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1. 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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  • [Cites] Int J Gynecol Pathol. 1989;8(4):299-310 [2553628.001]
  • [Cites] Arch Gynecol Obstet. 1991;248(3):117-21 [1902079.001]
  • [Cites] Obstet Gynecol. 1992 Oct;80(4):660-4 [1328975.001]
  • [Cites] Hum Reprod. 2002 Jun;17(6):1468-71 [12042263.001]
  • [Cites] South Med J. 2000 Dec;93(12):1201-4 [11142457.001]
  • [Cites] Am J Surg Pathol. 1987 Nov;11(11):835-45 [2823622.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Nov;41(5):571-6 [7828344.001]
  • [Cites] Mol Endocrinol. 1993 Mar;7(3):423-33 [8387159.001]
  • (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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2. 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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  • [Cites] Anticancer Res. 1999 Jul-Aug;19(4C):3627-30 [10629663.001]
  • [Cites] N Engl J Med. 1996 Jan 4;334(1):1-6 [7494563.001]
  • [Cites] J Natl Cancer Inst. 2000 May 3;92(9):699-708 [10793106.001]
  • [Cites] Gynecol Oncol. 2000 Aug;78(2):194-202 [10926802.001]
  • [Cites] Am J Reprod Immunol. 2000 Aug;44(2):104-13 [10994638.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Nov;85(11):4280-6 [11095468.001]
  • [Cites] Cochrane Database Syst Rev. 2001;(1):CD001034 [11279703.001]
  • [Cites] CA Cancer J Clin. 2001 Jan-Feb;51(1):15-36 [11577478.001]
  • [Cites] Gynecol Oncol. 2002 Feb;84(2):201-9 [11812075.001]
  • [Cites] Mol Cell Endocrinol. 2002 May 31;191(1):97-103 [12044923.001]
  • [Cites] Gynecol Oncol. 2002 Sep;86(3):297-301 [12217751.001]
  • [Cites] Anticancer Res. 1988 May-Jun;8(3):417-34 [3291746.001]
  • [Cites] J Clin Oncol. 1989 Jan;7(1):115-8 [2491882.001]
  • [Cites] Eur J Cancer Clin Oncol. 1988 Oct;24(10):1567-72 [3208800.001]
  • [Cites] Eur J Cancer Clin Oncol. 1989 Feb;25(2):215-21 [2649375.001]
  • [Cites] BMJ. 1991 Feb 2;302(6771):259-62 [1998789.001]
  • [Cites] Cancer. 1991 Jul 15;68(2):269-71 [2070324.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Apr;81(4):1401-5 [8636341.001]
  • [Cites] Gynecol Oncol. 1997 Jan;64(1):64-9 [8995549.001]
  • [Cites] J Steroid Biochem Mol Biol. 1998 Apr;65(1-6):199-206 [9699874.001]
  • [Cites] Clin Chem. 1999 May;45(5):651-8 [10222351.001]
  • [Cites] Recent Results Cancer Res. 2000;153:83-94 [10626291.001]
  • [Cites] Br J Cancer. 1992 Apr;65(4):621-3 [1314071.001]
  • [Cites] Gynecol Endocrinol. 1992 Dec;6(4):271-4 [1492583.001]
  • [Cites] J Clin Oncol. 1993 Oct;11(10):1957-68 [7691999.001]
  • [Cites] N Engl J Med. 1993 Nov 18;329(21):1539-42 [8413476.001]
  • [Cites] Gynecol Oncol. 1994 Jul;54(1):80-6 [8020844.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jun;40(6):717-23 [8033361.001]
  • [Cites] Eur J Cancer. 1994;30A(5):682-6 [8080688.001]
  • [Cites] Cancer. 1994 Nov 1;74(9):2555-61 [7522953.001]
  • [Cites] Gynecol Oncol. 1994 Nov;55(2):285-9 [7959297.001]
  • [Cites] Hum Reprod. 1994 Jul;9(7):1364-79 [7962452.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Oct;80(10):2926-32 [7559876.001]
  • [Cites] Oncologist. 2000;5(1):26-35 [10706647.001]
  • (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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3. 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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  • [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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4. 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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5. 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


6. 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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7. 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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8. 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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  • [Cites] Pathology. 1979 Apr;11(2):251-82 [460950.001]
  • [Cites] Pathology. 1979 Jan;11(1):5-26 [431978.001]
  • [Cites] J Steroid Biochem. 1982 Jul;17(1):41-9 [7109591.001]
  • [Cites] Br J Obstet Gynaecol. 1989 Aug;96(8):889-92 [2775686.001]
  • [Cites] Blood. 1990 May 15;75(10):1947-50 [2337669.001]
  • [Cites] J Biol Chem. 1991 Jul 15;266(20):13011-8 [2071588.001]
  • [Cites] Crit Rev Biochem Mol Biol. 1992;27(4-5):283-335 [1521460.001]
  • [Cites] Ann Oncol. 1996 Apr;7(4):361-4 [8805927.001]
  • [Cites] J Clin Oncol. 1997 Jan;15(1):172-6 [8996139.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9118-23 [10430905.001]
  • [Cites] Stem Cells. 2004;22(7):1142-51 [15579635.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 17;102(20):7180-5 [15899981.001]
  • [Cites] Stem Cells. 2005 Jun-Jul;23(6):752-60 [15917471.001]
  • [Cites] Exp Hematol. 2005 Jul;33(7):836-43 [15963860.001]
  • [Cites] Blood. 2006 Mar 1;107(5):2162-9 [16269619.001]
  • [Cites] Cancer. 2006 May 1;106(9):1925-32 [16568440.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9339-44 [16990346.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):259-73 [17349583.001]
  • [Cites] Novartis Found Symp. 2007;285:23-40; discussion 40-51, 198-9 [17590985.001]
  • [Cites] Breast Cancer Res. 2007;9(3):303 [17540049.001]
  • [Cites] Stem Cell Rev. 2007 Jun;3(2):107-9 [17873341.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Mol Cancer Res. 2008 Jul;6(7):1146-53 [18644979.001]
  • [Cites] Cell Stem Cell. 2007 Nov;1(5):555-67 [18371393.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1670-80 [18971422.001]
  • [Cites] J Cell Mol Med. 2009 Aug;13(8B):2236-52 [18681906.001]
  • [Cites] J Biol Chem. 1999 Nov 19;274(47):33366-73 [10559215.001]
  • [Cites] Oncologist. 2002;7 Suppl 5:20-8 [12324630.001]
  • [Cites] Chem Biol Interact. 2003 Feb 1;143-144:201-10 [12604205.001]
  • [Cites] J Biochem Mol Toxicol. 2003;17(1):7-23 [12616643.001]
  • [Cites] J Neurochem. 2004 Jan;88(1):212-26 [14675165.001]
  • [Cites] Am J Surg Pathol. 2004 Apr;28(4):496-504 [15087669.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1648-55 [15178579.001]
  • [Cites] Natl Cancer Inst Monogr. 1975 Oct;42:5-7 [1234636.001]
  • [Cites] Pathology. 1979 Jul;11(3):493-532 [230444.001]
  • (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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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. 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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11. 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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12. Etemadmoghadam D, deFazio A, Beroukhim R, Mermel C, George J, Getz G, Tothill R, Okamoto A, Raeder MB, Harnett P, Lade S, Akslen LA, Tinker AV, Locandro B, Alsop K, Chiew YE, Traficante N, Fereday S, Johnson D, Fox S, Sellers W, Urashima M, Salvesen HB, Meyerson M, Bowtell D, AOCS Study Group: Integrated genome-wide DNA copy number and expression analysis identifies distinct mechanisms of primary chemoresistance in ovarian carcinomas. Clin Cancer Res; 2009 Feb 15;15(4):1417-27
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  • [Title] Integrated genome-wide DNA copy number and expression analysis identifies distinct mechanisms of primary chemoresistance in ovarian carcinomas.
  • PURPOSE: A significant number of women with serous ovarian cancer are intrinsically refractory to platinum-based treatment.
  • EXPERIMENTAL DESIGN: Genome-wide copy number variation was measured in 118 ovarian tumors using high-resolution oligonucleotide microarrays.
  • A well-defined subset of 85 advanced-stage serous tumors was then used to relate copy number variation to primary resistance to treatment.
  • Likely copy number variation targets and tumor molecular subtypes were further characterized by gene expression profiling.
  • RESULTS: Amplification of 19q12, containing cyclin E (CCNE1), and 20q11.22-q13.12, mapping immediately adjacent to the steroid receptor coactivator NCOA3, was significantly associated with poor response to primary treatment.
