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1. Bompas E, Freyer G, Vitrey D, Trillet-Lenoir V: [Granulosa cell tumour: review of the literature]. Bull Cancer; 2000 Oct;87(10):709-14
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  • [Title] [Granulosa cell tumour: review of the literature].
  • [Transliterated title] Tumeur à cellules de la granulosa: revue de la littérature.
  • Granulosa cell tumours account for only 5% of ovarian malignancies and there is currently no standard treatment.
  • It is thus important to better define the characteristics and prognostic factors of this histological subtype in order to recommend appropriate therapy.
  • Call-Exner bodies and "coffee bean" cells are characteristic of the histopathology of these tumors.
  • Surgery is the treatment for local disease.
  • Patients with locally advanced, recurrent or metastatic tumors require chemotherapy, although the optimal regimen remains to be determined.
  • [MeSH-major] Granulosa Cell Tumor / therapy. Ovarian Neoplasms / therapy
  • [MeSH-minor] Age Factors. Combined Modality Therapy. Female. Humans. Neoplasm Proteins / metabolism. Prognosis

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  • (PMID = 11084534.001).
  • [ISSN] 0007-4551
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] FRANCE
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 59
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2. Hersmus R, de Leeuw BH, Stoop H, Bernard P, van Doorn HC, Brüggenwirth HT, Drop SL, Oosterhuis JW, Harley VR, Looijenga LH: A novel SRY missense mutation affecting nuclear import in a 46,XY female patient with bilateral gonadoblastoma. Eur J Hum Genet; 2009 Dec;17(12):1642-9
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  • Patients with disorders of sex development (DSD), especially those with gonadal dysgenesis and hypovirilization, are at risk of developing the so-called type II germ cell tumors (GCTs).
  • Both carcinoma in situ and gonadoblastoma (GB) can be the precursor lesion, resulting in a seminomatous or non-seminomatous invasive cancer.
  • The premalignant lesion of the initially removed gonad was positive for OCT3/4, TSPY and stem cell factor in germ cells, and for FOXL2 in the stromal component (ie, granulosa cells), but not for SOX9.
  • The identified W70L mutation in the SRY gene resulted in a 50% reduction in the nuclear accumulation of the mutant protein compared with wild type.
  • This likely explains the diminished SOX9 expression, and therefore the lack of proper Sertoli cell differentiation during development.
  • This case shows the value of the proper diagnosis of human GCTs in identification of patients with DSD, which allows subsequent early diagnosis and prevention of the development of an invasive cancer, likely to be treated by chemotherapy at young age.
  • [MeSH-major] Cell Nucleus / metabolism. Gonadal Dysgenesis, 46,XY / complications. Gonadal Dysgenesis, 46,XY / genetics. Gonadoblastoma / complications. Gonadoblastoma / genetics. Mutation, Missense / genetics. Sex-Determining Region Y Protein / genetics
  • [MeSH-minor] Active Transport, Cell Nucleus / genetics. Adolescent. Adult. Base Sequence. DNA Mutational Analysis. Female. Gonads / pathology. Gonads / surgery. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Karyotyping. Molecular Sequence Data

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  • (PMID = 19513096.001).
  • [ISSN] 1476-5438
  • [Journal-full-title] European journal of human genetics : EJHG
  • [ISO-abbreviation] Eur. J. Hum. Genet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / SRY protein, human; 0 / Sex-Determining Region Y Protein
  • [Other-IDs] NLM/ PMC2987026
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3. Ray-Coquard I, Pautier P, Pujade-Lauraine E, Méeus P, Morice P, Treilleux I, Duvillard P, Alexandre J, Lhommé C, Selle F, Guastalla J: [Rare ovarian tumours: therapeutic strategies in 2010, national website observatory for rare ovarian cancers and delineation of referent centers in France]. Bull Cancer; 2010 Jan;97(1):123-35
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  • [Title] [Rare ovarian tumours: therapeutic strategies in 2010, national website observatory for rare ovarian cancers and delineation of referent centers in France].
  • [Transliterated title] Les tumeurs rares de l'ovaire: stratégies thérapeutiques en 2010, Observatoire francophone des tumeurs rares de l'ovaire et émergence des centres de références.
  • Majorities of the rare ovarian cancers were represented by germ cell tumours and sex cords ovarian tumours with borderline tumours, clear cell carcinoma and mucinous carcinoma and are extremely rare malignant diseases of the ovaries.
  • Tumors of the stromal (Leydig cells) and/or sex cords (Sertoli cells) represent approximately 7% of ovarian cancers and develop from the conjunctive tissue (respectively, interstitial and nurse cells) of the ovaries.
  • Treatment of rare ovarian tumors is currently as follows.
  • Surgery is the same as that for ovarian adenocarcinoma, with one major difference: conservation of reproductive function in women of reproductive age is usual case for this type of tumor.
  • Chemotherapy for germ cell and sex cords tumors, based on data reported in the literature is the same as that prescribed for testicular germ-cell tumors.
  • Surgery, chemotherapy and possible surgical intervention for residual lesions are highly complex.
  • Too rare to be included in randomized studies, treatment of these tumors has benefited from the therapeutic advancements made against testicular germ-cell tumors or with publications using retrospective data.
  • Because of the rarity of these tumours a specialized website (www.ovaire-rare.org) was developed in France in 2002.
  • The other new scientific data concern surgical procedures for sex cords tumors, evidence for presence of FOXL2 mutation in adult granulosa cell tumors, the use of paclitaxel plus carboplatin for sex cords tumors.
  • [MeSH-major] Cancer Care Facilities / organization & administration. Ovarian Neoplasms / therapy
  • [MeSH-minor] Adenocarcinoma, Clear Cell / pathology. Adenocarcinoma, Clear Cell / therapy. Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Mucinous / therapy. Adult. Antineoplastic Agents / therapeutic use. Female. France. Humans. Neoplasms, Germ Cell and Embryonal / pathology. Neoplasms, Germ Cell and Embryonal / therapy. Rare Diseases / pathology. Rare Diseases / therapy. Sarcoma / pathology. Sarcoma / therapy. Sex Cord-Gonadal Stromal Tumors / pathology. Sex Cord-Gonadal Stromal Tumors / therapy

