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1. Wang L, Chang X, Yuan G, Zhao Y, Wang P: Expression of peptidylarginine deiminase type 4 in ovarian tumors. Int J Biol Sci; 2010;6(5):454-64
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  • [Title] Expression of peptidylarginine deiminase type 4 in ovarian tumors.
  • Peptidylarginine deiminase type 4 (PADI4) converts arginine residues into citrulline.
  • We utilized immunohistochemistry, real-time PCR and western blotting to analyze the expression of PADI4 in the tumor tissues and in the cell line that were cultured with estrodial-17β.
  • PADI4 was detected in serious cystadenocarcinoma (n=39, positivity=100%), clear cell cancer (n=7, positivity= 100%), mucinous cystadenocarcinoma (n=6, positivity=100%), dysgerminoma (n=6, positivity=100%), squamous cell tumor (n=6, positivity=100%), sibnet-ring cell carcinoma (n=6, positivity=100%), endodermal sinus tumor (n=6, positivity=100%), germ cell tumors (n=6, positivity=100%) and immature teratoma (n=6, positivity=100%).
  • However, PADI4 was either not detected or detected at low levels in granulosa cell tumor (n=6), malignant thecoma (n=6), ovarian cystadenoma (n=5) and normal ovarian tissue (n=11).
  • PADI4 was evenly distributed in the cytoplasm of tumor cells of serious cystadenocarcinoma that were classified as being grade II and III by histopathological scoring.
  • However, PADI4 showed granular cellular distribution in the tumor tissues that were isolated from grade I cystadenocarcinoma.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Estradiol / pharmacology. Estradiol / physiology. Female. Gene Expression / drug effects. Humans. Immunohistochemistry. Polymerase Chain Reaction. RNA, Messenger / metabolism

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  • (PMID = 20827398.001).
  • [ISSN] 1449-2288
  • [Journal-full-title] International journal of biological sciences
  • [ISO-abbreviation] Int. J. Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / RNA, Messenger; 4TI98Z838E / Estradiol; EC 3.- / Hydrolases; EC 3.5.3.15 / peptidylarginine deiminase type IV
  • [Other-IDs] NLM/ PMC2935668
  • [Keywords] NOTNLM ; Peptidylarginine deiminase type 4 (PADI4/PAD4) / estrodial-17β. / ovarian cancer (OCa)
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2. Rafii A, Ferron G, Lacroix-Triki M, Dalenc F, Gladieff L, Querleu D: Abdominal wall metastasis of ovarian carcinoma after low transverse abdominal incision: report of two cases and review of literature. Int J Gynecol Cancer; 2006 Jan-Feb;16 Suppl 1:334-7
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  • [Title] Abdominal wall metastasis of ovarian carcinoma after low transverse abdominal incision: report of two cases and review of literature.
  • Occurrence of parietal metastases after surgery for a suspect adnexal mass may worsen the prognosis of the disease.
  • However, it is not clear whether abdominal wall metastases is related to specific biologic features or simply to surgical mismanagement involving small incisions and traumatic extraction of the specimen, resulting in direct seeding of cancer cells.
  • We report two cases with development of parietal dissemination of ovarian carcinomas after Pfannenstiel incision.
  • The parietal extension of the disease may need major parietal resection that can worsen the functional and general outcome of the patients.
  • [MeSH-major] Adenocarcinoma, Mucinous / secondary. Granulosa Cell Tumor / secondary. Neoplasm Seeding. Ovarian Neoplasms / pathology. Peritoneal Neoplasms / secondary
  • [MeSH-minor] Abdominal Wall. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bleomycin / administration & dosage. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Female. Gynecologic Surgical Procedures. Humans. Ifosfamide / administration & dosage. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / surgery. Paclitaxel / administration & dosage