  • Other genes previously associated with copy number variation and clinical outcome in ovarian cancer were not associated with primary treatment resistance.
  • Chemoresistant tumors with high CCNE1 copy number and protein expression were associated with increased cellular proliferation but so too was a subset of treatment-responsive patients, suggesting a cell-cycle independent role for CCNE1 in modulating chemoresponse.
  • Patients with a poor clinical outcome without CCNE1 amplification overexpressed genes involved in extracellular matrix deposition.
  • CONCLUSIONS: We have identified two distinct mechanisms of primary treatment failure in serous ovarian cancer, involving CCNE1 amplification and enhanced extracellular matrix deposition.
  • CCNE1 copy number is validated as a dominant marker of patient outcome in ovarian cancer.

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  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11417-22 [11572989.001]
  • [Cites] Methods Mol Biol. 2000;132:365-86 [10547847.001]
  • [Cites] J Natl Cancer Inst. 2000 Sep 20;92(18):1534-5 [10995813.001]
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5382-5 [11034075.001]
  • [Cites] Lancet Oncol. 2002 Sep;3(9):529-36 [12217790.001]
  • [Cites] Am J Clin Pathol. 2002 Dec;118(6):922-9 [12472286.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1235-41 [12649182.001]
  • [Cites] Cancer Cell. 2003 Apr;3(4):377-86 [12726863.001]
  • [Cites] Gynecol Oncol. 2003 Jul;90(1):3-9 [12821334.001]
  • [Cites] Cancer. 2003 Jul 1;98(1):18-23 [12833450.001]
  • [Cites] Oncogene. 2003 Jul 3;22(27):4281-6 [12833150.001]
  • [Cites] Gynecol Oncol. 2004 Jan;92(1):31-9 [14751135.001]
  • [Cites] Exp Mol Pathol. 2004 Apr;76(2):138-42 [15010292.001]
  • [Cites] Oncogene. 2004 Apr 8;23(15):2648-57 [15007381.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3060-71 [15126342.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Aug;40(4):342-8 [15188458.001]
  • [Cites] Science. 1989 May 12;244(4905):707-12 [2470152.001]
  • [Cites] Gynecol Oncol. 1990 Sep;38(3):340-2 [2227545.001]
  • [Cites] Ann Oncol. 1996 Apr;7(4):361-4 [8805927.001]
  • [Cites] Cancer Res. 1999 Oct 1;59(19):5002-11 [10519415.001]
  • [Cites] Nat Med. 2004 Nov;10(11):1251-6 [15502842.001]
  • [Cites] Oncol Rep. 2004 Dec;12(6):1177-82 [15547734.001]
  • [Cites] Nat Cell Biol. 2005 Jan;7(1):3-5 [15632940.001]
  • [Cites] Nat Methods. 2004 Nov;1(2):109-11 [15782172.001]
  • [Cites] Oncogene. 2005 Apr 18;24(17):2776-86 [15838514.001]
  • [Cites] Neoplasia. 2005 Jun;7(6):603-13 [16036111.001]
  • [Cites] Nat Rev Cancer. 2005 Jul;5(7):516-25 [15965493.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2005;6:331-54 [16124865.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12519-24 [16116079.001]
  • [Cites] Clin Cancer Res. 2005 Sep 1;11(17):6300-10 [16144934.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):14004-9 [16172393.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Dec;163(2):144-50 [16337857.001]
  • [Cites] Int J Gynecol Cancer. 2005 Nov-Dec;15 Suppl 3:212-20 [16343233.001]
  • [Cites] Nat Rev Cancer. 2006 Feb;6(2):99-106 [16491069.001]
  • [Cites] Am J Clin Pathol. 2006 Jul;126(1):101-9 [16753589.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6312-8 [16778208.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Oct;45(10):905-17 [16845658.001]
  • [Cites] Gynecol Oncol. 2006 Nov;103(2):559-64 [16714056.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Jan;46(1):1-9 [17044060.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D247-52 [17130144.001]
  • [Cites] Mol Cell. 2007 Jan 12;25(1):127-39 [17218276.001]
  • [Cites] Cancer Res. 2007 Apr 1;67(7):3074-84 [17409414.001]
  • [Cites] J Clin Oncol. 2007 Jun 1;25(16):2281-7 [17538174.001]
  • [Cites] Nat Rev Cancer. 2007 Aug;7(8):573-84 [17625587.001]
  • [Cites] Clin Cancer Res. 2007 Aug 15;13(16):4731-9 [17699850.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] J Cell Biol. 2008 Jan 28;180(2):267-72 [18209103.001]
  • [Cites] Clin Cancer Res. 2008 Aug 15;14(16):5198-208 [18698038.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1833-9 [10815905.001]
  • [Cites] Br J Cancer. 2000 Oct;83(7):921-7 [10970695.001]
  • (PMID = 19193619.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA109038-01A1; United States / NCI NIH HHS / CA / R01 CA109038; United States / NIGMS NIH HHS / GM / T32 GM007753; United States / NCI NIH HHS / CA / R01 CA109038-01A1
  • [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 / CCNE1 protein, human; 0 / Cyclin E; 0 / Ki-67 Antigen; 0 / Oncogene Proteins; 0 / Trans-Activators; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / NCOA3 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 3
  • [Other-IDs] NLM/ NIHMS90509; NLM/ PMC2670486
  • [Investigator] Bowtell D; Chenevix-Trench G; Green A; Webb P; deFazio A; Gertig D
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13. 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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  • [Cites] Cancer Res. 1996 Mar 1;56(5):950-4 [8640783.001]
  • [Cites] Anticancer Res. 1995 Nov-Dec;15(6B):2639-42 [8669839.001]
  • [Cites] Gynecol Oncol. 1996 Jul;62(1):4-6 [8690289.001]
  • [Cites] J Cell Biochem Suppl. 1995;23:208-18 [8747398.001]
  • [Cites] Cancer. 1997 May 15;79(10):1944-50 [9149021.001]
  • [Cites] Am J Epidemiol. 1998 Jun 1;147(11):1038-42 [9620047.001]
  • [Cites] Semin Surg Oncol. 2000 Jul-Aug;19(1):3-10 [10883018.001]
  • [Cites] J Natl Cancer Inst Monogr. 2000;(27):67-73 [10963620.001]
  • [Cites] Br J Cancer. 1998 Jul;78(2):277 [9683307.001]
  • [Cites] Gynecol Oncol. 1998 Aug;70(2):275-81 [9740705.001]
  • [Cites] J Soc Gynecol Investig. 1998 Sep-Oct;5(5):271-6 [9773403.001]
  • [Cites] J Natl Cancer Inst. 1998 Dec 2;90(23):1774-86 [9839517.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5722-7 [10318951.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3658-62 [10446978.001]
  • [Cites] Cancer. 2000 Oct 15;89(8):1783-91 [11042574.001]
  • [Cites] Br J Cancer. 2000 Dec;83(11):1488-94 [11076658.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):97-102 [11196205.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):667-72 [11342781.001]
  • [Cites] Int J Oncol. 2001 Jul;19(1):31-8 [11408919.001]
  • [Cites] Gynecol Oncol. 2001 Jul;82(1):127-38 [11426974.001]
  • [Cites] J Cell Biochem. 2001;82(3):445-51 [11500921.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6768-76 [11559549.001]
  • [Cites] Int J Cancer. 2001 Nov 20;95(6):394-7 [11668524.001]
  • [Cites] Biol Reprod. 2001 Nov;65(5):1417-24 [11673258.001]
  • [Cites] Zhonghua Fu Chan Ke Za Zhi. 2000 Jul;35(7):423-6 [11776191.001]
  • [Cites] Gynecol Oncol. 2002 Feb;84(2):201-9 [11812075.001]
  • [Cites] Wash Memo Alan Guttmacher Inst. 1992 Jul 29;(12):2-3 [12344814.001]
  • [Cites] Integration. 1996 Spring;(47):41 [12347310.001]
  • [Cites] Apoptosis. 2002 Apr;7(2):107-13 [11865194.001]
  • [Cites] Int J Gynecol Cancer. 2001 Nov-Dec;11(6):438-44 [11906546.001]
  • [Cites] J Natl Cancer Inst. 2002 Apr 17;94(8):617-29 [11959895.001]
  • [Cites] JAMA. 2002 May 1;287(17):2210-1; author reply 2211 [11980516.001]
  • [Cites] Reproduction. 2002 Jun;123(6):743-50 [12052228.001]
  • [Cites] Am J Clin Pathol. 2002 May;117(5):745-50 [12090423.001]
  • [Cites] JAMA. 2002 Jul 3;288(1):58-66 [12090863.001]
  • [Cites] Clin Cancer Res. 2002 Jul;8(7):2233-9 [12114425.001]
  • [Cites] JAMA. 2002 Jul 17;288(3):321-33 [12117397.001]
  • [Cites] Jpn J Cancer Res. 2002 Jul;93(7):807-15 [12149147.001]