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  • (PMID = 20007069.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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4. Pectasides D, Pectasides E, Psyrri A: Granulosa cell tumor of the ovary. Cancer Treat Rev; 2008 Feb;34(1):1-12
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  • [Title] Granulosa cell tumor of the ovary.
  • Ovarian granulosa cell tumors (GCTs) are uncommon neoplasms that arise from the sex-cord stromal cells of the ovary.
  • In postmenopausal women and those with more advanced disease a total abdominal hysterectomy with bilateral salpingo-oophorectomy is the appropriate surgical treatment.
  • Nevertheless, the use of adjuvant chemotherapy or radiotherapy has sometimes been associated with prolonged disease-free survival and possibly overall survival.
  • Chemotherapy should be considered for patients with advanced, recurrent or metastatic disease and the BEP (bleomycin, etoposide, cisplatin) is the currently preferable regimen.
  • [MeSH-major] Granulosa Cell Tumor / diagnosis. Granulosa Cell Tumor / therapy. Ovarian Neoplasms / diagnosis. Ovarian Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Chemotherapy, Adjuvant. Combined Modality Therapy. Disease-Free Survival. Estradiol / analysis. Female. Humans. Neoplasm Recurrence, Local. Prognosis. Radiotherapy, Adjuvant

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  • (PMID = 17945423.001).
  • [ISSN] 0305-7372
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 4TI98Z838E / Estradiol
  • [Number-of-references] 99
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5. Woods DC, Alvarez C, Johnson AL: Cisplatin-mediated sensitivity to TRAIL-induced cell death in human granulosa tumor cells. Gynecol Oncol; 2008 Mar;108(3):632-40
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  • [Title] Cisplatin-mediated sensitivity to TRAIL-induced cell death in human granulosa tumor cells.
  • OBJECTIVES: The goal of the present study was to determine the efficacy of combinatorial treatment using cisplatin and tumor necrosis factor-related apoptosis including ligand (TRAIL) to promote apoptosis in granulosa cell tumor (GCT) lines, in vitro.
  • The cytotoxic effects of each treatment were evaluated using a methyl tetrazolium salt (MTS) assay.
  • Overexpression and knockdown studies were conducted to evaluate the role of p53 in TRAIL-induced cell death.
  • Real-time PCR was used for gene expression analysis of the TRAIL receptor dr5 and the pro-apoptotic bax following treatment with cisplatin.
  • RESULTS: Treatment with TRAIL (100-200 ng/ml) led to a slight, but significant, loss of cell viability following an 18-h culture.
  • This effect was enhanced following pre-treatment with cisplatin (25 microM) for 2 or 18 h.
  • Moreover, pre-treatment with cisplatin decreased the maximal effective dose of TRAIL from 100 ng/ml to as low as 3 ng/ml in both cell lines.
  • While the level of p53 expression enhanced both the death-inducing and TRAIL-sensitizing effects of cisplatin, TRAIL-induced cell death was found to occur independent of p53.
  • CONCLUSIONS: These data suggest that the efficacy of cisplatin in GCT cells can be enhanced through combinatorial treatment with TRAIL.
  • Combinatorial treatment of GCTs with cisplatin and TRAIL may provide an efficacious addition to cisplatin-based regimens.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cisplatin / pharmacology. Granulosa Cell Tumor / drug therapy. Ovarian Neoplasms / drug therapy. TNF-Related Apoptosis-Inducing Ligand / pharmacology
  • [MeSH-minor] Cell Line, Tumor / drug effects. Female. Humans

