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1. Hasan J, Ton N, Mullamitha S, Clamp A, McNeilly A, Marshall E, Jayson GC: Phase II trial of tamoxifen and goserelin in recurrent epithelial ovarian cancer. Br J Cancer; 2005 Sep 19;93(6):647-51
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  • [Title] Phase II trial of tamoxifen and goserelin in recurrent epithelial ovarian cancer.
  • Endocrine therapy is a recognised option in the treatment of chemo-resistant ovarian cancer.
  • We conducted a nonrandomised phase II evaluation of combination endocrine therapy with tamoxifen and goserelin in patients with advanced ovarian cancer that had recurred following chemotherapy.
  • The median age was 63 years and enrolled patients had received a median of three chemotherapy regimens prior to trial entry.
  • Four patients received treatment for more than 2 years (range 1-31) and one of them is still on treatment.
  • In none of the four patients was there any evidence of recurrent or cumulative treatment related toxicity.
  • Treatment-limiting toxicity was not seen in any of the study population.
  • No consistent correlation could be established between LH/FSH suppression and tumour response.
  • Likewise no relationship was observed between Inhibin A/B and pro-alpha C levels and tumour response.
  • Inhibin is unlikely to be a useful surrogate marker for response in locally advanced or metastatic ovarian cancer.
  • Combination endocrine therapy with tamoxifen and goserelin is an active regimen in platinum-resistant ovarian cancer patients.
  • Hormonal therapy is advantageous in its relative lack of toxicity, ease of administration and tolerability, thus making it suitable for patients with heavily pretreated disease, compromised bone marrow function and other comorbid conditions that contraindicate cytotoxic therapy as well as in patients with indolent disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cystadenocarcinoma, Serous / drug therapy. Neoplasm Recurrence, Local / drug therapy. Neoplasms, Glandular and Epithelial / drug therapy. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Aged. Disease-Free Survival. Drug Resistance, Neoplasm. Female. Goserelin / administration & dosage. Humans. Maximum Tolerated Dose. Middle Aged. Salvage Therapy. Survival Rate. Tamoxifen / administration & dosage

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  • (PMID = 16222310.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen; 0F65R8P09N / Goserelin
  • [Other-IDs] NLM/ PMC2361624
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2. Baş F, Saka N, Darendeliler F, Tuzlali S, Ilhan R, Bundak R, Günöz H: Bilateral ovarian steroid cell tumor in congenital adrenal hyperplasia due to classic 11beta-hydroxylase deficiency. J Pediatr Endocrinol Metab; 2000 Jun;13(6):663-7
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  • [Title] Bilateral ovarian steroid cell tumor in congenital adrenal hyperplasia due to classic 11beta-hydroxylase deficiency.
  • Prednisolone and antihypertensive drugs were started.
  • Histopathological examination of both ovaries revealed steroid cell tumor.
  • The type of the tumor was "not otherwise specified" (NOS).
  • Basal hormone levels and ACTH test performed 10 months after the operation and 7 days off treatment reconfirmed the diagnosis of 11beta-hydroxylase deficiency.
  • Steroid cell tumors are extremely rare forms of steroid hormone-reducing ovarian neoplasms in childhood and may coexist with or imitate virilizing CAH.
  • [MeSH-major] Adrenal Hyperplasia, Congenital / complications. Ovarian Neoplasms / complications
  • [MeSH-minor] Adrenocorticotropic Hormone. Angiotensin I / blood. Child. Consanguinity. Female. Glucocorticoids / therapeutic use. Humans. Hydrocortisone / blood. Hypertension / drug therapy. Hypertension / etiology. Hysterectomy. Ovariectomy. Ovary / pathology. Prednisolone / therapeutic use. Testosterone / therapeutic use