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  • (PMID = 16515617.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin; UM20QQM95Y / Ifosfamide; BEP protocol
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3. Meijera C, van Luyn MJ, Nienhuis EF, Blom N, Mulder NH, de Vries EG: Ultrastructural morphology and localisation of cisplatin-induced platinum-DNA adducts in a cisplatin-sensitive and -resistant human small cell lung cancer cell line using electron microscopy. Biochem Pharmacol; 2001 Mar 1;61(5):573-8
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  • [Title] Ultrastructural morphology and localisation of cisplatin-induced platinum-DNA adducts in a cisplatin-sensitive and -resistant human small cell lung cancer cell line using electron microscopy.
  • Ultrastructural morphology (transmission electron microscopy) and localisation of cisplatin-induced platinum (Pt)-DNA adducts (immunoelectron microscopy) were analysed in the human small cell lung cancer cell line GLC(4) and its 40-fold in vitro acquired cisplatin-resistant subline GLC(4)-CDDP, which is characterised by, among other things, a decreased DNA platination.
  • Immunoelectron microscopy showed Pt-DNA adducts primarily in the nucleus, preferentially at loci with high-density chromatin (e.g. heterochromatin, pars granulosa around nucleoli, condensed DNA in proliferating and apoptotic cells), and in mitochondria.
  • The level of detectable Pt-DNA adducts was cell cycle status-dependent.
  • In both cell lines, Pt-DNA adduct levels increased from non-dividing interphase cells to dividing cells and were highest in cells undergoing apoptosis.
  • [MeSH-major] Carcinoma, Small Cell / ultrastructure. Cisplatin / pharmacology. DNA Adducts / ultrastructure. Drug Resistance, Neoplasm / physiology
  • [MeSH-minor] Antibodies / immunology. Antineoplastic Agents / pharmacology. DNA, Neoplasm / drug effects. DNA, Neoplasm / metabolism. Humans. Immunohistochemistry. Microscopy, Electron. Tumor Cells, Cultured

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  • (PMID = 11239500.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antineoplastic Agents; 0 / DNA Adducts; 0 / DNA, Neoplasm; Q20Q21Q62J / Cisplatin
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4. Piura B, Wiznitzer A, Shaco-Levy R: Juvenile granulosa cell tumor of the ovary associated with hypercalcemia. Arch Gynecol Obstet; 2008 Mar;277(3):257-62
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  • [Title] Juvenile granulosa cell tumor of the ovary associated with hypercalcemia.
  • INTRODUCTION: Juvenile granulosa cell tumors (JGCTs) are rare ovarian neoplasms that typically occur in children and young women.
  • Paraneoplastic hypercalcemia occurs in 5% of ovarian malignancies with small cell and clear cell carcinoma being the commonest ovarian tumors associated with hypercalcemia.
  • After rectifying the hypercalcemia with saline hydration, furosemide, and anti-hypercalcemic drugs, the patient underwent unilateral salpingo-oophorectomy that demonstrated Stage IC ovarian JGCT.
  • Since serum PTH-i level was suppressed and the hypercalcemia did not recur after resection of the tumor, it is concluded that the hypercalcemia was caused by parathyroid hormone-related protein (PTH-rP) produced by the tumor.
  • [MeSH-major] Granulosa Cell Tumor / diagnosis. Hypercalcemia / etiology. Ovarian Neoplasms / diagnosis. Paraneoplastic Syndromes / diagnosis

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  • (PMID = 17849133.001).
  • [ISSN] 0932-0067
  • [Journal-full-title] Archives of gynecology and obstetrics
  • [ISO-abbreviation] Arch. Gynecol. Obstet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Parathyroid Hormone
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5. Kossoy G, Anisimov VN, Ben-Hur H, Kossoy N, Zusman I: Effect of the synthetic pineal peptide epitalon on spontaneous carcinogenesis in female C3H/He mice. In Vivo; 2006 Mar-Apr;20(2):253-7
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  • Treatment with Epitalon decreased the number of tumor-bearing mice with malignant tumors and prevented the development of metastases.
  • The mammary gland tumors were different variants of invasive ductal carcinomas.
  • In the ovaries, granulosa-cell tumors were found.
  • In control mice, metastases were found in 3 out of 9 tumor-bearing mice, all of them being from tumors of the reproductive organs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Intraductal, Noninfiltrating / drug therapy. Mammary Neoplasms, Animal / drug therapy. Neoplasm Metastasis / drug therapy. Neoplasms / drug therapy. Oligopeptides / pharmacology
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Female. Lung Neoplasms / drug therapy. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mice. Mice, Inbred C3H