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  • (PMID = 18191995.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / TNF-Related Apoptosis-Inducing Ligand; Q20Q21Q62J / Cisplatin
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6. Koukourakis GV, Kouloulias VE, Koukourakis MJ, Zacharias GA, Papadimitriou C, Mystakidou K, Pistevou-Gompaki K, Kouvaris J, Gouliamos A: Granulosa cell tumor of the ovary: tumor review. Integr Cancer Ther; 2008 Sep;7(3):204-15
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  • [Title] Granulosa cell tumor of the ovary: tumor review.
  • Granulosa cell tumors of the ovary are rare neoplasms that originate from sex-cord stromal cells.
  • The long natural history of granulosa cell tumors and their tendency to recur years after the initial diagnosis are the most prominent of their characteristics.
  • Total abdominal hysterectomy with bilateral salpingo-oophorectomy is the appropriate surgical treatment for postmenopausal women and those with more advanced disease.
  • There are no clear conclusions regarding the role of postoperative chemotherapy or radiotherapy in stage I disease and in those with completely resected tumor.
  • The use of adjuvant chemotherapy or radiotherapy has sometimes been associated with prolonged disease-free survival and possibly overall survival.
  • Chemotherapy is the treatment of choice for patients with advanced, recurrent, or metastatic disease, and BEP (bleomycin, etoposide, and cisplatin) is the preferred regimen.
  • Although the overall rate of response to treatment is high, the impact of treatment on disease-free or overall survival is unknown.
  • [MeSH-major] Granulosa Cell Tumor / therapy. Ovarian Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor. Chemotherapy, Adjuvant. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Neoplasm Staging. Prognosis. Radiotherapy, Adjuvant

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  • (PMID = 18815151.001).
  • [ISSN] 1534-7354
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 99
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7. Kalfa N, Philibert P, Patte C, Ecochard A, Duvillard P, Baldet P, Jaubert F, Fellous M, Sultan C: Extinction of FOXL2 expression in aggressive ovarian granulosa cell tumors in children. Fertil Steril; 2007 Apr;87(4):896-901
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  • [Title] Extinction of FOXL2 expression in aggressive ovarian granulosa cell tumors in children.
  • OBJECTIVE: In the female gonad, FOXL2 is a key factor for proper differentiation of granulosa cells (GC) during folliculogenesis and its expression persists in the ovary after birth.
  • The aim of this multicentric nationwide study was to determine whether FOXL2 expression varies during tumoral proliferation of GC cells in juvenile ovarian GC tumors (OGCT).
  • PATIENT(S): Between 1994 and 2004, 26 patients with juvenile OGCT were reported in the TGM95 database of the French Society for Childhood Cancer (SFCE) and from eight pediatric endocrinology centers.
  • RESULT(S): FOXL2 expression was absent in the GC of 10 patients and was markedly reduced in the cells of 4 patients.
  • All patients requiring complementary treatment (n = 7; chemotherapy or complementary surgery) had reduced expression of FOXL2 in the tumor.
  • [MeSH-major] Forkhead Transcription Factors / analysis. Granulosa Cell Tumor / chemistry. Ovarian Neoplasms / chemistry
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Granulosa Cells / pathology. Humans. Immunohistochemistry. Infant. Neoplasm Staging. Prognosis. Retrospective Studies

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  • (PMID = 17430735.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXL2 protein, human; 0 / FOXO1 protein, human; 0 / Forkhead Transcription Factors
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8. Woods DC, Liu HK, Nishi Y, Yanase T, Johnson AL: Inhibition of proteasome activity sensitizes human granulosa tumor cells to TRAIL-induced cell death. Cancer Lett; 2008 Feb 18;260(1-2):20-7
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  • [Title] Inhibition of proteasome activity sensitizes human granulosa tumor cells to TRAIL-induced cell death.
  • Human granulosa tumor cell (GCT) lines (KGN and COV434) were utilized to establish the combinatorial effects of TRAIL treatment and a proteasome inhibitor on cell viability, in vitro.
  • TRAIL induced a slight, but consistent, decrease in viability for both cell lines, and pharmacologic inhibition of proteasome activity, using Z-LLF-CHO (Z-LLF), synergistically enhanced TRAIL-induced loss of viability.
  • Targeted reduction of p53 expression revealed that the ability of Z-LLF to enhance DR5 and Bax expression occurs independent of p53 activity.
  • These studies underscore the potential to develop targeted treatments for GCTs using established cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Granulosa Cell Tumor / drug therapy. Oligopeptides / pharmacology. Protease Inhibitors / pharmacology. Proteasome Inhibitors. TNF-Related Apoptosis-Inducing Ligand / metabolism
  • [MeSH-minor] Caspase 8 / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cytochromes c / metabolism. Dose-Response Relationship, Drug. Humans. Mitochondria / drug effects. Mitochondria / enzymology. Proteasome Endopeptidase Complex / metabolism. RNA Interference. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Recombinant Proteins. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Up-Regulation. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

