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2. Nishida T, Nishida N: Reinstatement of "germinal epithelium" of the ovary. Reprod Biol Endocrinol; 2006;4:42
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  • BACKGROUND: The existing dogma that the former term ovarian "germinal epithelium" resulted from a mistaken belief that it could give rise to new germ cells is now strongly challenged.
  • They showed the new oocyte with zona pellucida and granulosa cells, both originated from the surface epithelium arising from mesenchymal cells in the tunica albuginea, and stressed that the human ovary could form primary follicles throughout the reproductive period.
  • This gives a big impact not only to the field of reproductive medicine, but also to the oncologic area.
  • The surface epithelium is regarded as the major source of ovarian cancers, and most of the neoplasms exhibit the histology resembling müllerian epithelia.
  • Since the differentiating capability of the surface epithelium has now expanded, the histologic range of the neoplasms in this category may extend to include both germ cell tumors and sex cord-stromal cell tumors.
  • SUMMARY: Since the oogenic capability of ovarian surface cells has been proven, it is now believed that the oocytes can originate from them.
  • [MeSH-major] Epithelial Cells / cytology. Epithelium / growth & development. Ovary / cytology. Ovary / growth & development. Ovum / cytology. Ovum / growth & development
  • [MeSH-minor] Animals. Female. Humans. Oocytes / cytology. Oocytes / growth & development

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  • [Cites] Eur J Obstet Gynecol Reprod Biol. 2000 Jun;90(2):125-7 [10825629.001]
  • [Cites] Reprod Biol Endocrinol. 2004 Apr 28;2:20 [15115550.001]
  • [Cites] Endocrine. 2005 Apr;26(3):301-16 [16034186.001]
  • [Cites] Cancer. 1998 Sep 1;83(5):965-70 [9731901.001]
  • [Cites] Reprod Biol Endocrinol. 2005;3:17 [15871747.001]
  • [Cites] Am J Reprod Immunol. 1995 Apr;33(4):323-40 [7546251.001]
  • (PMID = 16923182.001).
  • [ISSN] 1477-7827
  • [Journal-full-title] Reproductive biology and endocrinology : RB&E
  • [ISO-abbreviation] Reprod. Biol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 17
  • [Other-IDs] NLM/ PMC1560142
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4. Dickinson RE, Myers M, Duncan WC: Novel regulated expression of the SLIT/ROBO pathway in the ovary: possible role during luteolysis in women. Endocrinology; 2008 Oct;149(10):5024-34
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  • In Drosophila the Slit gene product, a secreted glycoprotein, acts as a ligand for the roundabout (robo) transmembrane receptor.
  • Together they influence the guidance and migration of neuronal and nonneuronal cells.
  • ROBO1, SLIT2, and SLIT3 are also inactivated in human cancers and may regulate apoptosis and metastasis.
  • Because processes such as apoptosis and tissue remodeling occur during the regression of the CL, the aim of this study was to investigate the expression, regulation, and effects of the SLIT and ROBO genes in human luteal cells.
  • Immunohistochemistry and RT-PCR revealed that SLIT2, SLIT3, ROBO1, and ROBO2 are expressed in luteal steroidogenic cells and fibroblast-like cells of the human CL.
  • Additionally, hCG significantly inhibited SLIT2, SLIT3, and ROBO2 expression in cultured luteinized granulosa cells (P<0.05).
  • Blocking SLIT-ROBO activity increased migration and significantly decreased levels of apoptosis in primary cultures of luteal cells (P<0.05).
  • [MeSH-major] Corpus Luteum / cytology. Corpus Luteum / physiology. Luteolysis / physiology. Nerve Tissue Proteins / genetics. Receptors, Immunologic / genetics
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Cells, Cultured. Chorionic Gonadotropin / pharmacology. Female. Fibroblasts / cytology. Fibroblasts / physiology. Gene Expression / drug effects. Gene Expression / physiology. Granulosa Cells / cytology. Granulosa Cells / physiology. Humans. Hydrocortisone / pharmacology. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Luteal Cells / cytology. Luteal Cells / physiology. Membrane Proteins / genetics. Membrane Proteins / metabolism. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism