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  • (PMID = 16634527.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligopeptides; O65P17785G / alanyl-glutamyl-aspartyl-glycine
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6. Ohno K, Araki N, Yanase T, Nawata H, Iida M: A novel nonradioactive method for measuring aromatase activity using a human ovarian granulosa-like tumor cell line and an estrone ELISA. Toxicol Sci; 2004 Dec;82(2):443-50
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  • [Title] A novel nonradioactive method for measuring aromatase activity using a human ovarian granulosa-like tumor cell line and an estrone ELISA.
  • In the current studies, we developed a novel nonradioactive method for measuring aromatase activity that uses a specific ELISA for estrone along with KGN human ovary granulosa-like carcinoma cells.
  • This cell line has relatively high aromatase activity, and because it lacks 17alpha-hydroxylase, it secretes little or no androstenedione, 17beta-estradiol, or estrone.
  • [MeSH-major] Aromatase / analysis. Estrone / analysis. Granulosa Cell Tumor / enzymology. Ovarian Neoplasms / enzymology. Xenobiotics / pharmacology
  • [MeSH-minor] Benomyl / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Cross Reactions. Enzyme Induction / drug effects. Enzyme Inhibitors / pharmacology. Enzyme-Linked Immunosorbent Assay. Female. Fungicides, Industrial / pharmacology. Humans. Reference Standards. Reproducibility of Results

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  • [ErratumIn] Toxicol Sci. 2005 Jan;83(1):204
  • [ErratumIn] Toxicol Sci. 2005 Feb;83(2):406
  • (PMID = 15456920.001).
  • [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 / Enzyme Inhibitors; 0 / Fungicides, Industrial; 0 / Xenobiotics; 2DI9HA706A / Estrone; EC 1.14.14.1 / Aromatase; TLW21058F5 / Benomyl
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7. Looijenga LH: Human testicular (non)seminomatous germ cell tumours: the clinical implications of recent pathobiological insights. J Pathol; 2009 Jun;218(2):146-62
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  • [Title] Human testicular (non)seminomatous germ cell tumours: the clinical implications of recent pathobiological insights.
  • Human germ cell tumours (GCTs) comprise several types of neoplasias with different pathogeneses and clinical behaviours.
  • Here, the so-called type II testicular GCTs (TGCTs), ie the seminomas and non-seminomas, will be reviewed with emphasis on pathogenesis and clinical implications.
  • TGCTs are omnipotent, able to generate all differentiation lineages, both embryonic and extra-embryonic, as well as the germ cell lineage itself.
  • The precursor lesion, composed of primordial germ cells/gonocytes, is referred to as carcinoma in situ of the testis (CIS) and gonadoblastoma of the dysgenetic gonad.
  • These pre-malignant cells retain embryonic characteristics, which probably explains the unique responsiveness of the derived tumours to DNA-damaging agents.
  • Development of CIS and gonadoblastoma is crucially dependent on the micro-environment created by Sertoli cells in the testis, and granulosa cells in the dysgenetic gonad.
  • OCT3/4 has high sensitivity and specificity for CIS/gonadoblastoma, seminoma, and embryonal carcinoma, and is useful for the detection of CIS cells in semen, thus a promising tool for non-invasive screening.
  • Overdiagnosis of CIS due to germ cell maturation delay can be avoided using immunohistochemical detection of stem cell factor (SCF).
  • Immunohistochemistry is helpful in making the distinction between seminoma and embryonal carcinoma, especially SOX17 and SOX2.
  • The availability of representative cell lines, both for seminoma and for embryonal carcinoma, allows mechanistic studies into the initiation and progression of this disease.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / pathology. Testicular Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Carcinoma in Situ / chemistry. Carcinoma in Situ / pathology. Gonadoblastoma / chemistry. Gonadoblastoma / pathology. Humans. Immunohistochemistry. Male. SOXB1 Transcription Factors / analysis. SOXF Transcription Factors / analysis. Stem Cell Factor / analysis. Young Adult