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  • (PMID = 18031928.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / Oligopeptides; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 143839-79-6 / N-benzyloxycarbonyl-leucyl-leucyl-phenylalaninal; 9007-43-6 / Cytochromes c; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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9. Yoshida Y, Hosokawa K, Dantes A, Tajima K, Kotsuji F, Amsterdam A: Theophylline and cisplatin synergize in down regulation of BCL-2 induction of apoptosis in human granulosa cells transformed by a mutated p53 (p53 val135) and Ha-ras oncogene. Int J Oncol; 2000 Aug;17(2):227-35
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  • [Title] Theophylline and cisplatin synergize in down regulation of BCL-2 induction of apoptosis in human granulosa cells transformed by a mutated p53 (p53 val135) and Ha-ras oncogene.
  • Cisplatin is in common use in ovarian cancer therapy, although it is also implicated in cytotoxicity in normal tissue.
  • We have examined the effect of cisplatin alone and in combination with theophylline, a phoshodiesterase inhibitor, on modulation of Bcl-2/Bax expression and induction of apoptosis in human granulosa cells transformed by stable transfection with mutant p53 plus Ha-ras.
  • Theophylline elicited cell death only at relatively high concentrations with an EC50 of 200 microg/ml.
  • Using fluorescence-activated cell sorting analysis of DNA stained cells and the terminal deoxy-nucleotide tranferase-mediated dUTP nick end-labeling method, we found that even at concentrations of 0.
  • 3 and 1 microM cisplatin, theophylline at 15 and 50 microg/ml increased the incidence of apoptosis in these cells by 3-5-fold, while theophylline alone induced extremely low apoptosis.
  • Neither drug had any measurable effect on Bax protein expression.
  • The combination of theophylline and cisplatin resulted in a further dramatic reduction in Bcl-2, under-scoring the pronounced synergy of these two drugs.
  • These observations suggest that suppression of Bcl-2 expression may play an important role in mediating the synergistic effect of cisplatin and theophylline on induction of apoptosis in ovarian cancer cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cisplatin / pharmacology. Neoplasm Proteins / drug effects. Phosphodiesterase Inhibitors / pharmacology. Proto-Oncogene Proteins c-bcl-2 / drug effects. Theophylline / pharmacology
  • [MeSH-minor] Drug Therapy, Combination. Female. Genes, ras / drug effects. Genes, ras / physiology. Granulosa Cells / drug effects. Granulosa Cells / metabolism. Humans. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / metabolism. Tumor Cells, Cultured / drug effects. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 10891529.001).
  • [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 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Phosphodiesterase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; C137DTR5RG / Theophylline; Q20Q21Q62J / Cisplatin
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10. Utsunomiya T, Tanaka T, Utsunomiya H, Umesaki N: A novel molecular mechanism for anticancer drug-induced ovarian failure: Irinotecan HCl, an anticancer topoisomerase I inhibitor, induces specific FasL expression in granulosa cells of large ovarian follicles to enhance follicular apoptosis. Int J Oncol; 2008 May;32(5):991-1000
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  • [Title] A novel molecular mechanism for anticancer drug-induced ovarian failure: Irinotecan HCl, an anticancer topoisomerase I inhibitor, induces specific FasL expression in granulosa cells of large ovarian follicles to enhance follicular apoptosis.
  • Clinical use of CPT-11 combination chemotherapy frequently induces ovarian dysfunction in premenopausal and perimenopausal cancer patients, but its mechanism remains unclear.
  • Clinically therapeutic doses of CPT-11 were injected intraperitoneally into 8-week-old female MCH mice, and their ovaries were examined by the TUNEL assay to detect dead cells.
  • Furthermore, normal murine ovarian tissue fragments were incubated with recombinant soluble FasL in organ cultures and stained by the TUNEL assay to detect apoptotic cells.
  • Intraperitoneal CPT-11 injections induced specific TUNEL-positive cells and cell death with cleaved caspase 3 expression among large ovarian follicular granulosa cells.
  • Apoptotic follicles (follicles containing >/=10 TUNEL-positive cells per ovarian section) were only found among large follicles.
  • Fas antigen was expressed in most ovarian cells, with extremely high expression levels detected in luteal cells.
  • CPT-11 injections did not significantly increase the Fas expression levels in ovarian cells.
  • Although no FasL expression was detected in normal ovarian tissues, CPT-11 injections significantly induced specific FasL expression in granulosa cells.
  • Incubation of organ-cultured normal murine ovarian tissue fragments with recombinant mouse soluble FasL significantly increased the numbers of TUNEL-positive granulosa and luteal cells.
  • In conclusion, CPT-11 dose-dependently induced specific FasL expression in granulosa cells of developing ovarian follicles.
  • The induced FasL reacted with the Fas antigen constitutively expressed on granulosa cells, such that apoptosis can only be enhanced and induced in granulosa cells in an autocrine and/or paracrine manner.
  • This cell lineage-specific and differentiation stage-specific apoptosis in granulosa cells is thought to be the main molecular mechanism of the ovarian dysfunction induced by CPT-11 combination chemotherapy.
  • [MeSH-major] Apoptosis. Fas Ligand Protein / metabolism. Granulosa Cells / drug effects. Primary Ovarian Insufficiency / pathology
  • [MeSH-minor] Animals. Antigens, CD95 / metabolism. Antineoplastic Agents, Phytogenic / administration & dosage. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Caspase 3 / metabolism. DNA Topoisomerases, Type I / metabolism. Disease Models, Animal. Dose-Response Relationship, Drug. Enzyme Activation. Enzyme Inhibitors / administration & dosage. Female. Immunohistochemistry. In Situ Nick-End Labeling. Injections, Intraperitoneal. Mice. Organ Culture Techniques. Recombinant Proteins / metabolism. Topoisomerase I Inhibitors. Up-Regulation