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  • (PMID = 18566128.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / ROBO2 protein, human; 0 / ROBO3 protein, human; 0 / ROBO4 protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Immunologic; 0 / SLIT1 protein, human; 0 / SLIT3 protein, human; 0 / Slit homolog 2 protein; 0 / roundabout protein; WI4X0X7BPJ / Hydrocortisone
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5. Leuschner C, Hansel W: Targeting breast and prostate cancers through their hormone receptors. Biol Reprod; 2005 Nov;73(5):860-5
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  • [Title] Targeting breast and prostate cancers through their hormone receptors.
  • A targeted treatment that effectively destroys human breast, prostate, ovarian, and testicular cancer cells that express luteinizing hormone/chorionic gonadotropin (LH/CG) receptors has been developed.
  • Because these conjugates act primarily by destroying cell membranes, their effects are independent of cell proliferation.
  • In a series of independent experiments conducted in three different laboratories, the validity of the concept has been established, and it has been shown that the LH/CG receptor capacity of the cancer cells is directly related to the sensitivity of the lytic peptide conjugates.
  • Sensitivity to the drugs can be increased by pretreating prostate or breast cancer cells with FSH or estradiol to up-regulate LH/CG receptors.
  • A series of 23 in vivo experiments involving a total of 1630 nude mice bearing xenografts of human prostate or breast cancer cells showed convincingly that all three lytic peptide-betaCG compounds were highly effective in destroying tumors and reducing tumor burden.
  • Hecate-betaCG was less effective in mice bearing ovarian epithelial cancer cell xenografts, but was highly effective in treating granulosa cell tumors in transgenic mice.
  • In addition, Hecate-betaCG and Phor14-betaCG were highly effective in targeting and destroying prostate and breast cancer cell metastases in the presence or absence of the primary tumors.
  • Although effective in vitro, neither Hecate nor Phor14 alone were effective in reducing primary tumor volume or burden in nude mice bearing prostate or breast cancer xenografts.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Prostatic Neoplasms / drug therapy. Receptors, LH / drug effects
  • [MeSH-minor] Animals. Cell Membrane / drug effects. Chorionic Gonadotropin, beta Subunit, Human / pharmacology. Drug Screening Assays, Antitumor. Female. Humans. Male. Melitten / analogs & derivatives. Melitten / pharmacology. Peptides / pharmacology. Testicular Neoplasms / drug therapy. Testicular Neoplasms / metabolism

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  • (PMID = 16033998.001).
  • [ISSN] 0006-3363
  • [Journal-full-title] Biology of reproduction
  • [ISO-abbreviation] Biol. Reprod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Peptides; 0 / Receptors, LH; 0 / hecate-chorionic gonadotropin beta-subunit conjugate; 20449-79-0 / Melitten
  • [Number-of-references] 38
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6. Zaleska M, Bodek G, Jana B, Hansel W, Ziecik AJ: Targeted destruction of normal and cancer cells through lutropin/choriogonadotropin receptors using Hecate-betaCG conjugate. Exp Clin Endocrinol Diabetes; 2003 May;111(3):146-53
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  • [Title] Targeted destruction of normal and cancer cells through lutropin/choriogonadotropin receptors using Hecate-betaCG conjugate.
  • A recent approach to cancer treatment is destruction of malignant and non-malignant tumors by hormonally targeted lytic peptides.
  • The presence of lutropin/choriogonadotropin (LH/CG) receptors has been confirmed in several cancer cells (e.g. breast, ovarian, and prostate).
  • To test the hypothesis that Hecate-betaCG selectively destroys porcine granulosa and luteal cells, and Leydig cancer cell line (BLT-1) possessing LH/CG receptors, the conjugate was added to culture media at different concentrations of 0.5 to 10 micro M.
  • Spleen cells and late passage of granulosa cancer cell line (KK-1) not-possessing LH/CG receptors were used as controls.
  • The toxicity of Hecate-betaCG conjugate was concentration-dependent in all cell types but different among various cells.
  • The toxicity of the conjugate to treated cells was closely correlated with the number of LH/CG receptors per cell.
  • At low concentration (1 micro M), Hecate-betaCG was more cytotoxic to cells bearing LH/CG receptors than to controls (p < 0.01).
  • In contrast to cells possessing LH/CG receptors, cancer cell line KK-1 and spleen cells were sensitive only at concentration of 5 micro M (p < 0.001).
  • We conclude that Hecate-betaCG selectively kills cells expressing LH/CG receptors; its toxicity is dependent on the number of binding sites for LH/CG.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Chorionic Gonadotropin / metabolism. Chorionic Gonadotropin / pharmacology. Melitten / analogs & derivatives. Melitten / pharmacology. Neoplasms / physiopathology. Receptors, Gonadotropin / metabolism. Receptors, LH / drug effects
  • [MeSH-minor] Animals. Cell Death. Cells, Cultured. Corpus Luteum / cytology. Corpus Luteum / drug effects. Dose-Response Relationship, Drug. Drug Combinations. Female. Granulosa Cells / drug effects. Leydig Cells / drug effects. Male. Osmolar Concentration. Protein Isoforms / administration & dosage. Protein Isoforms / pharmacology. Spleen / cytology. Spleen / drug effects. Swine