  • [Cites] Int J Oncol. 2002 Sep;21(3):583-9 [12168103.001]
  • [Cites] Obstet Gynecol Clin North Am. 2002 Sep;29(3):425-36 [12353666.001]
  • [Cites] Maturitas. 2002 Aug 30;43 Suppl 1:S35-52 [12361887.001]
  • [Cites] Gynecol Oncol. 2002 Oct;87(1):57-63 [12468343.001]
  • [Cites] Curr Opin Obstet Gynecol. 2003 Feb;15(1):63-8 [12544504.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):845-52 [12576458.001]
  • [Cites] Exp Biol Med (Maywood). 2003 Mar;228(3):308-14 [12626776.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Mar;12(3):226-7 [12646513.001]
  • [Cites] Acta Obstet Gynecol Scand. 2003 Apr;82(4):335-44 [12716318.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2003 Mar;17(1):139-47 [12763517.001]
  • [Cites] JAMA. 2003 May 28;289(20):2651-62 [12771112.001]
  • [Cites] Chin Med J (Engl). 2003 Mar;116(3):388-91 [12781043.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Aug;59(2):145-55 [12864790.001]
  • [Cites] Oncogene. 2003 Oct 9;22(44):6883-90 [14534535.001]
  • [Cites] Am J Obstet Gynecol. 1978 May 1;131(1):69-72 [645786.001]
  • [Cites] Am J Epidemiol. 1981 Sep;114(3):398-405 [7304575.001]
  • [Cites] J Natl Cancer Inst. 1983 Oct;71(4):711-6 [6578366.001]
  • [Cites] Gynecol Oncol. 1987 Oct;28(2):151-5 [3311923.001]
  • [Cites] Am J Epidemiol. 1988 May;127(5):990-8 [3358417.001]
  • [Cites] Am J Epidemiol. 1988 Dec;128(6):1216-27 [3195563.001]
  • [Cites] J Exp Med. 1989 May 1;169(5):1747-56 [2469768.001]
  • [Cites] Obstet Gynecol. 1989 Jun;73(6):1009-16 [2542854.001]
  • [Cites] Endocr Rev. 1991 Feb;12(1):14-26 [1851084.001]
  • [Cites] Cancer. 1991 Jul 15;68(2):269-71 [2070324.001]
  • [Cites] Hum Pathol. 1991 Aug;22(8):750-62 [1869263.001]
  • [Cites] J Steroid Biochem Mol Biol. 1993 Mar;44(4-6):657-60 [8476778.001]
  • [Cites] Cell. 1993 Dec 17;75(6):1169-78 [7505205.001]
  • [Cites] Lancet. 1994 Nov 5;344(8932):1250-4 [7967985.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 1994 Aug 30;345(1313):281-7 [7531345.001]
  • [Cites] Br J Cancer. 1995 Mar;71(3):451-5 [7880723.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2743-5 [7796397.001]
  • [Cites] Br J Cancer. 1995 Aug;72(2):367-75 [7640220.001]
  • [Cites] Int J Fertil Menopausal Stud. 1995;40 Suppl 1:40-53 [7581588.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):741-4 [8631007.001]
  • (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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14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] Proc Natl Acad Sci U S A. 2009 Sep 22;106(38):16281-6 [19805294.001]
  • [Cites] Clin Cancer Res. 2010 Jan 1;16(1):45-55 [20028757.001]
  • [Cites] PLoS One. 2010;5(4):e10277 [20422001.001]
  • [Cites] Biochem Biophys Res Commun. 2010 Jun 11;396(4):843-8 [20450887.001]
  • [Cites] Head Neck. 2010 Sep;32(9):1195-201 [20073073.001]
  • [Cites] Cancer Lett. 2005 Feb 10;218(2):127-39 [15670890.001]
  • [Cites] Stem Cells. 2005 Jun-Jul;23(6):752-60 [15917471.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5506-11 [15994920.001]
  • [Cites] FEBS J. 2005 Sep;272(18):4725-40 [16156793.001]
  • [Cites] J Natl Cancer Inst. 2000 Sep 20;92(18):1535-6 [10995814.001]
  • [Cites] Clin Cancer Res. 2001 Jan;7(1):145-52 [11205902.001]
  • [Cites] Cell Signal. 2001 Jun;13(6):389-400 [11384837.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6635-9 [11559526.001]
  • [Cites] Int J Cancer. 2002 Jan 10;97(2):261-5 [11774273.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585.001]
  • [Cites] Int J Oncol. 2002 May;20(5):913-20 [11956583.001]
  • [Cites] J Natl Cancer Inst. 2002 Nov 6;94(21):1652-4; author reply 1654 [12419794.001]
  • [Cites] Cytokine Growth Factor Rev. 2003 Feb;14(1):53-66 [12485619.001]
  • [Cites] Bioinformatics. 2003 Jan 22;19(2):185-93 [12538238.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Biostatistics. 2003 Apr;4(2):249-64 [12925520.001]
  • [Cites] Cell. 2004 Jun 25;117(7):927-39 [15210113.001]
  • [Cites] Drug Metab Rev. 2004 May;36(2):279-99 [15237855.001]
  • [Cites] Cancer Res. 1985 Feb;45(2):584-90 [3967234.001]
  • [Cites] J Biol Chem. 1986 Jun 15;261(17):7762-70 [3711108.001]
  • [Cites] Cell. 1991 Jul 12;66(1):85-94 [1712673.001]
  • [Cites] J Natl Cancer Inst. 1992 Oct 7;84(19):1506-12 [1359153.001]
  • [Cites] J Steroid Biochem Mol Biol. 1993 Mar;44(4-6):671-3 [8476781.001]
  • [Cites] Curr Opin Cell Biol. 1993 Oct;5(5):806-11 [8240824.001]
  • [Cites] Cancer Res. 1994 Jan 1;54(1):152-8 [7903202.001]
  • [Cites] J Natl Cancer Inst. 1994 Jan 19;86(2):110-7 [7903701.001]
  • [Cites] Biochim Biophys Acta. 1994 May 27;1198(1):11-26 [8199193.001]
  • [Cites] Int J Cancer. 1994 Aug 1;58(3):400-6 [7914183.001]
  • [Cites] Science. 1997 Jan 17;275(5298):343-9 [8994024.001]
  • [Cites] Dev Biol. 2005 Jan 15;277(2):443-56 [15617686.001]
  • [Cites] Curr Opin Cell Biol. 2005 Oct;17(5):548-58 [16098727.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11230-5 [16357123.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):1883-90; discussion 1895-6 [16488983.001]
  • [Cites] Exp Hematol. 2006 May;34(5):622-30 [16647568.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8788-95 [16951195.001]
  • [Cites] BMC Mol Biol. 2006;7:29 [16978418.001]
  • [Cites] J Biol Chem. 2006 Dec 1;281(48):36501-9 [16956878.001]
  • [Cites] J Natl Cancer Inst. 2006 Dec 20;98(24):1777-85 [17179479.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):350-2 [16504380.001]
  • [Cites] Breast Cancer Res. 2006;8(5):R59 [17062128.001]
  • [Cites] Cells Tissues Organs. 2007;185(1-3):191-203 [17587825.001]
  • [Cites] Cancer Res. 2007 Aug 1;67(15):7212-22 [17671189.001]
  • [Cites] Cancer J. 2007 Sep-Oct;13(5):271-5 [17921723.001]
  • [Cites] Curr Drug Deliv. 2007 Oct;4(4):324-33 [17979652.001]
  • [Cites] Mol Endocrinol. 2007 Dec;21(12):2907-18 [17761946.001]
  • [Cites] Leuk Res. 2008 Mar;32(3):475-80 [17709137.001]
  • [Cites] Cancer Res. 2008 Mar 1;68(5):1378-87 [18316601.001]
  • [Cites] Breast Cancer Res. 2008;10(1):R10 [18241344.001]
  • [Cites] Br J Cancer. 2008 May 6;98(9):1515-24 [18382425.001]
  • [Cites] J Natl Cancer Inst. 2008 May 7;100(9):672-9 [18445819.001]
  • [Cites] Int J Gynecol Cancer. 2008 May-Jun;18(3):506-14 [17868344.001]
  • [Cites] Breast Cancer Res. 2008;10(2):R25 [18366788.001]
  • [Cites] Nat Clin Pract Oncol. 2008 Jun;5(6):337-47 [18431377.001]
  • [Cites] J Clin Oncol. 2008 Jun 10;26(17):2890-4 [18539969.001]
  • [Cites] PLoS One. 2008;3(8):e3077 [18728788.001]
  • [Cites] Oncogene. 2008 Oct 16;27(47):6120-30 [18591932.001]
  • [Cites] Cell Stem Cell. 2007 Nov;1(5):555-67 [18371393.001]
  • [Cites] J Cancer Res Clin Oncol. 2009 Jan;135(1):81-90 [18560890.001]
  • [Cites] Breast Dis. 2008;29:83-9 [19029627.001]
  • [Cites] Chem Biol Interact. 2009 Mar 16;178(1-3):48-55 [18952074.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2009 Mar;14(1):3-9 [19224345.001]
  • [Cites] Cancer Immunol Immunother. 2009 Aug;58(8):1185-94 [19048252.001]
  • [Cites] Cell. 2009 Aug 21;138(4):645-59 [19682730.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):13820-5 [19666588.001]
  • (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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15. Chan DW, Liu VW, To RM, Chiu PM, Lee WY, Yao KM, Cheung AN, Ngan HY: Overexpression of FOXG1 contributes to TGF-beta resistance through inhibition of p21WAF1/CIP1 expression in ovarian cancer. Br J Cancer; 2009 Oct 20;101(8):1433-43
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  • [Title] Overexpression of FOXG1 contributes to TGF-beta resistance through inhibition of p21WAF1/CIP1 expression in ovarian cancer.