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  • (PMID = 18425325.001).
  • [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 / Antigens, CD95; 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / Recombinant Proteins; 0 / Topoisomerase I Inhibitors; 7673326042 / irinotecan; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 5.99.1.2 / DNA Topoisomerases, Type I; XT3Z54Z28A / Camptothecin
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11. Rice S, Amon A, Whitehead SA: Ethanolic extracts of black cohosh (Actaea racemosa) inhibit growth and oestradiol synthesis from oestrone sulphate in breast cancer cells. Maturitas; 2007 Apr 20;56(4):359-67
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  • [Title] Ethanolic extracts of black cohosh (Actaea racemosa) inhibit growth and oestradiol synthesis from oestrone sulphate in breast cancer cells.
  • Extracts of black cohosh (Actaea racemosa) and soy are used as 'natural' alternatives to conventional hormone replacement therapy (HRT) and there is some evidence that soy may protect against breast cancer by inhibiting the production of active oestrogens.
  • This study compares the action of ethanolic extracts of black cohosh (BCE) and genistein on growth and enzyme activity in MCF-7 and MDA-MB-123 breast cancer cells.
  • 50 and 100 microg/ml, whilst genistein stimulated growth in the oestrogen receptor positive (ER(+)) MCF-7 cells, but at high doses it inhibited growth in both cell lines.
  • BCE did not affect the conversion of androstenedione to oestradiol and only the highest doses (50 and 100 microg/ml) significantly inhibited the conversion of oestrone to oestradiol in MDA cells.
  • In contrast, BCE induced a dose-dependent inhibition of the conversion of oestrone sulphate to oestradiol in both cell lines, whilst in human granulosa lutein (GL) cells enzyme activity was only inhibited at the highest dose of BCE.
  • Genistein had no significant effect on enzyme activity in breast cancer cells and like BCE only the highest doses (10 and 50 microM) inhibited enzyme activity in human GL cells.
  • In vivo genistein may have growth stimulatory effects on breast tissue but BCE not only inhibits growth but inhibits the conversion of oestrone sulphate to active oestradiol, considered by some, to be the preferred pathway of oestradiol synthesis in breast tissue.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Cimicifuga. Estradiol Dehydrogenases / biosynthesis. Estrogen Replacement Therapy. Genistein / pharmacology. Phytotherapy. Plant Extracts / pharmacology
  • [MeSH-minor] Breast Neoplasms / prevention & control. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. Cell Proliferation. Dose-Response Relationship, Drug. Female. Humans. Neoplasms, Hormone-Dependent / prevention & control. Sulfatases / antagonists & inhibitors. Sulfatases / metabolism

