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1. 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


2. O'Brien N, Jones ST, Williams DG, Cunningham HB, Moreno K, Visentin B, Gentile A, Vekich J, Shestowsky W, Hiraiwa M, Matteo R, Cavalli A, Grotjahn D, Grant M, Hansen G, Campbell MA, Sabbadini R: Production and characterization of monoclonal anti-sphingosine-1-phosphate antibodies. J Lipid Res; 2009 Nov;50(11):2245-57
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  • Sphingosine-1-phosphate (S1P) is a pleiotropic bioactive lipid involved in multiple physiological processes.
  • This report describes the successful production and characterization of a murine monoclonal antibody, LT1002, directed against S1P, using novel immunization and screening methods applied to bioactive lipids.
  • Using an in vitro bioassay, LT1002 and LT1009 were effective in blocking S1P-mediated release of the pro-angiogenic and prometastatic cytokine, interleukin-8, from human ovarian carcinoma cells, showing that both antibodies can out-compete S1P receptors in binding to S1P.
  • The anti-S1P antibody shows promise as a novel, first-in-class therapeutic acting as a "molecular sponge" to selectively deplete S1P from blood and other compartments where pathological S1P levels have been implicated in disease progression or in disorders where immune modulation may be beneficial.

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  • (PMID = 19509417.001).
  • [ISSN] 1539-7262
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R44 CA110298; United States / NCI NIH HHS / CA / R44CA110298-3
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Heavy Chains; 0 / Interleukins; 0 / Lysophospholipids; 26993-30-6 / sphingosine 1-phosphate; NGZ37HRE42 / Sphingosine
  • [Other-IDs] NLM/ PMC2759830
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3. Koudelka S, Turánek-Knötigová P, Masek J, Korvasová Z, Skrabalová M, Plocková J, Bartheldyová E, Turánek J: Liposomes with high encapsulation capacity for paclitaxel: Preparation, characterisation and in vivo anticancer effect. J Pharm Sci; 2010 May;99(5):2309-19
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  • Paclitaxel (PTX) is approved for the treatment of ovarian and breast cancer.
  • The commercially available preparation of PTX, Cremophor EL(R) is associated with hypersensitivity reactions in spite of a suitable premedication.
  • In general, the developed liposomal PTX formulations are troubled with low PTX encapsulation capacity (maximal content, 3 mol%) and accompanied by PTX crystallisation.
  • Sucrose was found to be a suitable cryoprotectant at the lipid:sugar molar ratios of 1:5-1:10.
  • A dose-dependent anticancer effect was found in both hollow fibre implants and syngenic B16F10 melanoma mouse tumour models.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Drug Compounding. Drug Stability. Freeze Drying. Lipids / chemistry. Liposomes. Melanoma, Experimental / drug therapy. Melanoma, Experimental / metabolism. Mice. Mice, Inbred C57BL. Nanotechnology. Particle Size. Xenograft Model Antitumor Assays

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  • (PMID = 19904827.001).
  • [ISSN] 1520-6017
  • [Journal-full-title] Journal of pharmaceutical sciences
  • [ISO-abbreviation] J Pharm Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Lipids; 0 / Liposomes; P88XT4IS4D / Paclitaxel
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4. Zhigaltsev IV, Winters G, Srinivasulu M, Crawford J, Wong M, Amankwa L, Waterhouse D, Masin D, Webb M, Harasym N, Heller L, Bally MB, Ciufolini MA, Cullis PR, Maurer N: Development of a weak-base docetaxel derivative that can be loaded into lipid nanoparticles. J Control Release; 2010 Jun 15;144(3):332-40
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  • [Title] Development of a weak-base docetaxel derivative that can be loaded into lipid nanoparticles.
  • Hydrophobic uncharged drugs such as docetaxel are difficult to encapsulate and retain in liposomal nanoparticles (LNP).
  • In this work we show that a weak base derivative of docetaxel can be actively loaded into LNP using pH gradient loading techniques to achieve stable drug encapsulation and controlled release properties.
  • Docetaxel was derivatized at the hydroxyl group in the C-2' position to form an N-methyl-piperazinyl butanoic acid ester.
  • The free hydroxyl group in this position is essential for anticancer activity and the prodrug has, therefore, to be converted into the parent drug (docetaxel) to restore activity.
  • Cytotoxicity testing against a panel of cancer cell lines (breast, prostate and ovarian cancer) demonstrated that the prodrug is readily converted into active drug; the derivative was found to be as active as the parent drug in vitro.
  • The docetaxel derivative can be efficiently loaded at high drug-to-lipid ratios (up to 0.4 mg/mg) into LNP using pH loading techniques.
  • Pharmacokinetic, tolerability and efficacy studies in mice demonstrate that the LNP-encapsulated prodrug has the long drug circulation half-life required for efficient tumor accumulation (50-100 times higher drug plasma levels compared with free derivative and Taxotere, the commercial docetaxel formulation), is active in a xenograft model of breast cancer (MDA-MB-435/LCC6), and is well tolerated at i.v. doses of 3 times higher than the maximum tolerated dose (MTD) of the parent drug.
  • This is the first demonstration that a therapeutically active, remote-loaded, controlled-release LNP formulation of a taxane can be achieved.
  • The approach reported here has broad applicability to other approved drugs as well as new chemical entities.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Carriers / chemistry. Lipids / chemistry. Nanoparticles / chemistry. Taxoids / administration & dosage
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Cryoelectron Microscopy. Drug Compounding. Drug Stability. Female. Humans. Hydrogen-Ion Concentration. Mice. Molecular Structure. Solubility. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright (c) 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20202473.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / DDP-82935; Canada / Canadian Institutes of Health Research / / PPP-86167
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; 0 / Lipids; 0 / Taxoids; 15H5577CQD / docetaxel
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5. Dong X, Mattingly CA, Tseng MT, Cho MJ, Liu Y, Adams VR, Mumper RJ: Doxorubicin and paclitaxel-loaded lipid-based nanoparticles overcome multidrug resistance by inhibiting P-glycoprotein and depleting ATP. Cancer Res; 2009 May 1;69(9):3918-26
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  • [Title] Doxorubicin and paclitaxel-loaded lipid-based nanoparticles overcome multidrug resistance by inhibiting P-glycoprotein and depleting ATP.
  • To test the ability of nanoparticle formulations to overcome P-glycoprotein (P-gp)-mediated multidrug resistance, several different doxorubicin and paclitaxel-loaded lipid nanoparticles were prepared.
  • A series of in vitro cell assays were used including quantitative studies on uptake and efflux, inhibition of calcein acetoxymethylester efflux, alteration of ATP levels, membrane integrity, mitochondrial membrane potential, apoptosis, and cytotoxicity.
  • Calcein acetoxymethylester and ATP assays confirmed that blank nanoparticles inhibited P-gp and transiently depleted ATP. I.v. injection of pegylated paclitaxel nanoparticles showed marked anticancer efficacy in nude mice bearing resistant NCI/ADR-RES tumors versus all control groups.
  • Nanoparticles may be used to target both drug and biological mechanisms to overcome multidrug resistance via P-gp inhibition and ATP depletion.