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  • (PMID = 19253916.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / SOXB1 Transcription Factors; 0 / SOXF Transcription Factors; 0 / Stem Cell Factor
  • [Number-of-references] 200
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8. Watari H, Blanchette-Mackie EJ, Dwyer NK, Watari M, Burd CG, Patel S, Pentchev PG, Strauss JF 3rd: Determinants of NPC1 expression and action: key promoter regions, posttranscriptional control, and the importance of a "cysteine-rich" loop. Exp Cell Res; 2000 Aug 25;259(1):247-56
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  • Mutations in the NPC1 gene cause Niemann-Pick type C disease, which is characterized by the accumulation of free cholesterol and other lipids in lysosomes.
  • Treatment of proliferating granulosa cells with 30 microM progesterone, which induces a reversible phenocopy of the cholesterol trafficking defect of Niemann-Pick type C disease, increased NPC1 mRNA levels threefold.
  • Cysteine residues in a "cysteine-rich" loop predicted to reside in the intralumenal compartment of vesicles containing NPC1 were mutated, resulting in proteins that were incapable of correcting the cholesterol trafficking defect in CT60 cells, a Chinese hamster cell line in which the endogenous NPC1 gene is inactivated.
  • The I1061T mutation is one of the most common mutations in Niemann-Pick type C disease.
  • [MeSH-major] Carrier Proteins. Membrane Glycoproteins. Niemann-Pick Diseases / genetics. Promoter Regions, Genetic / genetics. Proteins
  • [MeSH-minor] Animals. CHO Cells. Carcinoma, Hepatocellular. Cricetinae. Cysteine. Gene Expression Regulation / drug effects. Gene Expression Regulation / physiology. Humans. Lysosomes / physiology. Plasmids. Progesterone / pharmacology. Protein Structure, Tertiary. RNA Processing, Post-Transcriptional / drug effects. RNA Processing, Post-Transcriptional / genetics. RNA, Messenger / genetics. Transfection. Tumor Cells, Cultured. Zinc / metabolism

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 10942596.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / HD06274; United States / NINDS NIH HHS / NS / NS34339
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Membrane Glycoproteins; 0 / NPC1 protein, human; 0 / Proteins; 0 / RNA, Messenger; 4G7DS2Q64Y / Progesterone; J41CSQ7QDS / Zinc; K848JZ4886 / Cysteine
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9. Kesterson JP, Mhawech-Fauceglia P, Lele S: The use of bevacizumab in refractory ovarian granulosa-cell carcinoma with symptomatic relief of ascites: a case report. Gynecol Oncol; 2008 Dec;111(3):527-9
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  • [Title] The use of bevacizumab in refractory ovarian granulosa-cell carcinoma with symptomatic relief of ascites: a case report.
  • BACKGROUND: The potential role of bevacizumab in the treatment of ovarian granulosa-cell tumors has not been evaluated.
  • CASE: An 82 year old woman with refractory ovarian granulosa-cell carcinoma was treated with bevacizumab with symptomatic relief of ascites.
  • CONCLUSION: Bevacizumab may have a role in the management of malignant ascites in the patient with refractory granulosa-cell carcinoma of the ovary which should be confirmed in a larger series of well selected patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Granulosa Cell Tumor / drug therapy. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Ascites / drug therapy. Bevacizumab. Female. Humans. Paclitaxel / administration & dosage