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  • (PMID = 17125943.001).
  • [ISSN] 0378-5122
  • [Journal-full-title] Maturitas
  • [ISO-abbreviation] Maturitas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts; DH2M523P0H / Genistein; EC 1.1.1.62 / Estradiol Dehydrogenases; EC 3.1.6.- / Sulfatases; EC 3.1.6.- / estrogen sulfatase
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12. Bukovsky A: Oogenesis from human somatic stem cells and a role of immune adaptation in premature ovarian failure. Curr Stem Cell Res Ther; 2006 Sep;1(3):289-303
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oogenesis from human somatic stem cells and a role of immune adaptation in premature ovarian failure.
  • With the assistance of immune system-related cells, primitive granulosa and germ cells appear to originate from OSE stem cells in the fetal and adult human gonads.
  • Premature ovarian failure (POF) may result from premature termination of follicular renewal during adulthood, possibly due to the alteration of fetal follicular development during immune adaptation (idiopathic POF), or due to the alteration of the adult immune system by cytostatic chemotherapy.
  • Factors responsible for the diminution of follicular renewal may be responsible for the aging of other tissues and the whole body in general.
  • However, our recent research shows that OSE stem cells may produce new eggs in vitro, even when derived from ovaries lacking primary follicles.
  • [MeSH-major] Embryonic Stem Cells / physiology. Oogenesis / physiology. Primary Ovarian Insufficiency / immunology. Primary Ovarian Insufficiency / physiopathology
  • [MeSH-minor] Adult. Animals. Cell Differentiation. Child. Embryo, Mammalian. Female. Granulosa Cells / cytology. Granulosa Cells / physiology. Humans. Mice. Ovarian Follicle / cytology. Ovarian Follicle / embryology. Ovarian Follicle / immunology. Ovary / cytology. Ovary / embryology. Ovary / physiology. Pregnancy

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  • (PMID = 18220874.001).
  • [ISSN] 1574-888X
  • [Journal-full-title] Current stem cell research & therapy
  • [ISO-abbreviation] Curr Stem Cell Res Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Number-of-references] 95
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13. Fabbri R, Venturoli S, D'Errico A, Iannascoli C, Gabusi E, Valeri B, Seracchioli R, Grigioni WF: Ovarian tissue banking and fertility preservation in cancer patients: histological and immunohistochemical evaluation. Gynecol Oncol; 2003 May;89(2):259-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ovarian tissue banking and fertility preservation in cancer patients: histological and immunohistochemical evaluation.
  • OBJECTIVE: A combination of chemotherapy and radiotherapy in young females with cancer has greatly enhanced the life expectancy of these patients, even if these treatments have a highly deleterious effect on the ovary and cause a severe depletion of the follicular store.
  • Cryopreservation of ovarian tissue before chemotherapy and/or radiotherapy, followed by autograft after remission or in in vitro maturation, could restore gonadal function and fertility.
  • The aim of this study is to verify the efficiency of the ovarian tissue cryopreservation procedure by histological and immunohistochemical analyses.
  • METHODS: Ovarian tissue was obtained by laparoscopy from 22 patients affected with different malignant diseases.
  • Tissue specimens were frozen using a combination of PROH (1,2-propanediol) and sucrose as cryoprotectants, and the cryopreservation protocol used consisted of a slow freezing-rapid thawing program.
  • Both fresh and frozen/thawed tissues were embedded in paraffin blocks for histological and immunohistochemical analyses.
  • RESULTS: Good stromal and follicular morphology was found in fresh and frozen/thawed tissue.
  • No significant differences were found in follicular density, distribution, and diameters in fresh and frozen/thawed tissue.
  • Regarding the Ki67 protein, positive staining was found in both the granulosa cells and/or the oocytes (36% in fresh and 56% in frozen/thawed).
  • For the Bcl2 protein, positive staining was observed in the follicle granulosa cells but not in the oocytes in 74% of the fresh and in 79% of the frozen/thawed specimens.
  • For the stromal cells, ER showed a negative staining distribution in 97% of the fresh and 100% of the frozen/thawed specimens.
  • CONCLUSIONS: These results suggest that human ovarian tissue morphology, antigenicity, cellular proliferation, and anti-apoptotic index were well preserved by cryopreservation in PROH and sucrose.
  • [MeSH-minor] Adult. Antibodies. Cell Division / physiology. Female. Humans. Immunohistochemistry. Neoplasms / drug therapy. Neoplasms / radiotherapy. Receptors, Estrogen / immunology. Receptors, Progesterone / immunology