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  • (PMID = 19383919.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115197-05; United States / NCI NIH HHS / CA / R01 CA115197; United States / NCI NIH HHS / CA / R01 CA115197-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fluoresceins; 0 / P-Glycoprotein; 148504-34-1 / calcein AM; 80168379AG / Doxorubicin; 8L70Q75FXE / Adenosine Triphosphate; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS139361; NLM/ PMC2758164
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6. Ye L, Wu XL, Xu L, Huang Q, Sun L, He Y, Yang KX: [Ovarian steroid cell tumor, not otherwise specified: a clinicopathologic study]. Zhonghua Bing Li Xue Za Zhi; 2007 Aug;36(8):516-20
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  • [Title] [Ovarian steroid cell tumor, not otherwise specified: a clinicopathologic study].
  • OBJECTIVE: To study the clinicopathologic features, diagnostic criteria, differential diagnosis and treatment options of ovarian steroid cell tumor, not otherwise specified (NOS).
  • METHODS: Light microscopy and immunohistochemical study was carried out in 8 cases of ovarian steroid cell tumor, NOS.
  • RESULTS: The 7 cases of benign ovarian steroid cell tumor, NOS were composed mainly of polygonal cells with granular eosinophilic cytoplasm and larger cells with vacuolated cytoplasm.
  • They resembled the architecture of normal adrenal gland, with formation of cell nests and trabeculae.
  • The single case of malignant ovarian steroid cell tumor had evidence of significant cellular pleomorphism, haemorrhage and coagulative tumor necrosis.
  • Immunohistochemical study showed that the tumor cells expressed calretinin and alpha-inhibin.
  • Differential diagnosis included oxyphilic granulosa cell tumor, thecoma, Sertoli cell tumor and clear cell carcinoma.
  • The treatment options of benign ovarian steroid cell tumor, NOS was local excision or ipsilateral salpingo-oophorectomy, while the malignant counterpart should be treated with a combination of surgery and chemotherapy, including administration of GnRH agonist.
  • CONCLUSIONS: Ovarian steroid cell tumor, NOS, is the most common type of ovarian steroid cell tumors.
  • Most of which are associated with a benign clinical outcome.
  • Immunohistochemistry is an important adjunct for diagnosis.
  • The treatment options of ovarian steroid cell tumor, NOS depend on its malignant potential.
  • [MeSH-major] Inhibins / metabolism. Ovarian Neoplasms / pathology. Ovary / pathology. S100 Calcium Binding Protein G / metabolism. Sex Cord-Gonadal Stromal Tumors / pathology
  • [MeSH-minor] Adolescent. Adult. Calbindin 2. Diagnosis, Differential. Female. Granulosa Cell Tumor / pathology. Humans. Ovariectomy / methods. Sertoli Cell Tumor / pathology. Thecoma / pathology. Young Adult

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  • (PMID = 17980097.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / S100 Calcium Binding Protein G; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
  • [Number-of-references] 27
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7. Hooks SB, Callihan P, Altman MK, Hurst JH, Ali MW, Murph MM: Regulators of G-Protein signaling RGS10 and RGS17 regulate chemoresistance in ovarian cancer cells. Mol Cancer; 2010 Nov 02;9:289
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  • [Title] Regulators of G-Protein signaling RGS10 and RGS17 regulate chemoresistance in ovarian cancer cells.
  • BACKGROUND: A critical therapeutic challenge in epithelial ovarian carcinoma is the development of chemoresistance among tumor cells following exposure to first line chemotherapeutics.
  • We have recently shown that Regulators of G-protein Signaling (RGS) proteins negatively regulate signaling by lysophosphatidic acid (LPA), a growth factor elevated in malignant ascites fluid that triggers oncogenic growth and survival signaling in ovarian cancer cells.
  • The goal of this study was to determine the role of RGS protein expression in ovarian cancer chemoresistance.
  • RESULTS: In this study, we find that RGS2, RGS5, RGS10 and RGS17 transcripts are expressed at significantly lower levels in cells resistant to chemotherapy compared with parental, chemo-sensitive cells in gene expression datasets of multiple models of chemoresistance.
  • Further, exposure of SKOV-3 cells to cytotoxic chemotherapy causes acute, persistent downregulation of RGS10 and RGS17 transcript expression.
  • Direct inhibition of RGS10 or RGS17 expression using siRNA knock-down significantly reduces chemotherapy-induced cell toxicity.
  • The effects of cisplatin, vincristine, and docetaxel are inhibited following RGS10 and RGS17 knock-down in cell viability assays and phosphatidyl serine externalization assays in SKOV-3 cells and MDR-HeyA8 cells.
  • CONCLUSIONS: Taken together, our data suggest that chemotherapy exposure triggers loss of RGS10 and RGS17 expression in ovarian cancer cells, and that loss of expression contributes to the development of chemoresistance, possibly through amplification of endogenous AKT signals.
  • Our results establish RGS10 and RGS17 as novel regulators of cell survival and chemoresistance in ovarian cancer cells and suggest that their reduced expression may be diagnostic of chemoresistance.