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  • (PMID = 18710781.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA108456
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab; P88XT4IS4D / Paclitaxel
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10. Hirsh L, Dantes A, Suh BS, Yoshida Y, Hosokawa K, Tajima K, Kotsuji F, Merimsky O, Amsterdam A: Phosphodiesterase inhibitors as anti-cancer drugs. Biochem Pharmacol; 2004 Sep 15;68(6):981-8
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  • [Title] Phosphodiesterase inhibitors as anti-cancer drugs.
  • Unfortunately substances elevating cAMP such as forskolin, 8-bromo-cAMP, 8-chloro-cAMP, monobutiryl or dibutiryl cAMP are not recommended to be used as anti-cancer drugs because of their high cytotoxicity.
  • In contrast blockers of phosphodieterases such as theophylline and aminophylline, which could elevate intracellular cAMP, are commonly used as anti-asthma drugs reaching concentrations in the blood of 10-20 microg/ml.
  • We tested the effectiveness of theophylline and aminophylline to induce cell death alone or in combination with common anti-cancer drugs such as cisplatin and gemcitabine (gemzar).
  • We examined such drug combinations in the induction of cell death in a variety of carcinoma cell lines derived from human ovarian, prostate and lung cancer and in granulosa cell line transformed by SV40 and Ras oncogene.
  • While theophylline could induce moderate cell death alone, at 20-25 microg/ml concentrations, aminophylline was ineffective at this concentration.
  • Theophylline (at 15-25 ng/ml) was found in all four representative cell lines to synergize with gemcitabine or cisplatin to induce programmed cell death, which permits a reduction in the effective doses of cisplatin and gemcitabine by 2-3-fold.
  • Such a reduction was proportional to the extent of apoptosis induced by theophylline as well as by the combined drug treatments.
  • Therefore, we propose that theophylline should be considered as a potential anti-cancer drug in combination with other chemotherapeutic drugs.
  • A clinical trial, using theophylline as an anti-cancer drug, is currently being conducted in lung cancer patients.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Phosphodiesterase Inhibitors / pharmacology. Xanthines / pharmacology
  • [MeSH-minor] Animals. Cell Division / drug effects. Drug Synergism. Female. Humans. Lung Neoplasms / pathology. Male. Ovarian Neoplasms / pathology. Theophylline / pharmacology. Tumor Cells, Cultured

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  • (PMID = 15313391.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phosphodiesterase Inhibitors; 0 / Xanthines; 28109-92-4 / methylxanthine; C137DTR5RG / Theophylline
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11. Crist KA, Zhang Z, You M, Gunning WT, Conran PB, Steele VE, Lubet RA: Characterization of rat ovarian adenocarcinomas developed in response to direct instillation of 7,12-dimethylbenz[a]anthracene (DMBA) coated suture. Carcinogenesis; 2005 May;26(5):951-7
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  • Human ovarian cancer is predominantly of epithelial cell origin (>90% of malignant tumors) and most often presents at an advanced stage with poor prognosis.
  • Most animal models of ovarian carcinoma yield thecal/granulosa cell tumors, rather than adenocarcinomas.
  • DMBA-treated ovaries showed a nearly complete loss of primary follicles and degeneration of granulosa cells at 16 weeks, consistent with the known toxic response of the ovary to direct DMBA application.
  • Ovarian tumors in DMBA-treated rats were first noted at 26 weeks post implantation reaching a cumulative tumor incidence of 77% (23/30) at 52 weeks.
  • Controls showed no evidence of tumor at 52 weeks (0/31).
  • Tumor histology was distributed as well differentiated adenocarcinoma (1/23), poorly differentiated adenocarcinoma (8/23), thecal/granulosa cell tumor (8/23), undifferentiated sarcoma (5/23) and one undifferentiated carcinoma with no adeno character.
  • Epithelial derived tumor cells positively react with antibodies to cytokeratin (8/8), epithelial cell adhesion molecule (Ep-CAM 5/5) and prostaglandin synthetase-1 (COX-1 4/4).
  • Vimentin positive epithelial cells when present in adenocarcinomas (4/7), showed perinuclear staining, quite distinct from the uniformly stained stromal cells in thecal/granulosa cell tumors (8/8).
  • The thecal/granulosa cell tumors were Ep-CAM negative (0/5) and weakly COX-1 positive (4/4).
  • Thus, the DMBA suture model in rats yields epithelial derived tumors histologically similar to humans and should prove suitable for the testing of preventive or therapeutic agents.
  • [MeSH-minor] Animals. Female. Immunohistochemistry. Rats. Rats, Inbred WF. Sutures