  • Here, we showed that the overexpressed FOXG1 was involved in attenuating the anti-proliferative control of TGF-beta/Smads signalling in ovarian cancer.
  • METHODS: FOXG1 and p21(WAF1/CIP1) expressions were evaluated by real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR), western blot and immunohistochemical analyses.
  • Cell lines stably expressing or short hairpin RNA interference-mediated knockdown FOXG1 were established for studying the gain-or-loss functional effects of FOXG1.
  • XTT cell proliferation assay was used to measure cell growth of ovarian cancer cells.
  • RESULTS: Quantitative RT-PCR and western blot analyses showed that FOXG1 was upregulated and inversely associated with the expression levels of p21(WAF1/CIP1) in ovarian cancer.
  • The overexpression of FOXG1 was significantly correlated with high-grade ovarian cancer (P=0.025).
  • Immunohistochemical analysis on ovarian cancer tissue array was further evidenced that FOXG1 was highly expressed and significantly correlated with high-grade ovarian cancer (P=0.048).
  • Functionally, enforced expression of FOXG1 selectively blocked the TGF-beta-induced p21(WAF1/CIP1) expressions and increased cell proliferation in ovarian cancer cells.
  • Conversely, FOXG1 knockdown resulted in a 20-26% decrease in cell proliferation together with 16-33% increase in p21(WAF1/CIP1) expression.
  • CONCLUSION: Our results suggest that FOXG1 acts as an oncoprotein inhibiting TGF-beta-mediated anti-proliferative responses in ovarian cancer cells through suppressing p21(WAF1/CIP1) transcription.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p21 / antagonists & inhibitors. Forkhead Transcription Factors / physiology. Nerve Tissue Proteins / physiology. Ovarian Neoplasms / drug therapy. Transforming Growth Factor beta / pharmacology
  • [MeSH-minor] Active Transport, Cell Nucleus. Adult. Aged. Cell Line, Tumor. Cell Proliferation. Drug Resistance, Neoplasm. Female. Humans. Immunohistochemistry. Middle Aged. Promoter Regions, Genetic. Signal Transduction

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  • [Cites] Endocr Rev. 1998 Jun;19(3):349-63 [9626558.001]
  • [Cites] Cancer Lett. 1998 Jan 9;122(1-2):157-63 [9464505.001]
  • [Cites] Annu Rev Biochem. 1998;67:753-91 [9759503.001]
  • [Cites] Clin Cancer Res. 1996 Aug;2(8):1255-61 [9816295.001]
  • [Cites] Int J Oncol. 1999 Jan;14(1):93-101 [9863014.001]
  • [Cites] Int J Cancer. 1999 Jul 19;82(2):197-202 [10389752.001]
  • [Cites] Br J Cancer. 1999 Apr;80(1-2):194-205 [10389996.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):222-7 [10508522.001]
  • [Cites] Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):108-18 [15650400.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):2078-93 [15774796.001]
  • [Cites] J Neurosci. 2005 Apr 27;25(17):4435-41 [15858069.001]
  • [Cites] Gynecol Oncol. 2005 Sep;98(3):427-33 [15993480.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2006;9(2):185-9 [16550207.001]
  • [Cites] Cancer Biol Ther. 2006 Jun;5(6):601-7 [16627986.001]
  • [Cites] Hum Pathol. 2007 Mar;38(3):400-9 [17217994.001]
  • [Cites] Nat Cell Biol. 2007 May;9(5):531-40 [17435750.001]
  • [Cites] J Steroid Biochem Mol Biol. 2007 May;104(3-5):195-207 [17482455.001]
  • [Cites] J Neurooncol. 2007 Nov;85(2):111-22 [17522785.001]
  • [Cites] WormBook. 2005;:1-12 [18050404.001]
  • [Cites] Cancer Res. 2008 Feb 1;68(3):783-9 [18245479.001]
  • [Cites] Anticancer Res. 2000 Jan-Feb;20(1A):43-51 [10769633.001]
  • [Cites] Mol Cell Biol. 2000 Sep;20(17):6201-11 [10938097.001]
  • [Cites] J Biol Chem. 2000 Sep 22;275(38):29244-56 [10878024.001]
  • [Cites] Cell. 2000 Oct 13;103(2):295-309 [11057902.001]
  • [Cites] EMBO J. 2000 Oct 2;19(19):5178-93 [11013220.001]
  • [Cites] Mol Cell Biol. 2001 Mar;21(6):1962-72 [11238932.001]
  • [Cites] Blood. 2001 Apr 1;97(7):2137-44 [11264182.001]
  • [Cites] J Biol Chem. 2001 Aug 10;276(32):30224-30 [11387330.001]
  • [Cites] J Biol Chem. 2001 Nov 16;276(46):43175-81 [11553622.001]
  • [Cites] J Neurosci. 2002 Aug 1;22(15):6526-36 [12151532.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38557-64 [12145312.001]
  • [Cites] Mod Pathol. 2003 Jan;16(1):86-96 [12527718.001]
  • [Cites] J Exp Clin Cancer Res. 2003 Jun;22(2):315-20 [12866583.001]
  • [Cites] J Biol Chem. 2003 Aug 15;278(33):30540-7 [12764135.001]
  • [Cites] J Clin Invest. 2003 Oct;112(7):1116-24 [14523048.001]
  • [Cites] J Biol Chem. 2003 Nov 7;278(45):44377-84 [12947087.001]
  • [Cites] Cell. 2004 Apr 16;117(2):211-23 [15084259.001]
  • [Cites] Mol Cell. 2004 May 21;14(4):416-8 [15149589.001]
  • [Cites] J Cell Physiol Suppl. 1987;Suppl 5:1-7 [3316252.001]
  • [Cites] J Biol Chem. 1994 Oct 14;269(41):25392-9 [7929236.001]
  • [Cites] Genes Dev. 1995 Aug 1;9(15):1831-45 [7649471.001]
  • [Cites] Oncogene. 1996 Jul 18;13(2):441-4 [8710385.001]
  • [Cites] Am J Surg. 1996 Dec;172(6):641-5 [8988667.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10885-8 [9380729.001]
  • [Cites] J Cell Physiol. 1998 Aug;176(2):424-34 [9648930.001]
  • (PMID = 19755996.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXG1 protein, human; 0 / Forkhead Transcription Factors; 0 / Nerve Tissue Proteins; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC2768441
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16. 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

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  • [Cites] In Vitro. 1983 Mar;19(3 Pt 1):147-58 [6339371.001]
  • [Cites] Exp Cell Res. 1994 Dec;215(2):303-9 [7526992.001]
  • [Cites] Lab Invest. 1985 Mar;52(3):243-56 [2579289.001]
  • [Cites] Cancer Detect Prev. 1987;10(3-4):237-46 [3568022.001]
  • [Cites] Annu Rev Biochem. 1987;56:779-827 [3304147.001]
  • [Cites] Cancer Genet Cytogenet. 1987 Oct;28(2):201-12 [3476184.001]
  • [Cites] Asia Oceania J Obstet Gynaecol. 1989 Dec;15(4):403-16 [2624581.001]
  • [Cites] Semin Cancer Biol. 1990 Jun;1(3):165-79 [1715788.001]
  • [Cites] Gynecol Oncol. 1992 Nov;47(2):179-85 [1361478.001]
  • [Cites] J Cell Sci. 1992 Oct;103 ( Pt 2):293-8 [1282514.001]
  • [Cites] Mol Endocrinol. 1993 Oct;7(10):1244-55 [8264658.001]