3. Yousef GM, Kyriakopoulou LG, Scorilas A, Fracchioli S, Ghiringhello B, Zarghooni M, Chang A, Diamandis M, Giardina G, Hartwick WJ, Richiardi G, Massobrio M, Diamandis EP, Katsaros D: Quantitative expression of the human kallikrein gene 9 (KLK9) in ovarian cancer: a new independent and favorable prognostic marker. Cancer Res; 2001 Nov 1;61(21):7811-8
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  • [Title] Quantitative expression of the human kallikrein gene 9 (KLK9) in ovarian cancer: a new independent and favorable prognostic marker.
  • KLK9 is a newly discovered human kallikrein gene that is expressed in several tissues including thymus, testis, spinal cord, salivary gland, ovary, and skin.
  • Like other kallikreins, the KLK9 gene was found to be regulated by steroid hormones in cancer cell lines.
  • Our purpose is to examine whether quantitative analysis of KLK9 expression has prognostic value in ovarian cancer.
  • We studied the expression of KLK9 by quantitative reverse transcription-PCR in 168 consecutive ovarian tumors of different stages, grades, and histological types, and correlated the expression with clinicopathological parameters, response to chemotherapy, and patients' survival.
  • Kaplan-Meier survival curves demonstrated that patients with KLK9-positive tumors have substantially longer progression-free and overall survival (P < 0.001 and P = 0.016, respectively).
  • When the Cox proportional hazard regression analysis was applied to subgroups of patients, KLK9 expression was found to be a significant predictor of progression-free survival in the subgroup of patients with low-grade tumors [hazard ratio (HR), 0.13; P = 0.0015], early stage (HR, 0.099; P = 0.031); and those with optimal debulking (HR, 0.26; P = 0.012).
  • Our results indicate that KLK9 is under steroid hormone regulation in ovarian and breast cancer cell lines.
  • Immmunohistochemically, human kallikrein protein (hK9) was localized in the cytoplasm, but not in the nuclei, of the epithelial cells of ovarian cancer tissues.
  • We conclude that KLK9 is a potential new independent favorable prognostic marker for early stage, low-grade, optimally debulked ovarian cancer patients.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Kallikreins / biosynthesis. Neoplasm Proteins. Ovarian Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Analysis of Variance. Estrogens / physiology. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Middle Aged. Neoplasm Staging. Progestins / physiology. Prognosis. Survival Rate. Up-Regulation

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  • (PMID = 11691797.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogens; 0 / Neoplasm Proteins; 0 / Progestins; EC 3.4.21.- / KLK9 protein, human; EC 3.4.21.- / Kallikreins
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4. Shitara K, Munakata M, Ishiguro A, Kudo T, Okada R, Tomioka R, Mitobe S, Yokoyama S, Sakata Y: [Colonic perforation in a patient treated with combination chemotherapy for recurrent ovarian clear cell adenocarcinoma]. Gan To Kagaku Ryoho; 2006 Oct;33(10):1497-1500
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  • [Title] [Colonic perforation in a patient treated with combination chemotherapy for recurrent ovarian clear cell adenocarcinoma].
  • BACKGROUND: Colonic perforation due to colitis is a known and reported side effect of chemotherapy.
  • CASE REPORT: A 53-year-old woman was treated with combination chemotherapy of irinotecan plus cisplatin for a recurrent ovarian clear cell adenocarcinoma.
  • Steroid was also used for suspected interstitial pneumonia.
  • After two cycles of treatment, she developed a colonic perforation.
  • Oral intake could be restarted for a while, but she died from tumor progression one and a half months after the diagnosis of perforation.
  • [MeSH-major] Adenocarcinoma, Clear Cell / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cecal Diseases / etiology. Intestinal Perforation / etiology. Neoplasm Recurrence, Local / drug therapy. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Cisplatin / administration & dosage. Colonoscopy. Drainage. Drug Administration Schedule. Fatal Outcome. Female. Humans. Lung Neoplasms / secondary. Middle Aged. Pleural Effusion, Malignant / etiology

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  • (PMID = 17033246.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 7673326042 / irinotecan; Q20Q21Q62J / Cisplatin; XT3Z54Z28A / Camptothecin
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5. Ye L, Wu XL, Xu L, Huang Q, Sun L, He Y, Yang KX: [Ovarian steroid cell tumor, not otherwise specified: a clinicopathologic study]. Zhonghua Bing Li Xue Za Zhi; 2007 Aug;36(8):516-20
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  • [Title] [Ovarian steroid cell tumor, not otherwise specified: a clinicopathologic study].
  • OBJECTIVE: To study the clinicopathologic features, diagnostic criteria, differential diagnosis and treatment options of ovarian steroid cell tumor, not otherwise specified (NOS).
  • METHODS: Light microscopy and immunohistochemical study was carried out in 8 cases of ovarian steroid cell tumor, NOS.
  • RESULTS: The 7 cases of benign ovarian steroid cell tumor, NOS were composed mainly of polygonal cells with granular eosinophilic cytoplasm and larger cells with vacuolated cytoplasm.
  • They resembled the architecture of normal adrenal gland, with formation of cell nests and trabeculae.
  • The single case of malignant ovarian steroid cell tumor had evidence of significant cellular pleomorphism, haemorrhage and coagulative tumor necrosis.
  • Immunohistochemical study showed that the tumor cells expressed calretinin and alpha-inhibin.
  • Differential diagnosis included oxyphilic granulosa cell tumor, thecoma, Sertoli cell tumor and clear cell carcinoma.
  • The treatment options of benign ovarian steroid cell tumor, NOS was local excision or ipsilateral salpingo-oophorectomy, while the malignant counterpart should be treated with a combination of surgery and chemotherapy, including administration of GnRH agonist.
  • CONCLUSIONS: Ovarian steroid cell tumor, NOS, is the most common type of ovarian steroid cell tumors.
  • Most of which are associated with a benign clinical outcome.
  • Immunohistochemistry is an important adjunct for diagnosis.
  • The treatment options of ovarian steroid cell tumor, NOS depend on its malignant potential.
  • [MeSH-major] Inhibins / metabolism. Ovarian Neoplasms / pathology. Ovary / pathology. S100 Calcium Binding Protein G / metabolism. Sex Cord-Gonadal Stromal Tumors / pathology
  • [MeSH-minor] Adolescent. Adult. Calbindin 2. Diagnosis, Differential. Female. Granulosa Cell Tumor / pathology. Humans. Ovariectomy / methods. Sertoli Cell Tumor / pathology. Thecoma / pathology. Young Adult