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  • (PMID = 15695234.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-05103
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene
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12. Turbiner J, Moreno-Bueno G, Dahiya S, Sánchez-Estevez C, Hardisson D, Prat J, Oliva E, Palacios J: Clinicopathological and molecular analysis of endometrial carcinoma associated with tamoxifen. Mod Pathol; 2008 Aug;21(8):925-36
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  • [Title] Clinicopathological and molecular analysis of endometrial carcinoma associated with tamoxifen.
  • Tamoxifen has been associated with increased risk of endometrial carcinoma, although the exact mechanism of action is unknown.
  • The aim of our study was to seek a possible correlation between endometrial carcinoma, tamoxifen exposure and MSI, PTEN, beta-catenin and K-ras abnormalities.
  • A group of 18 patients with endometrial carcinoma following treatment with tamoxifen were selected.
  • A control group included 15 patients with endometrial carcinoma and associated ovarian hyperthecosis and one patient with endometrial carcinoma and adult granulosa cell tumor of the ovary, chosen because both conditions are associated with increased production of estrogen and increased risk of endometrial carcinoma development.
  • The second control group included 27 randomly selected consecutive patients with endometrial carcinoma without identifiable associated conditions.
  • There were 16 endometrioid endometrial carcinomas, one mixed carcinoma and one clear cell carcinoma among patients in the tamoxifen group.
  • All patients with ovarian hyperthecosis and adult granulosa cell tumor had endometrioid endometrial carcinoma.
  • In the random control group, there were 26 endometrioid endometrial carcinomas and one carcinosarcoma.
  • In conclusion, there was a direct relationship between tamoxifen exposure and overexpression of beta-catenin oncoprotein, which is known to play a major role in the pathogenesis of estrogen-driven, type I endometrial adenocarcinoma.
  • [MeSH-major] Antineoplastic Agents, Hormonal / adverse effects. Endometrial Neoplasms / chemically induced. Endometrial Neoplasms / pathology. Tamoxifen / adverse effects
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Carcinoma, Endometrioid / chemically induced. Carcinoma, Endometrioid / genetics. Carcinoma, Endometrioid / pathology. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Microsatellite Instability. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm Staging. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / metabolism. Proto-Oncogene Proteins p21(ras) / genetics. Proto-Oncogene Proteins p21(ras) / metabolism. Survival Rate. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 18500270.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Neoplasm Proteins; 0 / beta Catenin; 094ZI81Y45 / Tamoxifen; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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13. Dong Y, Kaushal A, Bui L, Chu S, Fuller PJ, Nicklin J, Samaratunga H, Clements JA: Human kallikrein 4 (KLK4) is highly expressed in serous ovarian carcinomas. Clin Cancer Res; 2001 Aug;7(8):2363-71
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  • [Title] Human kallikrein 4 (KLK4) is highly expressed in serous ovarian carcinomas.
  • Previous studies indicated that a new member of the human kallikrein (KLK) gene family, KLK4, was expressed in prostate, breast, and endometrial carcinoma cell lines and may have potential as a tumor marker.
  • The aim of this study was to examine the expression of KLK4 in the normal ovary and ovarian tumors of different histology, stage, and differentiation and to determine its association with ovarian tumor progression.
  • Using reverse transcription-PCR, Southern blot, and densitometry analyses, we found the level of KLK4 expression was higher in late stage serous (SER) epithelial-derived ovarian carcinomas than in normal ovaries, mucinous epithelial tumors, and granulosa cell tumors.
  • KLK4 was highly expressed in all of the SER ovarian carcinoma cell lines (eight of eight), SER epithelial carcinomas (11 of 11), and two adenomas, whereas it was expressed at a lower level (or not at all) in normal ovaries (four of six), mucinous epithelial tumors (three of four), endometrioid carcinomas (four of five), clear cell carcinomas (two of three), or granulosa cell tumors (three of six).
  • Of particular interest, KLK4 mRNA variants were detected in SER ovarian carcinoma cell lines and primary cultured ovarian tumor cells, but they were not present in normal ovaries.
  • In situ hybridization analysis showed that KLK4 mRNA transcripts are localized to adenocarcinoma cells of ovarian tumor tissues.
  • Similarly, immunohistochemical staining of ovarian carcinoma sections showed immunoreactivity to KLK4 protein product (hK4) antipeptide antibodies.
  • In addition, intracellular hK4 levels, as detected on Western blot analysis, were induced by 100 nM estrogen treatment of the estrogen receptor positive ovarian carcinoma cell line OVCAR-3, >8-24 h.
  • Moreover, hK4 may be a candidate marker for the diagnosis and/or monitoring of ovarian epithelial carcinomas.
  • [MeSH-minor] Amino Acid Sequence. Blotting, Western. DNA, Complementary / chemistry. DNA, Complementary / genetics. Estradiol / pharmacology. Female. Gene Expression Regulation, Neoplastic / drug effects. Genetic Variation. Humans. Immunohistochemistry. In Situ Hybridization. Molecular Sequence Data. Ovary / metabolism. Ovary / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Sequence Alignment. Sequence Analysis, DNA. Sequence Homology, Amino Acid. Transcription, Genetic. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism