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  • (PMID = 21044322.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA151006-01; United States / NCI NIH HHS / CA / R15 CA151006; United States / NCI NIH HHS / CA / R15 CA151006-01; United States / NCI NIH HHS / CA / R15CA15006-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lysophospholipids; 0 / RGS Proteins; 0 / RGS10 protein, human; 0 / RGS17 protein, human; 0 / Taxoids; 15H5577CQD / docetaxel; 22002-87-5 / lysophosphatidic acid; 5J49Q6B70F / Vincristine; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2988731
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8. 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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9. Cattel L, Ceruti M, Dosio F: From conventional to stealth liposomes: a new frontier in cancer chemotherapy. Tumori; 2003 May-Jun;89(3):237-49
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  • [Title] From conventional to stealth liposomes: a new frontier in cancer chemotherapy.
  • Many attempts have been made to achieve good selectivity to targeted tumor cells by preparing specialized carrier agents that are therapeutically profitable for anticancer therapy.
  • Among these, liposomes are the most studied colloidal particles thus far applied in medicine and in particular in antitumor therapy.
  • Although they were first described in the 1960s, only at the beginning of 1990s did the first therapeutic liposomes appear on the market.
  • The first-generation liposomes (conventional liposomes) comprised a liposome-containing amphotericin B, Ambisome (Nexstar, Boulder, CO, USA), used as an antifungal drug, and Myocet (Elan Pharma Int, Princeton, NJ, USA), a doxorubicin-containing liposome, used in clinical trials to treat metastatic breast cancer.
  • The second-generation liposomes ("pure lipid approach") were long-circulating liposomes, such as Daunoxome, a daunorubicin-containing liposome approved in the US and Europe to treat AIDS-related Kaposi's sarcoma.
  • Actually, the only stealth liposome on the market is Caelyx/Doxil (Schering-Plough, Madison NJ, USA), used to cure AIDS-related Kaposi's sarcoma, resistant ovarian cancer and metastatic breast cancer.
  • Pegylated liposomal doxorubicin is characterized by a very long-circulation half-life, favorable pharmacokinetic behavior and specific accumulation in tumor tissues.
  • Active and cell targeted liposomes can be obtained by attaching some antigen-directed monoclonal antibodies (Moab or Moab fragments) or small proteins and molecules (folate, epidermal growth factor, transferrin) to the distal end of polyethylene glycol in pegylated liposomal doxorubicin.
  • The most promising therapeutic application of liposomes is as non-viral vector agents in gene therapy, characterized by the use of cationic phospholipids complexed with the negatively charged DNA plasmid.
  • The use of liposome formulations in local-regional anticancer therapy is also discussed.
  • Finally, pegylated liposomal doxorubicin containing radionuclides are used in clinical trials as tumor-imaging agents or in positron emission tomography.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Delivery Systems. Neoplasms / drug therapy

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  • (PMID = 12908776.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Liposomes; 30IQX730WE / Polyethylene Glycols
  • [Number-of-references] 121
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10. Schneider DT, Jänig U, Calaminus G, Göbel U, Harms D: Ovarian sex cord-stromal tumors--a clinicopathological study of 72 cases from the Kiel Pediatric Tumor Registry. Virchows Arch; 2003 Oct;443(4):549-60
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  • [Title] Ovarian sex cord-stromal tumors--a clinicopathological study of 72 cases from the Kiel Pediatric Tumor Registry.
  • We analyzed 72 patients with ovarian sex cord-stromal tumors (OSCST) registered at the German Pediatric Tumor Registry in Kiel over a 20-year period.
  • Juvenile granulosa cell tumors (JGCT, n=48) were the most frequent histological subtype.
  • In addition, there were 14 Sertoli-Leydig cell tumors, 5 sclerosing stromal tumors, 2 sex cord tumors with annular tubules, 2 thecomas and 1 steroid cell tumor.
  • Compared with adult granulosa cell tumors, JGCT showed pronounced mitotic activity [mean 9.8 mitoses/10 high power field (HPF)], which was significantly higher than in other histological subtypes (2.7/10 HPF, P=0.001).
  • Immunohistochemical analysis revealed frequent coexpression of vimentin (positive in 52/52 examined tumors), cytokeratin (27/33), and inhibin (19/20).
  • Of patients, 12 with Ic or higher stage tumors received adjuvant cisplatinum-based chemotherapy.
  • In conclusion, this analysis confirms that the majority of patients with OSCST present at low tumor stage and that prognosis in these patients is excellent.
  • Refractory tumors are characterized by high proliferative activity.
  • Therefore, histopathological evaluation substantially contributes to risk assessment in patients with OSCST and might be useful for therapy stratification in prospective therapeutic protocols.
  • [MeSH-major] Ovarian Neoplasms / pathology. Sex Cord-Gonadal Stromal Tumors / pathology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Infant. Sertoli-Leydig Cell Tumor / pathology