  • [Cites] Science. 1995 Dec 1;270(5241):1491-4 [7491495.001]
  • [Cites] EMBO J. 1996 May 1;15(9):2174-83 [8641283.001]
  • [Cites] N Engl J Med. 1996 Aug 29;335(9):640-9 [8692240.001]
  • [Cites] Cancer. 1997 Feb 1;79(3):462-7 [9028355.001]
  • [Cites] Cancer Res. 1997 Sep 15;57(18):3935-40 [9307275.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4736-8 [9354433.001]
  • [Cites] J Steroid Biochem Mol Biol. 1997 Aug;62(5-6):449-54 [9449248.001]
  • [Cites] J Biol Chem. 1998 Jun 26;273(26):15879-82 [9632630.001]
  • [Cites] Cancer Res. 1998 Aug 1;58(15):3254-8 [9699651.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Nov 10;95(23):13513-8 [9811831.001]
  • [Cites] Cancer Res. 1998 Dec 1;58(23):5285-90 [9850049.001]
  • [Cites] Oncology. 1999;56(1):59-65 [9885379.001]
  • [Cites] Subcell Biochem. 1998;31:105-40 [9932491.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):668-75 [10080613.001]
  • [Cites] Int J Gynecol Pathol. 1999 Apr;18(2):138-43 [10202671.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10182-7 [10468583.001]
  • [Cites] J Natl Cancer Inst. 1964 Sep;33:441-56 [14207855.001]
  • [Cites] Rom J Morphol Embryol. 1998 Jan-Dec;44(1-4):101-7 [15678850.001]
  • [Cites] Breast Dis. 2004;20:25-31 [15687704.001]
  • [Cites] Eur J Cancer. 2005 Mar;41(5):673-5 [15763641.001]
  • [Cites] Ann Oncol. 2006 Apr;17(4):637-45 [16407419.001]
  • [Cites] Int J Gynecol Cancer. 2006 Sep-Oct;16(5):1911-7 [17009991.001]
  • [Cites] Cell. 1999 Oct 29;99(3):323-34 [10555148.001]
  • [Cites] Mod Pathol. 2000 Mar;13(3):295-308 [10757340.001]
  • [Cites] Clin Cancer Res. 2000 Oct;6(10):3937-43 [11051241.001]
  • [Cites] Mol Endocrinol. 2000 Dec;14(12):1954-61 [11117526.001]
  • [Cites] J Steroid Biochem Mol Biol. 2000 Dec 31;75(4-5):209-12 [11282273.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4576-82 [11389093.001]
  • [Cites] Int J Biochem Cell Biol. 2001 Oct;33(10):960-70 [11470230.001]
  • [Cites] Gynecol Oncol. 2001 Dec;83(3):523-32 [11733966.001]
  • [Cites] Am J Hum Genet. 2002 Apr;70(4):829-44 [11875759.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):6-11 [12517768.001]
  • [Cites] Hum Cell. 2002 Sep;15(3):104-17 [12703541.001]
  • [Cites] J Exp Clin Cancer Res. 2003 Jun;22(2):265-71 [12866577.001]
  • [Cites] Int J Oncol. 2003 Sep;23(3):803-10 [12888921.001]
  • [Cites] Endocr Rev. 2003 Aug;24(4):428-65 [12920150.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 2003 Dec 10;111(2):109-21 [14597237.001]
  • [Cites] Gynecol Oncol. 2004 Feb;92(2):719-25 [14766275.001]
  • [Cites] CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29 [14974761.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Mar;49(3):179-86 [15036258.001]
  • [Cites] Int J Oncol. 2004 May;24(5):1311-24 [15067356.001]
  • [Cites] Mol Cancer. 2004 Mar 11;3:7 [15016316.001]
  • [Cites] Gynecol Oncol. 2004 Sep;94(3):699-704 [15350361.001]
  • [Cites] Gynecol Oncol. 2004 Sep;94(3):785-95 [15350374.001]
  • [Cites] Cancer. 1971 May;27(5):1064-73 [4325742.001]
  • [Cites] Am J Obstet Gynecol. 1972 Dec 15;114(8):1012-9 [4673779.001]
  • [Cites] J Biol Chem. 2007 Feb 16;282(7):4794-802 [17150964.001]
  • [Cites] Gynecol Oncol. 1984 Feb;17(2):213-30 [6706226.001]
  • (PMID = 17894888.001).
  • [ISSN] 1477-7827
  • [Journal-full-title] Reproductive biology and endocrinology : RB&E
  • [ISO-abbreviation] Reprod. Biol. Endocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones
  • [Other-IDs] NLM/ PMC2092433
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17. 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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  • [Cites] Am J Surg Pathol. 1985 Aug;9(8):543-69 [3911780.001]
  • [Cites] Scand J Gastroenterol Suppl. 1999;230:64-70 [10499464.001]
  • [Cites] Gynecol Oncol. 1997 Feb;64(2):282-4 [9038278.001]
  • [Cites] Obstet Gynecol Surv. 1998 Apr;53(4):240-7 [9560834.001]
  • [Cites] Gynecol Oncol. 1997 Jun;65(3):447-52 [9190974.001]
  • [Cites] Am J Obstet Gynecol. 1997 Dec;177(6):1450-7 [9423750.001]
  • [Cites] Acta Obstet Gynecol Scand. 2001 Nov;80(11):1069-74 [11703210.001]
  • [Cites] Tumori. 2001 Jan-Feb;87(1):47-53 [11669558.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4041-6 [11549623.001]
  • [Cites] Cancer. 1997 May 15;79(10):1951-5 [9149022.001]
  • [Cites] Am J Surg Pathol. 1984 Aug;8(8):575-96 [6465418.001]
  • [Cites] J Pathol. 1987 Aug;152(4):253-63 [2444685.001]
  • [Cites] Am J Surg Pathol. 1985 Oct;9(10):737-43 [4061731.001]
  • [Cites] Obstet Gynecol. 1996 Apr;87(4):527-31 [8602303.001]
  • [Cites] Int J Gynaecol Obstet. 2000 Aug;70(2):209-62 [11041682.001]
  • [Cites] Int J Gynecol Pathol. 1998 Jan;17 (1):46-53 [9475192.001]
  • [Cites] Pediatr Pathol. 1993 Jul-Aug;13(4):389-400 [8372023.001]
  • [Cites] Gynecol Oncol. 1993 Jan;48(1):119-23 [8423014.001]
  • [Cites] Virchows Arch. 1997 Apr;430(4):301-9 [9134041.001]
  • [Cites] Anticancer Drugs. 1998 Aug;9(7):621-3 [9773806.001]
  • [Cites] Gynecol Oncol. 1995 Jun;57(3):417-22 [7774848.001]
  • [Cites] Eur J Cell Biol. 1985 May;37:175-90 [3896804.001]
  • [Cites] Virchows Arch. 1996 Feb;427(5):497-502 [8624579.001]
  • [Cites] Gynecol Oncol. 2001 Apr;81(1):113-6 [11277661.001]
  • [Cites] Mod Pathol. 1997 Nov;10(11):1101-5 [9388060.001]
  • [Cites] Klin Padiatr. 2002 Jul-Aug;214(4):173-8 [12165898.001]
  • [Cites] Arch Fr Pediatr. 1992 Nov;49(9):793-8 [1300967.001]
  • [Cites] J Clin Oncol. 1988 Jun;6(6):990-5 [3373268.001]
  • (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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18. 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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19. Chatzistamou I, Schally AV, Sun B, Armatis P, Szepeshazi K: Inhibition of growth of OV-1063 human epithelial ovarian cancers and c- jun and c- fos oncogene expression by bombesin antagonists. Br J Cancer; 2000 Oct;83(7):906-13
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  • [Title] Inhibition of growth of OV-1063 human epithelial ovarian cancers and c- jun and c- fos oncogene expression by bombesin antagonists.