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  • (PMID = 11489814.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / RNA, Messenger; 4TI98Z838E / Estradiol; EC 3.4.21.- / Kallikreins; EC 3.4.21.- / kallikrein 4
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14. Nishi Y, Yanase T, Mu Y, Oba K, Ichino I, Saito M, Nomura M, Mukasa C, Okabe T, Goto K, Takayanagi R, Kashimura Y, Haji M, Nawata H: Establishment and characterization of a steroidogenic human granulosa-like tumor cell line, KGN, that expresses functional follicle-stimulating hormone receptor. Endocrinology; 2001 Jan;142(1):437-45
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  • [Title] Establishment and characterization of a steroidogenic human granulosa-like tumor cell line, KGN, that expresses functional follicle-stimulating hormone receptor.
  • We established a steroidogenic human ovarian granulosa-like tumor cell line, designated KGN, from a patient with invasive ovarian granulosa cell carcinoma.
  • These findings showed a pattern similar to that of steroidogenesis in human granulosa cells, thus allowing analysis of naturally occurring steroidogenesis in human granulosa cells.
  • Fas-mediated apoptosis of KGN was also observed, which mimicked the physiological regulation of apoptosis in normal human granulosa cells.
  • Based on these findings, this cell line is considered to be a very useful model for understanding the regulation of steroidogenesis, cell growth, and apoptosis in human granulosa cells.
  • [MeSH-major] Granulosa Cell Tumor / pathology. Ovarian Neoplasms / pathology. Receptors, FSH / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Aromatase / metabolism. Bucladesine / pharmacology. Cell Culture Techniques / methods. Cell Division. Chromosome Aberrations. Cyclic AMP / metabolism. Female. Follicle Stimulating Hormone / metabolism. Humans. Interferon-gamma / pharmacology. Karyotyping. Middle Aged. Pregnenolone / secretion. Progesterone / metabolism. Progesterone / secretion. Recombinant Proteins. Tetradecanoylphorbol Acetate / pharmacology. Tumor Cells, Cultured

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  • (PMID = 11145608.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, FSH; 0 / Recombinant Proteins; 4G7DS2Q64Y / Progesterone; 63X7MBT2LQ / Bucladesine; 73R90F7MQ8 / Pregnenolone; 82115-62-6 / Interferon-gamma; 9002-68-0 / Follicle Stimulating Hormone; E0399OZS9N / Cyclic AMP; EC 1.14.14.1 / Aromatase; NI40JAQ945 / Tetradecanoylphorbol Acetate
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15. Ghanayem BI, Nyska A, Haseman JK, Bucher JR: Acrylonitrile is a multisite carcinogen in male and female B6C3F1 mice. Toxicol Sci; 2002 Jul;68(1):59-68
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  • In general, there were dose-related increases in urinary thiocyanate and N-acetyl-S-(2-cyanoethyl)-L-cysteine concentrations in all dosed groups of mice and at all time points.
  • The incidence of forestomach papillomas and carcinomas was increased in mice of both sexes in association with an increase in forestomach epithelial hyperplasia.
  • The incidence of Harderian gland adenomas and carcinomas was also markedly increased in the acrylonitrile-dosed groups.
  • In female mice, the incidence of benign or malignant granulosa cell tumors (combined) in the ovary in the 10 mg/kg dose group was greater than that in the vehicle control group, but because of a lack of dose response, this was considered an equivocal finding.
  • The incidences of alveolar/bronchiolar adenoma or carcinoma (combined) were significantly increased in female mice treated with acrylonitrile at 10 mg/kg/day for 2 years.
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Female. Longevity / drug effects. Male. Mice. Mice, Inbred Strains