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  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
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11. Colomer R, Menéndez JA: Mediterranean diet, olive oil and cancer. Clin Transl Oncol; 2006 Jan;8(1):15-21
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  • Olive oil is an integral ingredient of the "Mediterranean diet" and accumulating evidence suggests that it may have a potential role in lowering the risk of several types of cancers.
  • Supporting our hypothesis, exogenous supplementation of cultured breast cancer cells with physiological concentrations of OA was found to suppress the overexpression of HER2 (Her-2/neu, erbB-2), a well-characterized oncogene playing a key role in the etiology, progression and response to chemotherapy and endocrine therapy in approximately 20% of breast carcinomas.
  • OA treatment was also found to synergistically enhance the efficacy of trastuzumab, a humanized monoclonal antibody binding with high affinity to the ectodomain (ECD) of the Her2-coded p185(HER2) oncoprotein.
  • Our most recent findings further reveal that OA exposure may suppresses HER2 at the transcriptional level by up-regulating the expression of the Ets protein PEA3 -a DNA-binding protein that specifically blocks HER2 promoter activity- in breast, ovarian and stomach cancer cell lines.
  • Indeed, OA-induced transcriptional repression of HER2 oncogene may represent a novel genomic explanation linking "Mediterranean diet", olive oil and cancer as it seems to equally operate in various types of Her-2/neu-related carcinomas.
  • [MeSH-major] Diet. Dietary Fats, Unsaturated / therapeutic use. Neoplasms / prevention & control. Plant Oils / therapeutic use
  • [MeSH-minor] Adult. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Breast Neoplasms / etiology. Breast Neoplasms / genetics. Breast Neoplasms / prevention & control. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. Child. Drug Synergism. Enzyme Activation / drug effects. Female. Genes, erbB-2 / drug effects. Humans. Hyperinsulinism / complications. Male. Neoplasm Invasiveness. Obesity / complications. Obesity / epidemiology. Oleic Acid / pharmacology. Oleic Acid / therapeutic use. Olive Oil. Receptor, ErbB-2 / antagonists & inhibitors. Trastuzumab

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  • (PMID = 16632435.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Dietary Fats, Unsaturated; 0 / Olive Oil; 0 / Plant Oils; 2UMI9U37CP / Oleic Acid; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
  • [Number-of-references] 70
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12. Tanyi JL, Morris AJ, Wolf JK, Fang X, Hasegawa Y, Lapushin R, Auersperg N, Sigal YJ, Newman RA, Felix EA, Atkinson EN, Mills GB: The human lipid phosphate phosphatase-3 decreases the growth, survival, and tumorigenesis of ovarian cancer cells: validation of the lysophosphatidic acid signaling cascade as a target for therapy in ovarian cancer. Cancer Res; 2003 Mar 1;63(5):1073-82
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  • [Title] The human lipid phosphate phosphatase-3 decreases the growth, survival, and tumorigenesis of ovarian cancer cells: validation of the lysophosphatidic acid signaling cascade as a target for therapy in ovarian cancer.
  • Lysophosphatidic acid (LPA) is present at elevated concentrations in the ascites and plasma of ovarian cancer patients.
  • Ovarian cancer cells produce and release LPA both constitutively and after stimulation.
  • LPA can induce proliferation, survival, invasiveness, and resistance to chemotherapy of ovarian cancer cells.
  • This suggests that LPA may be critically important for the development or progression of ovarian cancer and is thus a potential target for therapy.
  • In this study, we demonstrate that introduction of the integral membrane protein, human lipid phosphate phosphohydrolase-3 (hLPP-3) enzyme, which hydrolyzes phosphatidic acid, LPA, sphingosine, and ceramide phosphate in vitro with selectivity for LPA, into SKOV3 and OVCAR-3 ovarian cancer cells decreases colony-forming activity, increases apoptosis, and decreases tumor growth in vitro and in vivo.
  • Thus genetic or pharmacological manipulation of LPA metabolism, receptor activation, or downstream signaling is an attractive approach for therapy of ovarian cancer.
  • [MeSH-major] Lysophospholipids / physiology. Ovarian Neoplasms / enzymology. Phosphatidate Phosphatase / physiology. Receptors, G-Protein-Coupled
  • [MeSH-minor] Apoptosis / physiology. Cell Division / physiology. Enzyme Activation / drug effects. Female. Genetic Therapy / methods. Humans. Hydrolysis. Organothiophosphorus Compounds / pharmacology. Receptors, Cell Surface / agonists. Receptors, Lysophosphatidic Acid. Signal Transduction / physiology. Transfection. Tumor Cells, Cultured