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  • (PMID = 17980097.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / S100 Calcium Binding Protein G; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
  • [Number-of-references] 27
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6. Holmes WF, Soprano DR, Soprano KJ: Elucidation of molecular events mediating induction of apoptosis by synthetic retinoids using a CD437-resistant ovarian carcinoma cell line. J Biol Chem; 2002 Nov 22;277(47):45408-19
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  • [Title] Elucidation of molecular events mediating induction of apoptosis by synthetic retinoids using a CD437-resistant ovarian carcinoma cell line.
  • Retinoids have great promise in the area of cancer therapy and chemoprevention.
  • Although some tumor cells are sensitive to the growth inhibitory effect of all-trans-retinoic acid (ATRA), many ovarian tumor cells are not.
  • 6-((1-Admantyl)-4-hydroxyphenyl)-2-naphthalenecarboxylic acid (CD437) is a conformationally restricted synthetic retinoid that induces growth arrest and apoptosis in both ATRA-sensitive and ATRA-resistant ovarian tumor cell lines.
  • To better understand the mechanism by which CD437 induces apoptosis in ovarian tumor cell lines, we prepared a cell line, CA-CD437R, from the ATRA-sensitive ovarian cell line, CA-OV-3, which was resistant to CD437.
  • We found that the CD437-resistant cell line was also resistant to the induction of apoptosis by tumor necrosis factor-alpha but not resistant to the induction of apoptosis by another synthetic retinoid, fenretinide N-(4-hydroxyphenyl)retinamide.
  • We also show that this cell line remains ATRA-sensitive and exhibits no deficiencies in RAR function.
  • Analysis of this CD437-resistant cell line suggests that the pathway for induction of apoptosis by CD437 is similar to the pathway utilized by tumor necrosis factor-alpha and different from the pathway induced by the synthetic retinoid, fenretinide N-(4-hydroxyphenyl)retinamide.
  • The CA-CD437R cell line is a valuable tool, permitting us to further elucidate the molecular events that mediate apoptosis induced by CD437 and other synthetic retinoids.
  • Results of experiments utilizing this cell line suggest that the alteration responsible for resistance of CA-CD437R cells to CD437 induced event maps after the activation of p38 and TR3 expression, prior to mitochondrial depolarization, subsequent release of cytochrome c and activation of caspase-9 and caspase-3.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Ovarian Neoplasms / metabolism. Retinoids / pharmacology
  • [MeSH-minor] Caspases / metabolism. Cell Division / drug effects. Cell Division / physiology. Cytochrome c Group / metabolism. Drug Resistance, Neoplasm. Enzyme Activation. Female. Fenretinide / pharmacology. Humans. Membrane Potentials / drug effects. Mitochondria / drug effects. Mitochondria / metabolism. Mitogen-Activated Protein Kinases / metabolism. Nuclear Receptor Subfamily 4, Group A, Member 1. Oxygen / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Receptors, Steroid / genetics. Receptors, Steroid / metabolism. Receptors, Thyroid Hormone / genetics. Receptors, Thyroid Hormone / metabolism. Transcription, Genetic. Tretinoin / pharmacology. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology. p38 Mitogen-Activated Protein Kinases