  • Receptors for bombesin are present on human ovarian cancers and bombesin-like peptides could function as growth factors in this carcinoma.
  • Therefore, we investigated the effects of bombesin/gastrin-releasing peptide (GRP) antagonists RC-3940-II and RC-3095 on the growth of human ovarian carcinoma cell line OV-1063, xenografted into nude mice.
  • Treatment with RC-3940-II at doses of 10 microg and 20 microg per day s.c. decreased tumour volume by 60.9% (P< 0.05) and 73.5% (P< 0.05) respectively, after 25 days, compared to controls.
  • In OV-1063 cells cultured in vitro, GRP(14-27) induced the expression of mRNA for c- jun and c- fos oncogenes in a time-dependent manner.
  • In vivo, the levels of c- jun and c- fos mRNA in OV-1063 tumours were decreased by 43% (P< 0.05) and 45% (P = 0.
  • 05) respectively, after treatment with RC-3940-II at 20 microg per day.
  • Exposure of OV-1063, UCI-107 and ES-2 ovarian carcinoma cells to RC-3940-II at 1 microM concentration for 24 h in vitro, extended the latency period for the development of palpable tumours in nude mice.
  • Our results indicate that antagonists of bombesin/GRP inhibit the growth of OV-1063 ovarian cancers by mechanisms that probably involve the downregulation of c- jun and c- fos proto-oncogenes.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bombesin / analogs & derivatives. Bombesin / pharmacology. Genes, fos / drug effects. Genes, jun / drug effects. Gonadotropin-Releasing Hormone / analogs & derivatives. Ovarian Neoplasms / drug therapy. Peptide Fragments / pharmacology
  • [MeSH-minor] Animals. Cell Division / drug effects. Epithelium / pathology. Female. Gastrin-Releasing Peptide / antagonists & inhibitors. Gene Expression / drug effects. Hormone Antagonists / pharmacology. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Proto-Oncogene Proteins c-fos / biosynthesis. Proto-Oncogene Proteins c-fos / genetics. Proto-Oncogene Proteins c-jun / biosynthesis. Proto-Oncogene Proteins c-jun / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Bombesin / biosynthesis. Receptors, Bombesin / classification. Receptors, Bombesin / genetics. Tumor Cells, Cultured / drug effects

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  • [Copyright] Copyright 2000 Cancer Research Campaign.
  • [Cites] Oncogene. 1999 Nov 25;18(50):7168-73 [10597318.001]
  • [Cites] Cancer Res. 1999 Mar 1;59(5):1152-9 [10070977.001]
  • [Cites] Prostate. 2000 Mar 1;42(4):295-303 [10679759.001]
  • [Cites] Nature. 1985 Aug 29-Sep 4;316(6031):823-6 [2993906.001]
  • [Cites] Oncology. 1985;42(5):332-7 [2412195.001]
  • [Cites] Cancer Res. 1987 Feb 1;47(3):821-5 [3026617.001]
  • [Cites] Cell. 1988 Dec 2;55(5):917-24 [3142692.001]
  • [Cites] Cancer. 1989 May 1;63(9):1714-20 [2539244.001]
  • [Cites] Int J Pept Protein Res. 1988 Dec;32(6):425-35 [2469662.001]
  • [Cites] Cancer Chemother Pharmacol. 1989;24(3):148-54 [2544306.001]
  • [Cites] J Cancer Res Clin Oncol. 1992;118(1):35-43 [1309532.001]
  • [Cites] Int J Pept Protein Res. 1991 Dec;38(6):593-600 [1726427.001]
  • [Cites] Cancer Res. 1992 Aug 15;52(16):4545-7 [1643647.001]
  • [Cites] J Natl Cancer Inst. 1992 Dec 16;84(24):1915-22 [1460673.001]
  • [Cites] Recent Prog Horm Res. 1993;48:365-91 [8382830.001]
  • [Cites] Life Sci. 1993;52(14):1161-73 [8383784.001]
  • [Cites] Cancer. 1994 Feb 15;73(4):1229-38 [8313327.001]
  • [Cites] Cancer Res. 1994 Feb 15;54(4):1035-41 [8313359.001]
  • [Cites] J Biol Chem. 1994 Mar 18;269(11):8596-603 [8132585.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3804-8 [8170991.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jul 19;91(15):7090-4 [7518926.001]
  • [Cites] J Cancer Res Clin Oncol. 1994;120(9):519-28 [8045917.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12664-8 [7809097.001]
  • [Cites] Cancer Res. 1995 Jan 15;55(2):280-7 [7812958.001]
  • [Cites] Biomed Pharmacother. 1994;48(10):465-72 [7858155.001]
  • [Cites] Peptides. 1995;16(2):289-92 [7784258.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jun 20;92(13):6205-9 [7597102.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Sep;81(9):3215-21 [8784072.001]
  • [Cites] Int J Cancer. 1996 Sep 27;68(1):1-7 [8895531.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Feb 4;94(3):956-60 [9023364.001]
  • [Cites] Prostate. 1997 Aug 1;32(3):164-72 [9254895.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10913-8 [9380734.001]
  • [Cites] Eur J Cancer. 1997 Jun;33(7):1141-8 [9376196.001]
  • [Cites] Cancer. 1998 Mar 1;82(5):909-17 [9486581.001]
  • [Cites] Dig Dis Sci. 1998 Jul;43(7):1465-73 [9690380.001]
  • [Cites] J Steroid Biochem Mol Biol. 1998 Apr;65(1-6):199-206 [9699874.001]
  • [Cites] Eur J Cancer. 1998 Apr;34(5):710-7 [9713279.001]
  • [Cites] Cancer. 1998 Oct 1;83(7):1335-43 [9762934.001]
  • [Cites] CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1 [10200775.001]
  • [Cites] Eur J Cancer. 1999 Oct;35(10):1477-516 [10673980.001]
  • (PMID = 10970693.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] SCOTLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hormone Antagonists; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Messenger; 0 / Receptors, Bombesin; 0 / bombesin(6-14), Hca(6)-Leu(13)-psi(CH2N)-Tac(14)-; 138147-78-1 / bombesin (6-14), Tpi(6)-Leu(13)-psi(CH2NH)-Leu(14)-; 33515-09-2 / Gonadotropin-Releasing Hormone; 80043-53-4 / Gastrin-Releasing Peptide; OON1HFZ4BA / cetrorelix; PX9AZU7QPK / Bombesin
  • [Other-IDs] NLM/ PMC2374679
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20. McDonnel AC, Murdoch WJ: High-dose progesterone inhibition of urokinase secretion and invasive activity by SKOV-3 ovarian carcinoma cells: evidence for a receptor-independent nongenomic effect on the plasma membrane. J Steroid Biochem Mol Biol; 2001 Aug;78(2):185-91
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  • [Title] High-dose progesterone inhibition of urokinase secretion and invasive activity by SKOV-3 ovarian carcinoma cells: evidence for a receptor-independent nongenomic effect on the plasma membrane.
  • Urokinase plasminogen activator (uPA) has been implicated in the metastatic potential of ovarian carcinomas of surface epithelial origin.
  • The SKOV-3 human ovarian cancer cell line was tested for uPA secretory responses (enzyme immunoassay of conditioned media) after treatments with sex steroids, human menopausal gonadotropins (hMG), or gonadotropin-releasing hormone (GnRH).
  • [MeSH-major] Adenocarcinoma / drug therapy. Cell Membrane / drug effects. Ovarian Neoplasms / drug therapy. Progesterone / pharmacology. Urokinase-Type Plasminogen Activator / secretion
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Interactions. Estradiol / pharmacology. Female. Gonadotropin-Releasing Hormone / pharmacology. Gonadotropins / pharmacology. Humans. Mifepristone / pharmacology. Neoplasm Invasiveness / prevention & control. Receptors, Progesterone / antagonists & inhibitors. Testosterone / pharmacology. Tumor Cells, Cultured

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  • (PMID = 11566443.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gonadotropins; 0 / Receptors, Progesterone; 320T6RNW1F / Mifepristone; 33515-09-2 / Gonadotropin-Releasing Hormone; 3XMK78S47O / Testosterone; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
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21. 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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22. Yang YC, Wu CC, Chen CP, Chang CL, Wang KL: Reevaluating the safety of fertility-sparing hormonal therapy for early endometrial cancer. Gynecol Oncol; 2005 Nov;99(2):287-93
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  • [Title] Reevaluating the safety of fertility-sparing hormonal therapy for early endometrial cancer.