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  • (PMID = 12615725.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA64602; United States / NCI NIH HHS / CA / P30 CA16672
  • [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 / Lysophospholipids; 0 / Organothiophosphorus Compounds; 0 / Receptors, Cell Surface; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Lysophosphatidic Acid; 5994-73-0 / methylphosphonothiolate; EC 3.1.3.- / lipid phosphate phosphatase; EC 3.1.3.4 / Phosphatidate Phosphatase
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13. Mastrobattista E, Kapel RH, Eggenhuisen MH, Roholl PJ, Crommelin DJ, Hennink WE, Storm G: Lipid-coated polyplexes for targeted gene delivery to ovarian carcinoma cells. Cancer Gene Ther; 2001 Jun;8(6):405-13
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  • [Title] Lipid-coated polyplexes for targeted gene delivery to ovarian carcinoma cells.
  • A nonviral gene delivery vector has been developed in our laboratory based on the cationic polymer, poly(2-(dimethylethylamino)ethyl methacrylate) (p(DMAEMA)).
  • However, these polyplexes were unable to transfect OVCAR-3 cells growing in the peritoneal cavity of nude mice after intraperitoneal administration, which could be ascribed to inactivation by components (including hyaluronic acid) present in the tumor ascitic fluid.
  • The present work aimed at (a) protecting p(DMAEMA)-based polyplexes against destabilization or inactivation by polyanions such as hyaluronic acid present in tumor ascitic fluid and (b) enhancing cellular uptake of the protected p(DMAEMA)-based polyplexes by targeting with antibody Fab' fragments.
  • To fulfill these requirements, we have developed a detergent removal method to coat polyplexes with anionic lipids.
  • More importantly, the transfection efficiency of lipopolyplexes was unaffected in the presence of hyaluronic acid, indicating that lipid coating of polyplexes protects against destabilization by hyaluronic acid.
  • By conjugating antibody Fab' fragments directed against the epithelial glycoprotein-2 to the lipidic surface of these lipopolyplexes, target cell-specific transfection of OVCAR-3 cells could be obtained in vitro.
  • [MeSH-major] Gene Transfer Techniques. Lipid Metabolism. Ovarian Neoplasms / therapy
  • [MeSH-minor] Animals. DNA / metabolism. Dose-Response Relationship, Drug. Female. Glucosides / pharmacology. Humans. Hyaluronic Acid / pharmacology. Methacrylates / pharmacology. Mice. Mice, Nude. Micelles. Microscopy, Electron. Plasmids / metabolism. Transfection. Tumor Cells, Cultured

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  • (PMID = 11498760.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glucosides; 0 / Methacrylates; 0 / Micelles; 29836-26-8 / octyl-beta-D-glucoside; 9004-61-9 / Hyaluronic Acid; 9007-49-2 / DNA; O0V97PV2G1 / 2-(dimethylamino)ethyl methacrylate
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14. L'Espérance S, Bachvarova M, Tetu B, Mes-Masson AM, Bachvarov D: Global gene expression analysis of early response to chemotherapy treatment in ovarian cancer spheroids. BMC Genomics; 2008;9:99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global gene expression analysis of early response to chemotherapy treatment in ovarian cancer spheroids.
  • BACKGROUND: Chemotherapy (CT) resistance in ovarian cancer (OC) is broad and encompasses diverse unrelated drugs, suggesting more than one mechanism of resistance.
  • To better understand the molecular mechanisms controlling the immediate response of OC cells to CT exposure, we have performed gene expression profiling in spheroid cultures derived from six OC cell lines (OVCAR3, SKOV3, TOV-112, TOV-21, OV-90 and TOV-155), following treatment with 10,0 microM cisplatin, 2,5 microM paclitaxel or 5,0 microM topotecan for 72 hours.
  • RESULTS: Exposure of OC spheroids to these CT drugs resulted in differential expression of genes associated with cell growth and proliferation, cellular assembly and organization, cell death, cell cycle control and cell signaling.
  • Genes, functionally involved in DNA repair, DNA replication and cell cycle arrest were mostly overexpressed, while genes implicated in metabolism (especially lipid metabolism), signal transduction, immune and inflammatory response, transport, transcription regulation and protein biosynthesis, were commonly suppressed following all treatments.
  • Cisplatin and topotecan treatments triggered similar alterations in gene and pathway expression patterns, while paclitaxel action was mainly associated with induction of genes and pathways linked to cellular assembly and organization (including numerous tubulin genes), cell death and protein synthesis.
  • However, the induction of genes linked to mechanisms of DNA replication and repair in cisplatin- and topotecan-treated OC spheroids could be associated with immediate adaptive response to treatment.
  • Similarly, overexpression of different tubulin genes upon exposure to paclitaxel could represent an early compensatory effect to this drug action.
  • Finally, multicellular growth conditions that are known to alter gene expression (including cell adhesion and cytoskeleton organization), could substantially contribute in reducing the initial effectiveness of CT drugs in OC spheroids.
  • Results described in this study underscore the potential of the microarray technology for unraveling the complex mechanisms of CT drugs actions in OC spheroids and early cellular response to treatment.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gene Expression / drug effects. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / genetics
  • [MeSH-minor] Cell Line, Tumor. Cisplatin / therapeutic use. Drug Resistance, Neoplasm / genetics. Female. Gene Expression Profiling. Gene Regulatory Networks. Humans. Paclitaxel / therapeutic use. Spheroids, Cellular. Topotecan / therapeutic use

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  • (PMID = 18302766.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7M7YKX2N15 / Topotecan; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2279123
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15. Patwardhan G, Gupta V, Huang J, Gu X, Liu YY: Direct assessment of P-glycoprotein efflux to determine tumor response to chemotherapy. Biochem Pharmacol; 2010 Jul 1;80(1):72-9
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  • [Title] Direct assessment of P-glycoprotein efflux to determine tumor response to chemotherapy.
  • Multidrug resistance is a major impediment to the success of cancer chemotherapy.
  • The overproduced P-glycoprotein that extrudes anticancer drugs from cells, is the most common mechanism detected in multidrug-resistant cancers.
  • Direct measurement of cellular efflux of tumors in vivo, rather than estimation of MDR1 mRNA and P-glycoprotein levels in samples stored or embedded, can functionally characterize the mechanism of drug resistance and determine the choice of anticancer drugs for cancer patients.
  • Herewith, we introduce a new approach to directly determine P-glycoprotein efflux of tumors.
  • Employing Flutax-2 (Oregon green-488 paclitaxel) and fluorescence spectrophotometry, this method has successfully measured cellular transportability including efflux and accumulation in diverse cancer cell lines, tumors and other tissues with high reproducibility.
  • With this method, we have quantitatively determined cellular efflux that is correlated with P-glycoprotein levels and the reversal effects of agents in cell lines of breast, ovarian, cervical and colon cancers, and in tumor-bearing mice.
  • It has sensitively detected these alterations of P-glycoprotein efflux in approximately 5mg tumor or other tissues with high confidence.
  • This direct and quick functional assessment has a potential to determine drug resistance in different types of cancers after surgical resection.
  • Further validation of this method in clinic settings for the diagnosis of drug resistance purpose is needed.