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  • (PMID = 12784188.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chorionic Gonadotropin; 0 / Drug Combinations; 0 / Protein Isoforms; 0 / Receptors, Gonadotropin; 0 / Receptors, LH; 0 / hecate 1; 20449-79-0 / Melitten
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7. Yoshida Y, Hosokawa K, Dantes A, Kotsuji F, Kleinman HK, Amsterdam A: Role of laminin in ovarian cancer tumor growth and metastasis via regulation of Mdm2 and Bcl-2 expression. Int J Oncol; 2001 May;18(5):913-21
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  • [Title] Role of laminin in ovarian cancer tumor growth and metastasis via regulation of Mdm2 and Bcl-2 expression.
  • Ovarian cancer is among the most lethal cancers in women because of its high metastatic potential and lack of response to therapy.
  • An experimental model to study this disease was developed using a transformed granulosa cell line expressing a mutant p53 and Ha-ras.
  • In contrast, when cells were injected in the presence of gelatin, development of tumors was slower and no metastases were observed by day 21.
  • Cells were co-injected with laminin-1 and active laminin peptides from the alpha1; (A13: RQVFQVAYIIIKA, A12: WVTVTLDL RQVFQ, AG73: LQVQLSIR, IKVAV) and beta1 (YIGSR) chains.
  • [MeSH-major] Laminin / physiology. Nuclear Proteins. Ovarian Neoplasms / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Cell Division / drug effects. Disease Models, Animal. Female. Humans. Mice. Mice, Nude. Microscopy, Electron, Scanning. Neoplasm Metastasis. Neoplasm Transplantation. Peptide Fragments / physiology. Proto-Oncogene Proteins c-mdm2. Tumor Cells, Cultured / metabolism. Tumor Suppressor Protein p53 / metabolism. Up-Regulation. bcl-2-Associated X Protein

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  • (PMID = 11295035.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Laminin; 0 / Nuclear Proteins; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Mdm2 protein, mouse; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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8. Phan B, Rakenius A, Pietrowski D, Bettendorf H, Keck C, Herr D: hCG-dependent regulation of angiogenic factors in human granulosa lutein cells. Mol Reprod Dev; 2006 Jul;73(7):878-84
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  • [Title] hCG-dependent regulation of angiogenic factors in human granulosa lutein cells.
  • As prerequisite for development and maintenance of many diseases angiogenesis is of particular interest in medicine.
  • Pathologic angiogenesis takes place in chronic arthritis, collagen diseases, arteriosclerosis, retinopathy associated with diabetes, and particularly in cancers.
  • After ovulation the corpus luteum is formed by rapid vascularization of initially avascular granulosa lutein cell tissue.
  • In order to gain further insights in the regulatory mechanisms of angiogenesis in the ovary, we investigated these mechanisms in cell culture of human granulosa lutein cells.
  • Our results provide evidence that hCG determines growth and development of the corpus luteum by mediating angiogenic pathways in human granulosa lutein cells.
  • [MeSH-major] Angiogenesis Inducing Agents. Chorionic Gonadotropin / metabolism. Granulosa Cells / metabolism. Luteal Cells / metabolism. Neovascularization, Physiologic
  • [MeSH-minor] Cells, Cultured. Connective Tissue Growth Factor. Cytokines / genetics. Down-Regulation. Female. Fibroblast Growth Factors / genetics. Humans. Immediate-Early Proteins / genetics. Insulin-Like Growth Factor Binding Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Leptin / genetics. Tissue Inhibitor of Metalloproteinase-1 / genetics. Up-Regulation