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  • (PMID = 12075111.001).
  • [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, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; MP1U0D42PE / Acrylonitrile
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16. Kang SK, Tai CJ, Cheng KW, Leung PC: Gonadotropin-releasing hormone activates mitogen-activated protein kinase in human ovarian and placental cells. Mol Cell Endocrinol; 2000 Dec 22;170(1-2):143-51
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  • Considering that the action of gonadotropin-releasing hormone (GnRH) may be mediated via different signaling pathways in extrapituitary tissues, in the present study we investigated the role of the human GnRH receptor (GnRHR) in activating mitogen-activated protein kinases (MAPKs), which regulate cell growth, division, and differentiation.
  • Cell cultures were treated with various concentrations of a GnRH agonist, (D-Ala(6))-GnRH, for 5 min. (D-Ala(6))-GnRH stimulated a rapid activation of P-MAPK in human granulosa-luteal cells (hGLCs) and immortalized extravillous trophoblast (IEVT) cells.
  • Interestingly, (D-Ala(6))-GnRH treatment of ovarian cancer (OVCAR-3) and placental carcinoma (JEG-3) cells induced a biphasic regulatory pattern in P-MAPK activity.
  • To our knowledge, this is the first demonstration that (1) GnRH induces activation of the MAPK signaling pathway in normal and carcinoma cells of the human ovary and placenta, and (2) MAPK mediates the direct action of GnRH on progesterone production in hGLCs.
  • [MeSH-minor] Animals. Chorionic Gonadotropin / drug effects. Chorionic Gonadotropin / genetics. Dose-Response Relationship, Drug. Female. Humans. Immunoblotting. Mice. Pituitary Gland / cytology. Progesterone / secretion. RNA, Messenger / drug effects. Trophoblasts / cytology. Tumor Cells, Cultured

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  • (PMID = 11162898.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin; 0 / RNA, Messenger; 33515-09-2 / Gonadotropin-Releasing Hormone; 4G7DS2Q64Y / Progesterone; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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17. Toxicology and carcinogenesis studies of acrylonitrile (CAS No. 107-13-1) in B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2001 Oct;(506):1-201
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  • Pathology Findings The incidences of squamous cell papilloma, squamous cell carcinoma, and squamous cell papilloma or carcinoma (combined) of the forestomach occurred with positive trends in males and females, and were present in 50% or greater of mice administered 10 or 20 mg/kg.
  • The incidences of harderian gland adenoma and adenoma or carcinoma (combined) were significantly increased in all dosed groups of males and in 10 and 20 mg/kg females, and the incidence of harderian gland hyperplasia was significantly increased in 10 mg/kg males.
  • The incidence of benign or malignant granulosa cell tumor (combined) in the ovary of 10 mg/kg females was greater than that in the vehicle controls.
  • The incidence of alveolar/bronchiolar adenoma or carcinoma (combined) in 10 mg/kg females was significantly increased.
  • [MeSH-minor] Animals. Body Weight / drug effects. Carcinogenicity Tests. Female. Male. Mice. Mice, Inbred Strains. Mutagenicity Tests. Neoplasms / chemically induced. Neoplasms / pathology. Sex Characteristics. Survival Analysis. Time Factors

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  • (PMID = 11803701.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; MP1U0D42PE / Acrylonitrile
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18. Göcze P, Krommer K, Csermely T, Cziráky K, Garamvölgyi Z, Kovács K, Szabó I: [Ovulation induction therapy and malignant ovarian cancer]. Orv Hetil; 2000 Jan 9;141(2):71-5
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  • [Title] [Ovulation induction therapy and malignant ovarian cancer].
  • 92 of them had malignant granulosa cell tumor.
  • 236 questionnaires were shared out among patients with malignant ovarian tumor, who were treated between 1990 and 1997.
  • None of the 45 patients with granulosa cell tumors received induction therapy.
  • The number of patients admitted because of malignant ovarian tumor before and after the induction therapy was also compared.
  • Since 1986 in the in vitro fertilization program of the clinic nearly 1,500 patients were treated with effected ovulation induction drugs causing superovulation.
  • The authors don't know of any development of malignant ovarian tumor, and 732 woman have confirmed this fact.
  • [MeSH-major] Granulosa Cell Tumor / etiology. Ovarian Neoplasms / etiology. Ovulation Induction / adverse effects

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  • (PMID = 10686780.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] HUNGARY
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