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  • [Copyright] (c) 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20298675.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR016456; United States / NCRR NIH HHS / RR / P20 RR016456-085644; United States / NCRR NIH HHS / RR / RR016456-066973; United States / NCRR NIH HHS / RR / P20 RR16456; United States / NCRR NIH HHS / RR / RR016456-076138; United States / NCRR NIH HHS / RR / P20 RR016456-076138; United States / NCRR NIH HHS / RR / RR016456-085644; United States / NCRR NIH HHS / RR / P20 RR016456-066973
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flutax 2; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / Taxoids
  • [Other-IDs] NLM/ NIHMS188299; NLM/ PMC2860649
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16. Liu YY, Han TY, Yu JY, Bitterman A, Le A, Giuliano AE, Cabot MC: Oligonucleotides blocking glucosylceramide synthase expression selectively reverse drug resistance in cancer cells. J Lipid Res; 2004 May;45(5):933-40
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  • [Title] Oligonucleotides blocking glucosylceramide synthase expression selectively reverse drug resistance in cancer cells.
  • To examine whether GCS is a target for cancer therapy, we have designed and tested the effects of antisense oligodeoxyribonucleotides (ODNs) to GCS on gene expression and chemosensitivity in multidrug-resistant cancer cells.
  • Pretreatment with asGCS ODN-7 increased doxorubicin sensitivity by 17-fold in MCF-7-AdrR (doxorubicin-resistant) breast cancer cells and by 10-fold in A2780-AD (doxorubicin-resistant) ovarian cancer cells.
  • In MCF-7 drug-sensitive breast cancer cells, asGCS ODN-7 only increased doxorubicin sensitivity by 3-fold, and it did not influence doxorubicin cytotoxicity in normal human mammary epithelial cells. asGCS ODN-7 was shown to be more efficient in reversing drug resistance than either the GCS chemical inhibitor d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol or the P-glycoprotein blocking agents verapamil and cyclosporin A.
  • Experiments defining drug transport and lipid metabolism parameters showed that asGCS ODN-7 overcomes drug resistance mainly by enhancing drug uptake and ceramide-induced apoptosis.
  • [MeSH-major] Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation / drug effects. Glucosyltransferases / biosynthesis. Glucosyltransferases / genetics. Oligodeoxyribonucleotides, Antisense / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Breast Neoplasms / pathology. Cell Line, Tumor. Humans. Rhodamine 123 / metabolism. Substrate Specificity

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  • (PMID = 14967819.001).
  • [ISSN] 0022-2275
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-95339
  • [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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligodeoxyribonucleotides, Antisense; 1N3CZ14C5O / Rhodamine 123; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase
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17. Haji AG, Sharma S, Babu M, Vijaykumar D, Chitrathara K: Androgen secreting steroid cell tumor of the ovary in a young lactating women with acute onset of severe hyperandrogenism: a case report and review of literature. J Med Case Rep; 2007;1:182
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  • [Title] Androgen secreting steroid cell tumor of the ovary in a young lactating women with acute onset of severe hyperandrogenism: a case report and review of literature.
  • INTRODUCTION: Steroid cell tumors of the ovary account for less than 0.1% of all ovarian tumors 1 and these tumours may present at any age in association with interesting presentations related to the hormonal activity and virilizing properties of tumor.
  • The subtype, not otherwise specified, is associated with androgenic changes in approximately one half of patients with this tumour 1.
  • In a series of 63 cases from Massachusetts General Hospital, 94% of the tumors were found to be unilateral and 28.6% were malignant 3.
  • As most of these tumors are diagnosed at an early stage and do not recur or metastasize, little is known about their response to therapies such as chemotherapy or radiation 3.
  • CASE PRESENTATION: We present the case of a 22-year old lactating woman who presented with four months of amenorrhea associated with signs of virilization.
  • Clinical and diagnostic evaluation revealed a right adenexal mass and elevated serum levels of testosterone and she was diagnosed as having a stage 1A androgen secreting steroid cell tumor.
  • Histopathological examination and immunohistochemistry confirmed the diagnosis.
  • CONCLUSION: Surgery remains the mainstay of the treatment of gonadotrophin receptor positive steroid cell tumors although medical therapy using Gonadotrophin Releasing Hormone [GnRH analogues has been tried recently in recurrent or inoperable cases.
  • There is no described effective chemotherapy or radiotherapy for this condition.