  • OBJECTIVE: To evaluate the safety of fertility-sparing hormonal therapy for endometrial cancer in young patients.
  • METHODS: Six patients diagnosed with endometrial adenocarcinoma grade I and had undergone progestin treatment were reviewed.
  • Four patients failed progestin treatment and were then found at surgery to have both endometrial and ovarian cancers.
  • A clonality assay using the human androgen receptor gene as the X-linked polymorphic marker and immunohistochemistry for steroid hormone receptor expression were used to delineate the relation between the endometrial and ovarian lesions and to explore possible causes of treatment failure.
  • Four of the six responded to the treatment at a mean of 3.5 months.
  • Two patients did not respond to progestin treatment.
  • At surgery in those 4, both endometrial and ovarian tumors were found.
  • The clonality assay revealed an independent cell origin for the endometrial and ovarian lesions in 2 of the 4 women who failed progestin treatment.
  • Progesterone receptors were absent in both endometrial and ovarian tumors in 2 of these 4 patients.
  • CONCLUSION: The absence of progesterone receptors may relate to the failure of progestin treatment.
  • The use of progestin treatment for well-differentiated early endometrial carcinoma should be cautious and requires very careful clinical evaluation before and after treatment.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Endometrioid / drug therapy. Endometrial Neoplasms / drug therapy. Fertility. Megestrol Acetate / therapeutic use
  • [MeSH-minor] Adult. Chromosomes, Human, X / genetics. Estrogen Receptor alpha / biosynthesis. Female. Humans. Immunohistochemistry. Neoplasm Recurrence, Local. Ovarian Neoplasms / genetics. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / surgery. Prospective Studies. Receptors, Androgen / genetics. Receptors, Progesterone / biosynthesis. Treatment Failure. X Chromosome Inactivation

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  • (PMID = 16051341.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogen Receptor alpha; 0 / Receptors, Androgen; 0 / Receptors, Progesterone; TJ2M0FR8ES / Megestrol Acetate
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23. Namba R, Young LJ, Maglione JE, McGoldrick ET, Liu S, Wurz GT, DeGregorio MW, Borowsky AD, MacLeod CL, Cardiff RD, Gregg JP: Selective estrogen receptor modulators inhibit growth and progression of premalignant lesions in a mouse model of ductal carcinoma in situ. Breast Cancer Res; 2005;7(6):R881-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • DCIS accounts for nearly 20% of newly diagnosed breast cancer, but the lack of experimentally amenable in vivo DCIS models hinders the development of treatment strategies.
  • Here, we demonstrate the utility of a mouse transplantation model of DCIS for chemoprevention studies using selective estrogen receptor modulators (SERMs).
  • This model consists of a set of serially transplanted lines of genetically engineered mouse mammary intraepithelial neoplasia (MIN) outgrowth (MIN-O) tissue that have stable characteristics.
  • We studied the ovarian-hormone-responsiveness of one of the lines with a particular focus on the effects of two related SERMs, tamoxifen and ospemifene.
  • METHODS: The estrogen receptor (ER) status and ovarian-hormone-dependence of the mouse MIN outgrowth tissue were determined by immunohistochemistry and ovarian ablation.
  • The effects on ER status, cell proliferation, and apoptosis were studied with immunohistochemistry.
  • RESULTS: The MIN-O was ER-positive and ovarian ablation resulted in reduced MIN-O growth and tumor development.
  • Likewise, tamoxifen and ospemifene treatments decreased the MIN growth and tumor incidence in comparison with the control (P < 0.01).
  • Both SERMs significantly decreased cell proliferation.
  • Between the two SERM treatment groups, there were no statistically significant differences in MIN-O size, tumor latency, or proliferation rate.
  • In contrast, the ospemifene treatment significantly increased ER levels while tamoxifen significantly decreased them.
  • These data demonstrate the value of this model system for preclinical testing of antiestrogen or other therapies designed to prevent or delay the malignant transformation of premalignant mammary lesions in chemoprevention.

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  • [Cites] Endocrinology. 2000 Feb;141(2):809-20 [10650964.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1474-81 [10334533.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):968-88 [10713680.001]
  • [Cites] J Steroid Biochem Mol Biol. 2001 Jun;77(4-5):271-9 [11457665.001]
  • [Cites] Arch Toxicol. 2001 Aug;75(6):375-80 [11570696.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8298-305 [11719463.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6967-72 [12011455.001]
  • [Cites] Cancer Res. 2002 May 15;62(10):2798-805 [12019156.001]
  • [Cites] Lancet. 2005 Jan 1-7;365(9453):60-2 [15639680.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 2):951s-8s [15701892.001]
  • [Cites] J Clin Oncol. 2005 Apr 10;23(11):2469-76 [15753463.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3493-6 [15833886.001]
  • [Cites] Clin Breast Cancer. 2005 Apr;6(1):27-37 [15899070.001]
  • [Cites] Oncogene. 2005 Jun 16;24(26):4220-31 [15824740.001]
  • [Cites] Breast Cancer Res Treat. 2003 Mar;78(1):1-6 [12611451.001]
  • [Cites] Int J Cancer. 2003 Jun 20;105(3):384-9 [12704673.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2425-33 [12750262.001]
  • [Cites] Menopause. 2003 Sep-Oct;10(5):433-9 [14501605.001]
  • [Cites] Crit Rev Oncol Hematol. 2002 Jul;43(1):63-76 [12098608.001]
  • [Cites] Am J Pathol. 2002 Sep;161(3):1087-97 [12213737.001]
  • [Cites] Maturitas. 2002 Nov 20;43(3):207-14 [12443837.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):951-6 [12459733.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] Surg Oncol. 2003 Dec;12(4):213-9 [14998562.001]
  • [Cites] Mol Cancer Ther. 2004 Aug;3(8):941-53 [15299077.001]
  • [Cites] Mol Cancer Res. 2004 Aug;2(8):453-63 [15328372.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1558-68 [15466970.001]
  • [Cites] J Natl Cancer Inst. 1976 Aug;57(2):331-7 [826649.001]
  • [Cites] J Clin Oncol. 1986 Sep;4(9):1326-30 [3528402.001]
  • [Cites] Science. 1987 Jan 9;235(4785):177-82 [3798106.001]
  • [Cites] Breast Cancer Res Treat. 1997 Jul;44(3):201-10 [9266099.001]
  • [Cites] Lancet. 1998 May 16;351(9114):1451-67 [9605801.001]
  • [Cites] J Chromatogr B Biomed Sci Appl. 1999 Mar 5;724(1):163-71 [10202969.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):273-5 [10667575.001]
  • (PMID = 16280035.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA89140-01; United States / NCI NIH HHS / CA / R01 CA089140; United States / NCRR NIH HHS / RR / U42 RR014905; United States / NCRR NIH HHS / RR / U42RR14905; United States / NCI NIH HHS / CA / R01CA81376
  • [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] England
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen; B0P231ILBK / Ospemifene
  • [Other-IDs] NLM/ PMC1410776
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24. 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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  • [Cites] Cancer Res. 1985 Sep;45(9):4206-14 [3875407.001]
  • [Cites] Urology. 1986 Sep;28(3):228-31 [3489307.001]
  • [Cites] J Steroid Biochem. 1987 Mar;26(3):393-7 [3495702.001]