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  • (PMID = 16596638.001).
  • [ISSN] 1040-452X
  • [Journal-full-title] Molecular reproduction and development
  • [ISO-abbreviation] Mol. Reprod. Dev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / CTGF protein, human; 0 / Chorionic Gonadotropin; 0 / Cytokines; 0 / Immediate-Early Proteins; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Leptin; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / insulin-like growth factor binding protein-related protein 1; 137497-38-2 / midkine; 139568-91-5 / Connective Tissue Growth Factor; 62031-54-3 / Fibroblast Growth Factors
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9. Hutz RJ, Carvan MJ, Baldridge MG, Conley LK, Heiden TK: Environmental toxicants and effects on female reproductive function. Tren Reprod Bio; 2006;2:1-11
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  • From reports of large industrial and other accidents, or from experimental studies, dioxin exposure has been correlated in animal models and/or humans with chloracne of the skin, organ cancers, hepatotoxicity, gonadal and immune changes, pulmonary and other diseases such as diabetes, skewing of the sex ratio, and infertility.
  • We have demonstrated that the aromatic hydrocarbon receptor (AHR) that binds dioxin in tissues is localized in zebrafish, rat and rhesus monkey (Macaca mulatta) ovaries and in rat and human luteinizing granulosa cells (GC) (among other tissues), that labeled dioxin is specifically localized to granulosa cells of the ovarian follicle as observed by autoradiography, and that incubations of GC or ovarian fragments with environmentally relevant concentrations (fM to nM) of dioxin inhibit estradiol secretion significantly.

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  • (PMID = 18516253.001).
  • [Journal-full-title] Trends in reproductive biology
  • [ISO-abbreviation] Tren Reprod Bio
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R15 ES011569; United States / NCRR NIH HHS / RR / RR000167-440137; United States / NCRR NIH HHS / RR / RR000167-450137; United States / NIEHS NIH HHS / ES / ES011569-01; United States / NIEHS NIH HHS / ES / ES008342-04; United States / NIEHS NIH HHS / ES / P30 ES004184; United States / NCRR NIH HHS / RR / RR000167-465517
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] India
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10. 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.
  • The current study focused on the expression of PADI4 in various subtypes of ovary cancers, and this study investigated the effects of estrogen on PADI4 expression in SKOV-3 cells that originated from ovary tumors.
  • 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.
  • The study also detected an increased level of PADI4 in SKOV-3 cells that were incubated with estrodial-17β in the range of 10(-12) to 10(-4)M.
  • The results suggest an important role for PADI4 in the tumorigenesis of ovary cancers that are under the regulation of estrogen.
  • [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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11. 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.
  • It is well known that high intracellular levels of cAMP can effectively kill cancer cells in vitro.
  • 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.
  • Screening of other phosphodiesterase blockers, which are not severely toxic, could open a possibility to improved chemotherapeutic cancer treatments with reduced undesired side-effects.
  • 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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12. Yanase T, Mu YM, Nishi Y, Goto K, Nomura M, Okabe T, Takayanagi R, Nawata H: Regulation of aromatase by nuclear receptors. J Steroid Biochem Mol Biol; 2001 Dec;79(1-5):187-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We investigated the effects of a nuclear receptor system constituted by retinoid X receptor (RXR) and its heterodimer partner on the aromatase activity in a cultured MCF-7 human breast cancer cell line and also in human ovarian granulosa cells, using each selective ligand for retinoic acid receptor, RAR (TTNPB), retinoid X receptor, RXR (LG100268), PPARgamma (troglitazone), and vitamin D3 receptor (cholecalciferol).
  • In MCF-7 cells, the combined treatment with TTNPB and LG100268 caused a dramatic stimulation of the aromatase activity.
  • These results suggest that a nuclear receptor system constituted by a RAR:RXR heterodimer is involved in the regulation of aromatase activity in MCF-7 breast cancer cells.
  • In cultured human ovarian granulosa cells obtained from patients who underwent in vitro fertilization, troglitazone or LG100268 alone decreased the aromatase activity, while the combined treatment caused an even greater reduction in this activity.
  • Little effect of other specific ligands for RXR heterodimer partners may support the notion that the effects of troglitazone and/or LG100268 in human granulosa cells may be mediated through the specific activation of PPARgamma:RXR heterodimer system.
  • Since similar manners of effects of several PPARgamma ligands and/or LG100268 on the aromatase activity were observed in a newly established human ovarian granulosa cancer cell line, KGN, we performed the detailed analysis of the mechanisms of these effects using this cell line.
  • In conclusion, RAR:RXR and PPARgamma:RXR heterodimer nuclear receptor systems may be other important modulators of estrogen production in human breast cancer cells and ovarian granulosa cells, respectively.
  • [MeSH-major] Aromatase / metabolism. Breast Neoplasms / metabolism. Granulosa Cells / metabolism. Receptors, Cytoplasmic and Nuclear / metabolism. Thiazolidinediones
  • [MeSH-minor] Benzoates / pharmacology. Cholecalciferol / pharmacology. Chromans / pharmacology. Female. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Ligands. Nicotinic Acids / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, Calcitriol / metabolism. Receptors, Retinoic Acid / metabolism. Retinoid X Receptors. Retinoids / pharmacology. Tetrahydronaphthalenes / pharmacology. Thiazoles / pharmacology. Transcription Factors / metabolism. Tumor Cells, Cultured