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  • (PMID = 18088412.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2231374
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18. Kusumbe AP, Bapat SA: Cancer stem cells and aneuploid populations within developing tumors are the major determinants of tumor dormancy. Cancer Res; 2009 Dec 15;69(24):9245-53
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  • [Title] Cancer stem cells and aneuploid populations within developing tumors are the major determinants of tumor dormancy.
  • Tumor formation involves substantial cell division and genetic instability, but the relationship between quiescent cancer stem cells (CSC) and dividing progenitors in these events is poorly understood.
  • Likewise, the implication of aneuploid cells in solid tumors is uncertain.
  • CSCs are postulated to contribute to tumor dormancy and present a formidable obstacle in limiting treatment outcomes for a majority of cancers, whereas the genetic heterogeneity conjured by aneuploid cells may influence tumor drug resistance.
  • In the present study, we addressed the identification of tumor dormancy in terms of isolation of therapy-refractory residual tumor cells from tumors that persist in a state of quiescence as label-retaining cells.
  • The choices of label were PKH67/PKH26 dyes that irreversibly bind to the lipid bilayer on cell membranes and get equally partitioned among daughter cells subsequent to each cell division.
  • The former express a reversibility of quiescence through retention of functionality and also exhibit therapeutic refractoriness; the latter seem to be either quiescent or proliferation-arrested at steady-state.
  • Subsequent to exposure to selective pressure of chemotherapy, a fraction of these cells may acquire the potential to proliferate in a drug-refractory manner and acquire stem-like characteristics.
  • Collectively, the findings of the present study reveal that tumor-derived CSCs and aneuploid populations contribute to drug resistance and tumor dormancy in cancer progression.
  • [MeSH-major] Aneuploidy. Cystadenocarcinoma, Serous / pathology. Neoplastic Stem Cells / pathology. Ovarian Neoplasms / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / pharmacology. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line, Tumor. Female. Flow Cytometry. Fluorescent Dyes / chemistry. Fluorescent Dyes / metabolism. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Organic Chemicals / chemistry. Organic Chemicals / metabolism. Paclitaxel / pharmacology

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  • (PMID = 19951996.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Fluorescent Dyes; 0 / Organic Chemicals; 0 / PKH 26; 0 / PKH67; P88XT4IS4D / Paclitaxel
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19. Gauthaman K, Fong CY, Bongso A: Statins, stem cells, and cancer. J Cell Biochem; 2009 Apr 15;106(6):975-83
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  • Recent reports demonstrate an anticancer effect induced by the statins through inhibition of cell proliferation, induction of apoptosis, or inhibition of angiogenesis.
  • These effects are due to suppression of the mevalonate pathway leading to depletion of various downstream products that play an essential role in cell cycle progression, cell signaling, and membrane integrity.
  • Activation targets of NANOG, OCT4, SOX2, and c-MYC are more frequently overexpressed in certain tumors.
  • In the absence of bona fide cancer stem cell lines, human embryonic stem cells, which have similar properties to cancer and cancer stem cells, have been an excellent model throwing light on the anticancer affects of various putative anticancer agents.
  • It was shown that key cellular functions in karyotypically abnormal colorectal and ovarian cancer cells and human embryonic stem cells are inhibited by the statins and this is mediated via a suppression of this stemness pathway.
  • The strategy for treatment of cancers may thus be the targeting of a putative cancer stem cell within the tumor with specific agents such as the statins with or without chemotherapy.
  • The statins may thus play a dual prophylactic role as a lipid-lowering drug for the prevention of heart disease and as an anticancer agent to prevent certain cancers.
  • [MeSH-major] Embryonic Stem Cells / physiology. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use. Neoplasms / drug therapy. Neoplastic Stem Cells / physiology
  • [MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Apoptosis / drug effects. Cell Proliferation / drug effects. Cholesterol / biosynthesis. Humans. Neoplasm Metastasis / drug therapy. Neovascularization, Pathologic / drug therapy

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19224538.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 97C5T2UQ7J / Cholesterol
  • [Number-of-references] 61
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20. Gupta V, Patwardhan GA, Zhang QJ, Cabot MC, Jazwinski SM, Liu YY: Direct quantitative determination of ceramide glycosylation in vivo: a new approach to evaluate cellular enzyme activity of glucosylceramide synthase. J Lipid Res; 2010 Apr;51(4):866-74
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  • Due to its diverse roles in physiology and diseases, GCS may be a disease marker and drug target.
  • This cell-based method is able to quantitate glucosylceramide in pmol range, produced by approximately 50,000 cells or 1.0 mg tissue.
  • This method has been used successfully to evaluate the degrees of GCS enzyme in cells and in tumors subjected to gene manipulation and chemical inhibition.
  • These data indicate that this cell-based fluorescent method is direct, reproducible, and simple for assessing ceramide glycosylation.
  • It is applicable to validate GCS activity in drug-resistant cancers and in other disorders.