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  • (PMID = 12237293.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI 07101; United States / NCI NIH HHS / CA / CA 64945; United States / NIDCR NIH HHS / DE / DE 13139
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CD 437; 0 / Cytochrome c Group; 0 / NR4A1 protein, human; 0 / Nuclear Receptor Subfamily 4, Group A, Member 1; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Steroid; 0 / Receptors, Thyroid Hormone; 0 / Retinoids; 0 / Tumor Necrosis Factor-alpha; 187EJ7QEXL / Fenretinide; 5688UTC01R / Tretinoin; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; S88TT14065 / Oxygen
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7. Dery MC, Van Themsche C, Provencher D, Mes-Masson AM, Asselin E: Characterization of EN-1078D, a poorly differentiated human endometrial carcinoma cell line: a novel tool to study endometrial invasion in vitro. Reprod Biol Endocrinol; 2007;5:38
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  • [Title] Characterization of EN-1078D, a poorly differentiated human endometrial carcinoma cell line: a novel tool to study endometrial invasion in vitro.
  • BACKGROUND: To date, tools to study metastasis in endometrial cancers are insufficiently developed.
  • The aim of this study was to characterize the cell line EN-1078D, a new endometrial carcinoma cell line derived from a metastasis to the ovary.
  • In addition, this cell line expresses high levels of MMP-2 and MMP-14 mRNA, low levels of TIMP-1 and TIMP-2 transcripts and no detectable levels of MMP-9 mRNA.
  • Moreover, all nude mice developed tumors by subcutaneous injections and cell invasion was observed in vitro in response to TGF-beta 3.
  • Her-2/neu was not overamplified but mutations in the C-2 domain of PTEN gene as well as codon 12 of the K-Ras gene were found.
  • Finally, EN-1078D shows sensitivity to drugs commonly used in chemotherapy such as cisplatin and doxorubicin: IC50 of 2.8 microM of cisplatin after 72 hours of exposure and 0.54 microM of doxorubicin after 48 hours.
  • [MeSH-major] Endometrial Neoplasms / pathology. Endometrial Neoplasms / secondary. Endometrium / pathology. Ovarian Neoplasms / secondary
  • [MeSH-minor] Animals. Cell Differentiation / physiology. Female. Gonadal Steroid Hormones / metabolism. Gonadal Steroid Hormones / physiology. Humans. Mice. Mice, Nude. Middle Aged. Neoplasm Invasiveness. Tumor Cells, Cultured. Xenograft Model Antitumor Assays / methods


8. Ho SM: Estrogen, progesterone and epithelial ovarian cancer. Reprod Biol Endocrinol; 2003 Oct 07;1:73
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  • [Title] Estrogen, progesterone and epithelial ovarian cancer.
  • Ovarian carcinoma (OCa) continues to be the leading cause of death due to gynecologic malignancies and the vast majority of OCa is derived from the ovarian surface epithelium (OSE) and its cystic derivatives.
  • Epidemiological evidence strongly suggests that steroid hormones, primarily estrogens and progesterone, are implicated in ovarian carcinogenesis.
  • A limited number of clinical studies has demonstrated efficacies of antiestrogens, aromatase inhibitors, and progestins alone or in combination with chemotherapeutic drugs in the treatment of OCa.
  • As a result of increased life expectancy in most countries, the number of women taking hormone replacement therapies (HRT) continues to grow.
  • Thus, knowledge of the mechanism of action of steroid hormones on the OSE and OCa is of paramount significance to HRT risk assessment and to the development of novel therapies for the prevention and treatment of OCa.

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  • (PMID = 14577831.001).
  • [ISSN] 1477-7827
  • [Journal-full-title] Reproductive biology and endocrinology : RB&E
  • [ISO-abbreviation] Reprod. Biol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA094221; United States / NCI NIH HHS / CA / CA94221
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Estrogen Receptor Modulators; 0 / Estrogens; 0 / Neoplasm Proteins; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone
  • [Number-of-references] 75
  • [Other-IDs] NLM/ PMC239900
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9. Borgoño CA, Fracchioli S, Yousef GM, Rigault de la Longrais IA, Luo LY, Soosaipillai A, Puopolo M, Grass L, Scorilas A, Diamandis EP, Katsaros D: Favorable prognostic value of tissue human kallikrein 11 (hK11) in patients with ovarian carcinoma. Int J Cancer; 2003 Sep 10;106(4):605-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Favorable prognostic value of tissue human kallikrein 11 (hK11) in patients with ovarian carcinoma.
  • Recently, we developed a highly sensitive and specific immunoassay for hK11 and found that this protease is expressed in the prostate, stomach and trachea as well as in amniotic fluid and milk of lactating women.
  • Elevated serum hK11 levels were found in 60% of men with prostate cancer and 70% of women with ovarian cancer.
  • Also, hK11 expression was found to be under the regulation of steroid hormones, particularly estrogens, at the level of KLK11 transcription.
  • We hypothesized that hK11 may be implicated in endocrine-related malignancies and serve as a novel prostate and ovarian cancer serological marker.
  • The aim of our study was to examine if hK11 expression in ovarian tumors bears any prognostic significance.
  • The concentration of hK11 (ng per mg of total protein) in 104 ovarian tumor cytosolic extracts was quantified and correlated with clinicopathologic variables and outcome over a median follow-up period of 67 months.
  • hK11 concentration in ovarian tumor cytosols ranged from 0-21 ng/mg of total protein, with a median of 0.54 ng/mg.
  • An optimal cutoff value of 0.54 ng/mg was selected to categorize tumors as hK11-positive or -negative. hK11-positive tumors were more frequently associated with early stage (Stage I/II) disease, pre-/peri-menopausal status and patients who exhibited complete or partial response to chemotherapy (p < 0.05).
  • Univariate analysis revealed that patients with hK11-positive tumors had a significantly decreased risk of relapse with a hazard ratio (HR) of 0.45 (p = 0.007) and death (HR of 0.34, p = 0.005).
  • Kaplan-Meier survival curves further confirmed that women with hK11-positive tumors have longer PFS and OS (p = 0.005 and p = 0.003, respectively).
  • Similarly, in the subgroup of patients with grade 1-2 tumors, hK11-positivity was associated with higher OS in both univariate and multivariate analysis (HR of 0.23 and 0.17, p < 0.05).
  • Finally, in women with optimal debulking after surgery (<1 cm residual tumor), hK11 positivity was associated with a slower disease progression.
  • These results indicate that hK11 is a novel, independent marker of favorable prognosis in patients with ovarian cancer.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Neoplasm Proteins / metabolism. Ovarian Neoplasms / metabolism. Serine Endopeptidases / metabolism
  • [MeSH-minor] Adenocarcinoma, Clear Cell / metabolism. Adenocarcinoma, Clear Cell / pathology. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Adult. Aged. Aged, 80 and over. Carcinoma, Endometrioid / metabolism. Carcinoma, Endometrioid / pathology. Cystadenocarcinoma, Serous / metabolism. Cystadenocarcinoma, Serous / pathology. Disease Progression. Disease-Free Survival. Female. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate. Up-Regulation