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  • (PMID = 11850224.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzoates; 0 / Chromans; 0 / LG 100268; 0 / Ligands; 0 / Nicotinic Acids; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Calcitriol; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / Retinoids; 0 / Tetrahydronaphthalenes; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Transcription Factors; 1C6V77QF41 / Cholecalciferol; 71441-28-6 / 4-(2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl)benzoic acid; EC 1.14.14.1 / Aromatase; I66ZZ0ZN0E / troglitazone
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13. Freimann S, Ben-Ami I, Hirsh L, Dantes A, Halperin R, Amsterdam A: Drug development for ovarian hyper-stimulation and anti-cancer treatment: blocking of gonadotropin signaling for epiregulin and amphiregulin biosynthesis. Biochem Pharmacol; 2004 Sep 15;68(6):989-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drug development for ovarian hyper-stimulation and anti-cancer treatment: blocking of gonadotropin signaling for epiregulin and amphiregulin biosynthesis.
  • However, gonadotropin hyper-stimulation may be associated with higher risk for ovarian cancer development.
  • Moreover, we have recently discovered that gonadotropin stimulation can activate the MAPK cascade in target cells.
  • Using DNA microarray technology and RNA from human granulosa cells, we discovered that stimulation with saturating doses of gonadotropins dramatically elevates activity of genes coding for epiregulin and amphiregulin.
  • These gene products can bind and activate the EGF receptor and ERBB4, which are associated with the development of various cancers such as ovarian, breast endometrial and other non-gynecological malignancies.
  • Gonadotropin receptors are expressed not only in the gonads, but also in non-gonadal tissues and in cancer cells.
  • The discovery that gonadotropins activate certain mitogenic signal transduction pathways, may serve as a guide for novel anti-cancer therapy by (1) specific interference at the receptor level to block the gonadotropic response, or arresting the receptor expression and (2) blocking downstream mitogenic signals generated by these hormones, like attenuation of the expression of epiregulin and amphiregulin that belong to the EGF family, using anti-sense and/or SiRNA techniques targeted to suppress their expression.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Epidermal Growth Factor / biosynthesis. Glycoproteins / biosynthesis. Gonadotropins / antagonists & inhibitors. Intercellular Signaling Peptides and Proteins / biosynthesis. Signal Transduction / drug effects
  • [MeSH-minor] Amphiregulin. Cell Transformation, Neoplastic. Drug Design. EGF Family of Proteins. Epiregulin. Female. Gene Expression. Humans. Luteinizing Hormone / physiology. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / pathology. Transforming Growth Factor alpha / physiology

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  • (PMID = 15313392.001).
  • [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 / AREG protein, human; 0 / Amphiregulin; 0 / Antineoplastic Agents; 0 / EGF Family of Proteins; 0 / EREG protein, human; 0 / Epiregulin; 0 / Glycoproteins; 0 / Gonadotropins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Transforming Growth Factor alpha; 62229-50-9 / Epidermal Growth Factor; 9002-67-9 / Luteinizing Hormone
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