  • [Cites] Radiat Res. 1989 Jun;118(3):532-44 [2727274.001]
  • [Cites] Med Phys. 1994 Dec;21(12):1901-15 [7700197.001]
  • [Cites] Int J Cancer. 1996 Jul 29;67(3):357-64 [8707409.001]
  • [Cites] Endocrinology. 1996 Oct;137(10):4126-9 [8828467.001]
  • [Cites] Cytometry. 1996 Dec 15;26(4):281-5 [8979027.001]
  • [Cites] Oncology. 1997 May-Jun;54(3):199-202 [9143399.001]
  • [Cites] Am J Obstet Gynecol. 1997 Jun;176(6):1319-26; discussion 1326-7 [9215191.001]
  • [Cites] Gynecol Oncol. 1998 Oct;71(1):3-13 [9784312.001]
  • [Cites] J Natl Cancer Inst. 1998 Dec 2;90(23):1774-86 [9839517.001]
  • [Cites] J Endocrinol Invest. 1999 Mar;22(3):223-34 [10219893.001]
  • [Cites] J Org Chem. 2007 Jul 20;72(15):5546-54 [17585812.001]
  • [Cites] Neuroendocrinology. 2007;86(2):84-93 [17684316.001]
  • [Cites] Hum Pathol. 1993 Jan;24(1):90-5 [8418017.001]
  • [Cites] J Biol Chem. 1990 Apr 15;265(11):6048-54 [2156840.001]
  • [Cites] Cancer Res. 1990 Sep 1;50(17):5382-6 [2386943.001]
  • [Cites] Endocrinology. 1991 Jul;129(1):436-45 [1675988.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Aug 30;179(1):90-6 [1883394.001]
  • [Cites] J Urol. 1992 Mar;147(3 Pt 2):798-803 [1371552.001]
  • [Cites] Radiat Res. 1992 Mar;129(3):309-14 [1542718.001]
  • [Cites] J Med Chem. 1992 May 29;35(11):2113-29 [1597861.001]
  • [Cites] Exp Cell Res. 1956 Aug;11(2):297-305 [13375651.001]
  • [Cites] Biochem Pharmacol. 1962 Feb;11:155-9 [13904241.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Feb;90(2):893-903 [15585562.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2005 Mar;32(3):344-50 [15726353.001]
  • [Cites] Cell. 2005 Sep 9;122(5):751-62 [16143106.001]
  • [Cites] BMC Cancer. 2005;5:148 [16293185.001]
  • [Cites] Virchows Arch. 2006 Jul;449(1):24-30 [16628414.001]
  • [Cites] J Hepatol. 1993 Feb;17(2):187-91 [8383159.001]
  • [Cites] Nucl Med Biol. 1993 Jul;20(5):597-606 [8358345.001]
  • [Cites] Appl Radiat Isot. 1994 Jul;45(7):795-801 [8061661.001]
  • [Cites] Eur J Cancer. 1994;30A(7):911-4 [7946581.001]
  • [Cites] Am J Epidemiol. 2008 Jan 15;167(2):211-8 [17982156.001]
  • [Cites] Future Oncol. 2008 Feb;4(1):15-21 [18240997.001]
  • [Cites] J Hum Genet. 2008;53(3):220-6 [18217192.001]
  • [Cites] Breast Cancer Res. 2008;10(1):R16 [18275596.001]
  • [Cites] Adv Exp Med Biol. 2008;617:223-34 [18497046.001]
  • [Cites] Adv Exp Med Biol. 2008;617:557-64 [18497082.001]
  • [Cites] J Nucl Med. 2008 Jun;49(6):987-94 [18483103.001]
  • [Cites] J Clin Oncol. 2008 Aug 20;26(24):3923-9 [18711180.001]
  • [Cites] Curr Opin Pharmacol. 2008 Aug;8(4):440-8 [18674639.001]
  • [Cites] Urol Int. 2008;81(3):353-9 [18931557.001]
  • [Cites] Int J Clin Oncol. 2008 Oct;13(5):431-5 [18946753.001]
  • [Cites] Endocr Relat Cancer. 2008 Dec;15(4):1061-8 [18772244.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 2008 Dec;141(2):147-52 [18768247.001]
  • [Cites] Folia Histochem Cytobiol. 2008;46(3):269-76 [19056529.001]
  • [Cites] IUBMB Life. 2009 Jan;61(1):56-61 [19109827.001]
  • [Cites] Bioconjug Chem. 2009 Jan;20(1):78-86 [19117492.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):929-35 [10706107.001]
  • [Cites] BJU Int. 2000 May;85(7):932-44 [10792179.001]
  • [Cites] Br J Cancer. 2000 Oct;83(7):921-7 [10970695.001]
  • [Cites] J Urol. 2000 Dec;164(6):1992-5 [11061898.001]
  • [Cites] Nucl Med Biol. 2001 Jan;28(1):85-90 [11182568.001]
  • [Cites] Int J Cancer. 2002 Jun 10;99(5):652-7 [12115497.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26618-22 [12015315.001]
  • [Cites] Int J Cancer. 2002 Aug 10;100(5):507-14 [12124798.001]
  • [Cites] Mol Cell Endocrinol. 2002 Jul 31;193(1-2):121-8 [12161011.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2002 Sep;29(9):1174-81 [12192562.001]
  • [Cites] Radiat Res. 2003 Feb;159(2):251-61 [12537531.001]
  • [Cites] J Urol. 2003 Sep;170(3):990-3 [12913756.001]
  • [Cites] J Urol. 2003 Oct;170(4 Pt 1):1363-9 [14501770.001]
  • [Cites] Am J Clin Pathol. 2003 Nov;120(5):725-31 [14608899.001]
  • [Cites] Steroids. 2003 Dec;68(14):1163-71 [14643878.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2003;6(4):294-300 [14663470.001]
  • [Cites] J Endocrinol. 2004 Jan;180(1):77-85 [14709146.001]
  • [Cites] J Cell Biochem. 2004 Feb 15;91(3):483-90 [14755679.001]
  • [Cites] Int J Biol Markers. 2003 Oct-Dec;18(4):273-9 [14756542.001]
  • [Cites] J Cell Biochem. 2004 Mar 1;91(4):662-70 [14991758.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 3;101(31):11209-14 [15277682.001]
  • [Cites] J Cancer Res Clin Oncol. 2004 May;130(5):253-8 [14963700.001]
  • [Cites] J Cell Biol. 1974 Nov;63(2 Pt 1):515-23 [4138144.001]
  • [Cites] Proc Natl Acad Sci U S A. 1974 Dec;71(12):4836-8 [4531021.001]
  • [Cites] J Steroid Biochem. 1975 Mar-Apr;6(3-4):437-42 [171494.001]
  • [Cites] Biophys J. 1976 Sep;16(9):1003-12 [963201.001]
  • [Cites] Biochem Biophys Res Commun. 1978 Feb 28;80(4):849-57 [637870.001]
  • [Cites] Int J Appl Radiat Isot. 1981 Nov;32(11):811-5 [7309270.001]
  • [Cites] Cancer Res. 1983 Nov;43(11):5379-89 [6604576.001]
  • [Cites] J Neurooncol. 1983;1(3):179-89 [6088714.001]
  • (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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25. Spina CS, Ton L, Yao M, Maehr H, Wolfe MM, Uskokovic M, Adorini L, Holick MF: Selective vitamin D receptor modulators and their effects on colorectal tumor growth. J Steroid Biochem Mol Biol; 2007 Mar;103(3-5):757-62
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective vitamin D receptor modulators and their effects on colorectal tumor growth.
  • It is well documented that 1,25(OH)(2)D(3) also has anti-tumor effects on a number of cancers and cancer cell lines including breast, colorectal, gastric, liver, ovarian, prostate, and non-melanoma skin cancers.
  • Included in the anti-tumor activities of 1,25(OH)(2)D(3) are its ability to cause antiproliferation, prodifferentation and decrease angiogenesis.
  • Furthermore, through regulation of the plaminogen activator (PA) system and a class of proteolytic enzymes called matrix metalloproteinases (MMPs), 1,25(OH)(2)D(3) reduces the invasive spread of tumor cells.
  • Because of the calcemic limitations of using 1,25(OH)(2)D(3) as a therapy, we have tested the effects of a novel Gemini vitamin D analogue, Deuterated Gemini (DG), on mouse colorectal cancer.
  • We demonstrated that DG is more potent in reducing tumor volume and mass, compared to control and 1,25(OH)(2)D(3).
  • DG significantly prevented (100% reduction, p<0.05) the invasive spread of colorectal tumor cells into the surrounding muscle, and had no effect on serum calcium levels.
  • Thus, DG acts as a selective vitamin D receptor modulator (SVDRM) by enhancing select anti-tumor characteristic 1,25(OH)(2)D(3) activities, without inducing hypercalcemia.
  • Thus, DG shows promise in the development of colorectal cancer therapies.
  • [MeSH-major] Calcitriol / therapeutic use. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Receptors, Calcitriol / metabolism
  • [MeSH-minor] Animals. Calcium / blood. Cell Line, Tumor. Cell Proliferation. Disease Progression. Male. Mice. Mice, Inbred BALB C. Muscle Neoplasms / pathology. Muscle Neoplasms / secretion. Neoplasm Invasiveness

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
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  • (PMID = 17368190.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Calcitriol; FXC9231JVH / Calcitriol; SY7Q814VUP / Calcium
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