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12845660.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R1CA93568-O1A1
  • [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 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / trypsin-like serine protease; EC 3.4.21.- / Serine Endopeptidases
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10. Schneider DT, Jänig U, Calaminus G, Göbel U, Harms D: Ovarian sex cord-stromal tumors--a clinicopathological study of 72 cases from the Kiel Pediatric Tumor Registry. Virchows Arch; 2003 Oct;443(4):549-60
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  • [Title] Ovarian sex cord-stromal tumors--a clinicopathological study of 72 cases from the Kiel Pediatric Tumor Registry.
  • We analyzed 72 patients with ovarian sex cord-stromal tumors (OSCST) registered at the German Pediatric Tumor Registry in Kiel over a 20-year period.
  • Juvenile granulosa cell tumors (JGCT, n=48) were the most frequent histological subtype.
  • In addition, there were 14 Sertoli-Leydig cell tumors, 5 sclerosing stromal tumors, 2 sex cord tumors with annular tubules, 2 thecomas and 1 steroid cell tumor.
  • Compared with adult granulosa cell tumors, JGCT showed pronounced mitotic activity [mean 9.8 mitoses/10 high power field (HPF)], which was significantly higher than in other histological subtypes (2.7/10 HPF, P=0.001).
  • Immunohistochemical analysis revealed frequent coexpression of vimentin (positive in 52/52 examined tumors), cytokeratin (27/33), and inhibin (19/20).
  • Of patients, 12 with Ic or higher stage tumors received adjuvant cisplatinum-based chemotherapy.
  • In conclusion, this analysis confirms that the majority of patients with OSCST present at low tumor stage and that prognosis in these patients is excellent.
  • Refractory tumors are characterized by high proliferative activity.
  • Therefore, histopathological evaluation substantially contributes to risk assessment in patients with OSCST and might be useful for therapy stratification in prospective therapeutic protocols.
  • [MeSH-major] Ovarian Neoplasms / pathology. Sex Cord-Gonadal Stromal Tumors / pathology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Infant. Sertoli-Leydig Cell Tumor / pathology

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  • (PMID = 12910419.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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11. Chang B, Liu G, Xue F, Rosen DG, Xiao L, Wang X, Liu J: ALDH1 expression correlates with favorable prognosis in ovarian cancers. Mod Pathol; 2009 Jun;22(6):817-23
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  • [Title] ALDH1 expression correlates with favorable prognosis in ovarian cancers.
  • The authors hypothesized that the level of ALDH1 expression may be correlated with the clinical outcome of patients with ovarian cancer.
  • Immunohistochemical staining of ALDH1 expression was analyzed in 442 primary ovarian carcinomas using tissue microarray.
  • The associations between the expression of the ALDH1 and clinical factors (diagnosis, tumor grade, stage, and clinical response to chemotherapy), as well as overall and disease-free survival, were analyzed.
  • Fisher's exact test suggested that high expression of ALDH1 was significantly associated with endometrioid adenocarcinoma (P<0.0001), early-stage disease (P=0.006), complete response to chemotherapy (P<0.05), and a low serum level of CA125 (P=0.02).
  • High percentage of cells expressing ALDH1 was associated with a longer overall survival time (P=0.01) and disease-free survival time (P=0.006) by log-rank test.
  • In contrast to its function in breast cancer, ALDH1 was a favorable prognostic factor in ovarian carcinoma.
  • ALDH1 therefore may have a different function in ovarian cancer than it does in breast cancer.