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  • (PMID = 12713989.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone
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14. La Marca A, Volpe A: The Anti-Mullerian hormone and ovarian cancer. Hum Reprod Update; 2007 May-Jun;13(3):265-73
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  • [Title] The Anti-Mullerian hormone and ovarian cancer.
  • The Anti-Mullerian hormone (AMH), which is produced by fetal Sertoli cells, is responsible for regression of Mullerian ducts, the anlagen for uterus and Fallopian tubes, during male sex differentiation.
  • Ovarian granulosa cells also secrete AMH from late in fetal life.
  • The patterns of expression of AMH and its type II receptor in the post-natal ovary indicate that AMH may play an important role in ovarian folliculogenesis.
  • Recent advances in the physiological role of AMH has stimulated interest in the significance of AMH as a diagnostic marker and therapeutic agent for ovarian cancer.
  • Currently, AMH has been shown to be a circulating marker specifically for granulosa cell tumour (GCT).
  • Based on the physiological inhibitory role of AMH in the Mullerian ducts, it has been proposed that AMH may inhibit epithelial ovarian cancer cell both in vitro and in vivo.
  • These observations will be the basis for future research aiming to investigate the possible clinical role of AMH as neo-adjuvant, or most probably adjuvant, therapy for ovarian cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Glycoproteins / physiology. Glycoproteins / therapeutic use. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / physiopathology. Testicular Hormones / physiology. Testicular Hormones / therapeutic use

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  • (PMID = 17213257.001).
  • [ISSN] 1355-4786
  • [Journal-full-title] Human reproduction update
  • [ISO-abbreviation] Hum. Reprod. Update
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Testicular Hormones; 80497-65-0 / Anti-Mullerian Hormone
  • [Number-of-references] 61
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15. Bukovsky A: Sex steroid-mediated reprogramming of vascular smooth muscle cells to stem cells and neurons: possible utilization of sex steroid combinations for regenerative treatment without utilization of in vitro developed stem cells. Cell Cycle; 2009 Dec 15;8(24):4079-84
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  • [Title] Sex steroid-mediated reprogramming of vascular smooth muscle cells to stem cells and neurons: possible utilization of sex steroid combinations for regenerative treatment without utilization of in vitro developed stem cells.
  • Previous work from our laboratory demonstrated that sex steroid combinations, but not individual sex steroids alone, cause transdifferentiation of ovarian epithelial cells--ovarian surface epithelium (OSE) and follicular granulosa cells--into neural stem cells (NSC) and differentiating neurons.
  • In the present study we have chosen primary culture of human vascular smooth muscle cells (SMC), a non-epithelial mesenchymal cells in order to test them as a control cell type regarding their morphology and expression of NSC and neuronal markers.
  • However, the treatment with sex steroid combinations (PG + TS or E2 + PG + TS) caused transdifferentiation into neural/neuronal type cells.
  • By immunohistochemistry, these cells exhibited strong expression of stem cell markers and neural/neuronal glycoconjugates SSEA-1, SSEA-4, Thy-1, NeuN and NCAM.
  • In the Neurobasal/B27 medium both, the OSE and vascular SMC also transdifferentiated into neuronal cells.
  • Western blot analysis has shown significant increase of NeuN 48-kDa species after E2 + PG or PG + TS treatment.
  • Unlike OSE cells, the vascular SMC accompany as pericytes all vessels, including CNS microvasculature.
  • We also observed that sex steroid combinations could produce SMC stem type cells which differentiated within a few days back to mature vascular SMC.
  • Altogether, our observations suggest that sex steroid combinations could induce in vivo improvement of neurodegenerative, traumatic and ischemic neurological disorders and vascular diseases via their effect on resident pluripotent vascular SMC, i.e., without a need of in vitro developed stem cells.
  • [MeSH-major] Cell Differentiation / drug effects. Cell Lineage / drug effects. Gonadal Steroid Hormones / pharmacology. Muscle, Smooth, Vascular / drug effects. Neurons / drug effects. Stem Cells / drug effects
  • [MeSH-minor] Biomarkers / analysis. Biomarkers / metabolism. Cell Culture Techniques. Cells, Cultured. Culture Media / pharmacology. Drug Synergism. Drug Therapy, Combination / methods. Epithelial Cells / cytology. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Estradiol / metabolism. Estradiol / pharmacology. Female. Humans. Ovary / cytology. Ovary / drug effects. Ovary / metabolism. Pericytes / cytology. Pericytes / drug effects. Pericytes / metabolism. Progesterone / metabolism. Progesterone / pharmacology. Regeneration / drug effects. Regeneration / physiology. Regenerative Medicine / methods. Testosterone / metabolism. Testosterone / pharmacology

