expression was observed in greater than 50% of primary breast tumor lysates that were progesterone receptor (PR)+ but estrogen receptor negative.
  • [MeSH-major] Adenocarcinoma. Breast Neoplasms. Immediate-Early Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Progesterone Congeners / pharmacology. Promegestone / pharmacology
  • [MeSH-minor] Antibodies / pharmacology. Cell Division / drug effects. Cysteine-Rich Protein 61. Drug Synergism. Epidermal Growth Factor / pharmacology. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Neovascularization, Pathologic. S Phase / drug effects. Transcription, Genetic / drug effects. Transcriptional Activation. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / immunology. Up-Regulation / drug effects

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  • (PMID = 12374462.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / CYR61 protein, human; 0 / Cysteine-Rich Protein 61; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Progesterone Congeners; 62229-50-9 / Epidermal Growth Factor; 9XE0V2SQYX / Promegestone
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11. Ziółkowska E, Biedka M, Zyromska A, Makarewicz R: Psoriasis exacerbation after hormonotherapy in prostate cancer patient-Case report. Rep Pract Oncol Radiother; 2010;15(4):103-6
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  • Among systemic factors are endocrine and metabolic disturbances as well as many drugs.
  • A 57-year-old Caucasian man was admitted for curative radiation therapy of adenocarcinoma of the prostate after 3 months of initial hormonal therapy.
  • We decided to start the previously planned radiation therapy which included the prostate gland with 1.5 cm margin and provided for the total dose of 72 Gy in 36 fractions.

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  • (PMID = 24376933.001).
  • [ISSN] 1507-1367
  • [Journal-full-title] Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznań and Polish Society of Radiation Oncology
  • [ISO-abbreviation] Rep Pract Oncol Radiother
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC3863271
  • [Keywords] NOTNLM ; Hormonotherapy / Prostate cancer / Psoriasis
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12. Ito H, Nishimura T, Abe H, Oka F, Miura T, Uchikoba T, Oaki Y: Adenocarcinoma of the prostate with ectopic antidiuretic hormone production: a case report. Hinyokika Kiyo; 2000 Jul;46(7):499-503
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  • [Title] Adenocarcinoma of the prostate with ectopic antidiuretic hormone production: a case report.
  • An 88-year-old patient with a poorly differentiated adenocarcinoma of the prostate gland was found to have all cardinal findings of syndrome of inappropriate antidiuretic hormone secretion (SIADH).
  • [MeSH-major] Adenocarcinoma / secretion. Paraneoplastic Endocrine Syndromes. Prostatic Neoplasms / secretion. Vasopressins / secretion
  • [MeSH-minor] Aged. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Flutamide / therapeutic use. Humans. Inappropriate ADH Syndrome / drug therapy. Inappropriate ADH Syndrome / etiology. Leuprolide / therapeutic use. Male. Treatment Outcome

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  • (PMID = 10965460.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 11000-17-2 / Vasopressins; 76W6J0943E / Flutamide; EFY6W0M8TG / Leuprolide
  • [Number-of-references] 12
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13. Weyemi U, Caillou B, Talbot M, Ameziane-El-Hassani R, Lacroix L, Lagent-Chevallier O, Al Ghuzlan A, Roos D, Bidart JM, Virion A, Schlumberger M, Dupuy C: Intracellular expression of reactive oxygen species-generating NADPH oxidase NOX4 in normal and cancer thyroid tissues. Endocr Relat Cancer; 2010 Mar;17(1):27-37
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  • To date, in the thyroid gland, only DUOX1/2 NOX systems have been described.
  • ROS may have various biological effects, depending on the site of production.
  • [MeSH-major] Adenocarcinoma, Follicular / enzymology. Adenoma / enzymology. Carcinoma / enzymology. Carcinoma, Papillary / enzymology. NADPH Oxidase / biosynthesis. Neoplasm Proteins / biosynthesis. Reactive Oxygen Species / metabolism. Thyroid Gland / enzymology. Thyroid Neoplasms / enzymology
  • [MeSH-minor] Cells, Cultured / enzymology. Cytoplasm / enzymology. Enzyme Induction / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hydrogen Peroxide / metabolism. Oxidation-Reduction. RNA Interference. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. RNA, Small Interfering / pharmacology. Thyrotropin / pharmacology

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  • (PMID = 19779036.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 9002-71-5 / Thyrotropin; BBX060AN9V / Hydrogen Peroxide; EC 1.6.3.- / NOX4 protein, human; EC 1.6.3.1 / CYBA protein, human; EC 1.6.3.1 / DUOX1 protein, human; EC 1.6.3.1 / NADPH Oxidase
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