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  • (PMID = 19329942.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA131183-01A2; United States / NCI NIH HHS / CA / R01 CA131183; United States / NCI NIH HHS / CA / R01 CA131183-01A2; United States / NCI NIH HHS / CA / P50 CA083639-05; United States / NCI NIH HHS / CA / R01 CA131183-01; United States / NCI NIH HHS / CA / P50 CA083639
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Isoenzymes; EC 1.2.1.- / aldehyde dehydrogenase 1; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 1.2.1.36 / Retinal Dehydrogenase
  • [Other-IDs] NLM/ NIHMS96470; NLM/ PMC2692456
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12. Zhou H, Luo MP, Schönthal AH, Pike MC, Stallcup MR, Blumenthal M, Zheng W, Dubeau L: Effect of reproductive hormones on ovarian epithelial tumors: I. Effect on cell cycle activity. Cancer Biol Ther; 2002 May-Jun;1(3):300-6
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  • [Title] Effect of reproductive hormones on ovarian epithelial tumors: I. Effect on cell cycle activity.
  • We examined the effects of the 4 major female reproductive hormones, estradiol (E2), progesterone (P4), follicle stimulating hormone (FSH), and luteinizing hormone (LH) on thymidine incorporation in benign and malignant ovarian epithelial tumors cultured in vitro.
  • Treatment of these tumors with E2, FSH and LH resulted in increased thymidine incorporation while treatment with P4 inhibited growth as well as thymidine incorporation.
  • The inhibitory effect of progesterone could not be reproduced by treating the cells with ligands for other steroid hormone receptors known to interact with P4 such as the mineralocorticoid and glucocorticoid receptors.
  • Expression of a reporter gene downstream to an AP-1 responsive element in a plasmid construct transfected into ovarian epithelial tumor cells was induced by P4 and inhibited by RU486.
  • We conclude that P4 inhibits cell cycle activity in ovarian epithelial tumors, in part via down-regulation of the cdkl/cyclin B complex.
  • This inhibitory effect may have therapeutic utility against ovarian epithelial tumors.
  • [MeSH-major] Cell Cycle / drug effects. Cell Cycle Proteins / metabolism. Neoplasms, Glandular and Epithelial / pathology. Ovarian Neoplasms / pathology. Tumor Cells, Cultured / pathology
  • [MeSH-minor] Cell Division / drug effects. DNA, Neoplasm / metabolism. Down-Regulation. Estradiol / pharmacology. Female. Follicle Stimulating Hormone / pharmacology. Gonadal Steroid Hormones / pharmacology. Humans. Ligands. Luteinizing Hormone / pharmacology. Progesterone / pharmacology. Receptors, Glucocorticoid / agonists. Receptors, Mineralocorticoid / agonists. Receptors, Progesterone / agonists. Thymidine / metabolism. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism

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  • (PMID = 12432283.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30 CA14089-21; United States / NCI NIH HHS / CA / R01 CA 51167; United States / NCI NIH HHS / CA / R01 CA 79750; United States / NIDDK NIH HHS / DK / R01DK43093
  • [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 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Gonadal Steroid Hormones; 0 / Ligands; 0 / Receptors, Glucocorticoid; 0 / Receptors, Mineralocorticoid; 0 / Receptors, Progesterone; 0 / Transcription Factor AP-1; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; VC2W18DGKR / Thymidine
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13. Yousef GM, Fracchioli S, Scorilas A, Borgoño CA, Iskander L, Puopolo M, Massobrio M, Diamandis EP, Katsaros D: Steroid hormone regulation and prognostic value of the human kallikrein gene 14 in ovarian cancer. Am J Clin Pathol; 2003 Mar;119(3):346-55
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  • [Title] Steroid hormone regulation and prognostic value of the human kallikrein gene 14 in ovarian cancer.
  • To study KLK14 gene expression in endocrine-related cancers, we studied its hormonal regulation in breast and ovarian cancer cell lines.
  • We then studied the expression of KLK14 by quantitative reverse transcriptase-polymerase chain reaction in 155 consecutive ovarian tumors and correlated these findings with clinicopathologic parameters, response to chemotherapy, and survival.
  • A stepwise reduction was observed in the levels of KLK14 messenger RNA in normal, benign, and cancerous tissues (P < .001).
  • Expression levels were significantly higher in patients with early stage disease and optimal debulking and in patients who responded to chemotherapy.
  • Kaplan-Meier survival curves demonstrated longer progression-free and overall survival in patients with KLK14-positive tumors than in patients with KLK14-negative tumors (P < .001).
  • KLK14 is a new, independent, and favorable prognostic marker for ovarian cancer.
  • [MeSH-major] Biomarkers, Tumor. Carcinoma / genetics. Gene Expression Regulation, Neoplastic. Kallikreins / genetics. Ovarian Neoplasms / genetics. Steroids / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Disease-Free Survival. Female. Humans. Middle Aged. RNA, Messenger / metabolism. RNA, Neoplasm / analysis. Receptors, Androgen / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured / drug effects. Up-Regulation