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  • [CommentIn] Cell Cycle. 2009 Dec 15;8(24):4027-8 [19959936.001]
  • (PMID = 19946214.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Culture Media; 0 / Gonadal Steroid Hormones; 3XMK78S47O / Testosterone; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol
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16. 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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  • [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.
  • Moreover, since amphiregulin and epiregulin act as mediators of luteinizing hormone (LH) action in the mammalian ovulatory follicles, regulation of the expression of these factors may open new possibilities in treatment of ovarian malfunction implicated with ovarian hyper-stimulation.
  • [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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17. 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.
  • YIGSR and A12 reduced the expression of Bcl-2 by 7- and 3-fold, respectively, compared to treatment with laminin-1.
  • [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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18. Bar-Joseph H, Ben-Aharon I, Rizel S, Stemmer SM, Tzabari M, Shalgi R: Doxorubicin-induced apoptosis in germinal vesicle (GV) oocytes. Reprod Toxicol; 2010 Dec;30(4):566-72
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  • Ovarian failure is a-known side-effect observed in women treated for cancer.
  • We aimed at characterizing the effect of DXR on germinal vesicle (GV) oocytes that comprise the majority of oocytes within ovaries encountering chemotherapy.
  • We demonstrated that DXR crosses the blood-follicle barrier and accumulates in oocytes and granulosa cells.
  • [MeSH-major] Antineoplastic Agents / toxicity. Apoptosis / drug effects. Doxorubicin / toxicity. Oocytes / drug effects
  • [MeSH-minor] Animals. Biological Transport. Caspase 12 / metabolism. Chromatin / drug effects. Chromatin / metabolism. Female. Granulosa Cells / cytology. Granulosa Cells / metabolism. Mice. Mice, Inbred ICR. Microscopy, Confocal. Mitochondria / drug effects. Mitochondria / metabolism. Oogenesis. Organ Culture Techniques. Ovarian Follicle / cytology. Ovarian Follicle / drug effects. Ovarian Follicle / metabolism. Oxidative Stress / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Primary Ovarian Insufficiency / chemically induced. eIF-2 Kinase / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20656019.001).
  • [ISSN] 1873-1708
  • [Journal-full-title] Reproductive toxicology (Elmsford, N.Y.)
  • [ISO-abbreviation] Reprod. Toxicol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Casp12 protein, mouse; 0 / Chromatin; 80168379AG / Doxorubicin; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / eIF-2 Kinase; EC 3.4.22.- / Caspase 12
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19. 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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  • 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.
  • Pfannenstiel incisions for exploration of suspicious adnexal masses increase the risk of extensive parietal metastasis in case of malignancy because they require reflection of several sheaths of tissue.
  • [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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20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The treatment consists of a conjugate of a membrane-disrupting lytic peptide (Hecate, Phor14, or Phor21) and a 15-amino acid segment of the beta chain of CG.
  • 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

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
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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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21. Hinds L, Price J: Menopause, hormone replacement and gynaecological cancers. Menopause Int; 2010 Jun;16(2):89-93
MedlinePlus Health Information. consumer health - Menopause.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Menopause, hormone replacement and gynaecological cancers.
  • Approximately 18,000 women are diagnosed with a gynaecological cancer in the UK each year.
  • Predisposing risk factors for some of these gynaecological cancers include an early menarche/late menopause and hormone replacement therapy (HRT).
  • Furthermore, treatment of gynaecological malignancies often induces an iatrogenic menopause, which may be more severe than a natural onset.
  • HRT is an extremely effective treatment that may dramatically improve physical and psychological symptoms and ultimately quality of life in patients with cancer.
  • However, the safety of using HRT in patients with gynaecological cancer is a controversial issue and not entirely clear.
  • The main concern is the theoretical risk of the stimulation of residual cancer cells by estrogen replacement.
  • The review of the evidence in this article found that for most gynaecological cancers this hypothesis was not proven.
  • No study to date has found HRT to have a detrimental effect on survival in patients with early stage endometrial cancer, epithelial ovarian cancer, cervical cancer and vulval tumours.
  • HRT is only an absolute contraindication in low-grade endometrial stromal sarcomas and is best avoided in granulosa cell ovarian tumours.
  • Therefore, HRT should not be withheld in the majority of patients with gynaecological cancer.
  • If quality of life is being adversely affected by symptoms of the menopause, then patients with cancer should be counselled regarding the known risks and benefits of HRT to enable them to make an informed decision on their treatment.
  • [MeSH-major] Adenocarcinoma / chemically induced. Genital Neoplasms, Female / chemically induced. Hormone Replacement Therapy / adverse effects. Menopause / drug effects. Neoplasms, Squamous Cell / chemically induced. Sarcoma, Endometrial Stromal / chemically induced

  • MedlinePlus Health Information. consumer health - Hormone Replacement Therapy.
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  • (PMID = 20729501.001).
  • [ISSN] 1754-0461
  • [Journal-full-title] Menopause international
  • [ISO-abbreviation] Menopause Int
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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