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  • (PMID = 12645335.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Androgen; 0 / Steroids; EC 3.4.21.- / KLK14 protein, human; EC 3.4.21.- / Kallikreins
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14. Haji AG, Sharma S, Babu M, Vijaykumar D, Chitrathara K: Androgen secreting steroid cell tumor of the ovary in a young lactating women with acute onset of severe hyperandrogenism: a case report and review of literature. J Med Case Rep; 2007;1:182
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  • [Title] Androgen secreting steroid cell tumor of the ovary in a young lactating women with acute onset of severe hyperandrogenism: a case report and review of literature.
  • INTRODUCTION: Steroid cell tumors of the ovary account for less than 0.1% of all ovarian tumors 1 and these tumours may present at any age in association with interesting presentations related to the hormonal activity and virilizing properties of tumor.
  • The subtype, not otherwise specified, is associated with androgenic changes in approximately one half of patients with this tumour 1.
  • In a series of 63 cases from Massachusetts General Hospital, 94% of the tumors were found to be unilateral and 28.6% were malignant 3.
  • As most of these tumors are diagnosed at an early stage and do not recur or metastasize, little is known about their response to therapies such as chemotherapy or radiation 3.
  • CASE PRESENTATION: We present the case of a 22-year old lactating woman who presented with four months of amenorrhea associated with signs of virilization.
  • Clinical and diagnostic evaluation revealed a right adenexal mass and elevated serum levels of testosterone and she was diagnosed as having a stage 1A androgen secreting steroid cell tumor.
  • Histopathological examination and immunohistochemistry confirmed the diagnosis.
  • CONCLUSION: Surgery remains the mainstay of the treatment of gonadotrophin receptor positive steroid cell tumors although medical therapy using Gonadotrophin Releasing Hormone [GnRH analogues has been tried recently in recurrent or inoperable cases.
  • There is no described effective chemotherapy or radiotherapy for this condition.

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  • (PMID = 18088412.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2231374
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15. Powell JL, Dulaney DP, Shiro BC: Androgen-secreting steroid cell tumor of the ovary. South Med J; 2000 Dec;93(12):1201-4
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  • [Title] Androgen-secreting steroid cell tumor of the ovary.
  • We present the case of a 93-year-old virilized woman with an androgen-secreting ovarian tumor.
  • This rare ovarian sex cord stromal tumor behaved in a malignant fashion.
  • Various aspects of the presentation, diagnosis, and treatment of these tumors are discussed.
  • [MeSH-major] Androgens / secretion. Ovarian Neoplasms. Sex Cord-Gonadal Stromal Tumors. Virilism / etiology
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Female. Humans. Leuprolide / therapeutic use. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 11142457.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; EFY6W0M8TG / Leuprolide
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16. Chura JC, Ryu HS, Simard M, Poirier D, Tremblay Y, Brooker DC, Blomquist CH, Argenta PA: Steroid-converting enzymes in human ovarian carcinomas. Mol Cell Endocrinol; 2009 Mar 25;301(1-2):51-8
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  • [Title] Steroid-converting enzymes in human ovarian carcinomas.
  • Anti-estrogen therapies for treating ovarian carcinoma have had mixed outcomes suggesting some tumors may be estrogen-dependent.
  • We assayed the activity levels of 17beta-hydroxysteroid dehydrogenase (17beta-HSD), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD/3-KSR) and estrone sulfatase in a series of ovarian epithelial carcinomas.
  • A 17beta-HSD type 1 inhibition pattern was observed in 23% of the samples and a type 2 pattern in 25%.
  • 17beta-HSD type 1, type 2 and type 5 mRNA was detected in matched primary tumor and metastases.
  • Evaluation of 17beta-HSD and sulfatase activity levels, activity ratios and inhibition patterns may help predict tumor response to endocrine therapy.
  • [MeSH-major] 17-Hydroxysteroid Dehydrogenases / metabolism. 3-Hydroxysteroid Dehydrogenases / metabolism. Ovarian Neoplasms / enzymology. Sulfatases / metabolism
  • [MeSH-minor] Enzyme Inhibitors / pharmacology. Estradiol / metabolism. Estrogen Receptor alpha / metabolism. Female. Gene Expression Regulation, Enzymologic / drug effects. Humans. Neoplasm Metastasis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Substrate Specificity / drug effects. Testosterone / metabolism

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  • (PMID = 18723074.001).
  • [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 / Enzyme Inhibitors; 0 / Estrogen Receptor alpha; 0 / RNA, Messenger; 0 / estrogen receptor alpha, human; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; EC 1.1.- / 17-Hydroxysteroid Dehydrogenases; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.51 / 3 (or 17)-beta-hydroxysteroid dehydrogenase; EC 3.1.6.- / Sulfatases; EC 3.1.6.- / estrone sulfatase
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17. Calcagno AM, Salcido CD, Gillet JP, Wu CP, Fostel JM, Mumau MD, Gottesman MM, Varticovski L, Ambudkar SV: Prolonged drug selection of breast cancer cells and enrichment of cancer stem cell characteristics. J Natl Cancer Inst; 2010 Nov 3;102(21):1637-52
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  • [Title] Prolonged drug selection of breast cancer cells and enrichment of cancer stem cell characteristics.
  • BACKGROUND: Cancer stem cells are presumed to have virtually unlimited proliferative and self-renewal abilities and to be highly resistant to chemotherapy, a feature that is associated with overexpression of ATP-binding cassette transporters.
  • We investigated whether prolonged continuous selection of cells for drug resistance enriches cultures for cancer stem-like cells.
  • METHODS: Cancer stem cells were defined as CD44+/CD24⁻ cells that could self-renew (ie, generate cells with the tumorigenic CD44+/CD24⁻ phenotype), differentiate, invade, and form tumors in vivo.
  • Cells were examined for cell surface markers and side-population fractions by microarray and flow cytometry, with in vitro invasion assays, and for ability to form mammospheres.
  • Xenograft tumors were generated in mice to examine tumorigenicity (n = 52).
  • MCF-7/ADR cells were statistically significantly more invasive in Matrigel than parental MCF-7 cells (MCF-7 cells = 0.82 cell per field and MCF-7/ADR = 7.51 cells per field, difference = 6.69 cells per field, 95% confidence interval = 4.82 to 8.55 cells per field, P < .001).
  • CONCLUSION: The cell population with cancer stem cell characteristics increased after prolonged continuous selection for doxorubicin resistance.

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  • (PMID = 20935265.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / HHSN273200700046U; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / AC133 antigen; 0 / Antibiotics, Antineoplastic; 0 / Antigens, CD; 0 / Antigens, CD24; 0 / Antigens, CD44; 0 / Drug Combinations; 0 / Glycoproteins; 0 / Laminin; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Peptides; 0 / Proteoglycans; 0 / RNA, Messenger; 119978-18-6 / matrigel; 80168379AG / Doxorubicin; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ PMC2970576
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18. Kortylewicz ZP, Nearman J, Baranowska-Kortylewicz J: Radiolabeled 5-iodo-3'-O-(17beta-succinyl-5alpha-androstan-3-one)-2'-deoxyuridine and its 5'-monophosphate for imaging and therapy of androgen receptor-positive cancers: synthesis and biological evaluation. J Med Chem; 2009 Aug 27;52(16):5124-43
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  • [Title] Radiolabeled 5-iodo-3'-O-(17beta-succinyl-5alpha-androstan-3-one)-2'-deoxyuridine and its 5'-monophosphate for imaging and therapy of androgen receptor-positive cancers: synthesis and biological evaluation.
  • Both drugs were prepared at the no-carrier-added level.
  • Both drugs bind to sex hormone binding globulin.
  • Biodistribution and imaging studies show preferential uptake and retention of 8 and 13 in ip xenografts of human ovarian adenocarcinoma cells NIH:OVCAR-3, which overexpress AR.
  • When these drugs are administered at therapeutic dose levels, a significant tumor growth arrest is observed.

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  • (PMID = 19653647.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / P41 GM103422; United States / NCRR NIH HHS / RR / P41 RR000954; United States / NCRR NIH HHS / RR / 2P41RR000954
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / 5-iodo-3'-O-(17beta-succinyl-5alpha-androstan-3-one)-2'-deoxyuridine; 0 / 5-iodo-3'-O-(17beta-succinyl-5alpha-androstan-3-one)-2'-deoxyuridine 5'-monophosphate; 0 / Androstanols; 0 / Blood Proteins; 0 / Deoxyuracil Nucleotides; 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptors, Androgen; 0 / Sex Hormone-Binding Globulin; W78I7AY22C / Deoxyuridine
  • [Other-IDs] NLM/ NIHMS557395; NLM/ PMC3941710
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