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  • (PMID = 19826105.001).
  • [ISSN] 1539-7262
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR016456; United States / NIGMS NIH HHS / GM / R01 GM077391; United States / NIGMS NIH HHS / GM / GM77391; United States / NCRR NIH HHS / RR / P20 RR16456
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ceramides; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Oligonucleotides; 73257-80-4 / RV 538; 86701-10-2 / N-(7-(4-nitrobenzo-2-oxa-1,3-diazole))-6-aminocaproyl sphingosine; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase; EQF2794IRE / 4-Chloro-7-nitrobenzofurazan
  • [Other-IDs] NLM/ PMC2842142
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21. Takai N, Ueda T, Nasu K, Narahara H: Erucylphosphocholine shows a strong anti-growth activity in human endometrial and ovarian cancer cells. Gynecol Oncol; 2008 Nov;111(2):336-43
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  • [Title] Erucylphosphocholine shows a strong anti-growth activity in human endometrial and ovarian cancer cells.
  • OBJECTIVES: A membrane-targeted, lipophilic ether lipid of synthetic phospholipid analog, erucylphosphocholine (ErPC) induces apoptosis in some lines of human tumor cells.
  • We investigated the effect of ErPC on three endometrial cancer cell lines, two ovarian cancer cell lines, and normal human endometrial epithelial cells.
  • METHODS: Endometrial and ovarian cancer cells were treated with various concentrations of ErPC, and its effect on cell growth, cell cycle, apoptosis, and related measurements was investigated.
  • RESULTS: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that all endometrial and ovarian cancer cell lines were sensitive to the growth-inhibitory effect of ErPC, although normal endometrial epithelial cells were viable after treatment with the same doses of ErPC that induced growth inhibition in endometrial and ovarian cancer cells.
  • Cell cycle analysis indicated that their exposure to ErPC decreased the proportion of cells in the S-phase and increased the proportion in the G2/M phases of the cell cycle.
  • This induction occurred in concert with altered expression of genes related to cell growth, malignant phenotype, and apoptosis.
  • CONCLUSIONS: These results suggest that the anticancer activity of ErPC may occur with higher sensitivity of cancer cells compared with normal healthy cells, when using low concentration, rising hopes that ErPC may become a useful adjuvant therapy for endometrial and ovarian cancers.
  • [MeSH-major] Endometrial Neoplasms / drug therapy. Ovarian Neoplasms / drug therapy. Phosphorylcholine / analogs & derivatives
  • [MeSH-minor] Apoptosis / drug effects. Caspase 9 / metabolism. Cell Cycle / drug effects. Cell Cycle Proteins / biosynthesis. Cell Growth Processes / drug effects. Cell Line, Tumor. Cyclin B / biosynthesis. Cyclin B1. Dose-Response Relationship, Drug. Female. Flow Cytometry. Humans. Membrane Potential, Mitochondrial / drug effects. Protein-Serine-Threonine Kinases / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / biosynthesis

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  • [RetractionIn] Gynecol Oncol. 2013 Apr;129(1):268 [23638459.001]
  • (PMID = 18790523.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCNB1 protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin B; 0 / Cyclin B1; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 107-73-3 / Phosphorylcholine; 143317-74-2 / erucylphosphocholine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / polo-like kinase 1; EC 3.4.22.- / Caspase 9
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22. Nguyen GH, French R, Radhakrishna H: Protein kinase A inhibits lysophosphatidic acid induction of serum response factor via alterations in the actin cytoskeleton. Cell Signal; 2004 Oct;16(10):1141-51
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  • Lysophosphatidic acid (LPA; 1-acyl-2-hydroxy-sn-glycero-3-phosphate) is a lipid growth factor that stimulates the proliferation of ovarian cancer cells.
  • Recent studies indicate that elevation of cellular cAMP levels inhibits ovarian epithelial cancer cell growth.
  • In this study, we investigated the effects of elevating cellular cAMP levels on LPA stimulation of OVCAR-3 ovarian cancer cell growth and on LPA stimulation of the serum response factor (SRF) transcription factor.
  • Treatment of OVCAR-3 cells with forskolin and isobutylmethylxanthine (IBMX; 3-Isobutyl-1-methylxanthine) inhibited LPA stimulation of growth.
  • LPA stimulation of SRF-mediated transcription was also inhibited in OVCAR-3 cells that were incubated with forskolin, dibutyryl cyclic AMP (db-cAMP), or paired cAMP analogues (N(6)-mono-tert-butylcarbamoyladenosine-3', 5'-cyclic monophosphate [6-MBC-cAMP] and Sp-5,6-DCl-BIMPS), which selectively activate type II protein kinase A.
  • In contrast, incubation with a cAMP analogue (8-(4-chloro-phenylthio)-2'-O-methyadenosine-3',5'-cyclic monophosphate [8CPT-2Me-cAMP]) that specifically activates the cAMP inducible Rap1 exchange factor, Epac, did not inhibit SRF.
  • Similar results were obtained when HepG2 hepatoma cells, which do not express endogenous LPA receptors, were transfected with a single LPA receptor (LPA(1)).
  • We observed that treatment of OVCAR-3 cells with forskolin greatly reduced both F-actin staining and focal adhesion labeling with anti-paxillin antibodies.
  • Treatment of OVCAR-3 cells with the F-actin stabilizing compound, jasplakinolide, prevented the protein kinase A (PKA)-mediated inhibition of SRF.
  • These results suggest that PKA inhibits LPA stimulation of SRF by promoting the dissolution of F-actin and that this is likely to contribute to the cAMP-mediated inhibition of ovarian cancer cell growth.
  • [MeSH-minor] 1-Methyl-3-isobutylxanthine / pharmacology. Actin Cytoskeleton / drug effects. Actin Cytoskeleton / metabolism. Actins / metabolism. Animals. Carcinoma, Hepatocellular / drug therapy. Cell Adhesion / drug effects. Cell Adhesion / physiology. Cell Proliferation / drug effects. Colforsin / pharmacology. Cyclic AMP-Dependent Protein Kinase Type II. Cytoskeletal Proteins / metabolism. Female. Humans. Ovarian Neoplasms / drug therapy. Paxillin. Phosphoproteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 15240009.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL67134
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Cytoskeletal Proteins; 0 / Lysophospholipids; 0 / PXN protein, human; 0 / Paxillin; 0 / Phosphoproteins; 0 / Serum Response Factor; 1F7A44V6OU / Colforsin; 22002-87-5 / lysophosphatidic acid; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinase Type II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; TBT296U68M / 1-Methyl-3-isobutylxanthine
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23. Xing W, Gang WZ, Yong Z, Yi ZY, Shan XC, Tao RH: Treatment of xenografted ovarian carcinoma using paclitaxel-loaded ultrasound microbubbles. Acad Radiol; 2008 Dec;15(12):1574-9
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  • [Title] Treatment of xenografted ovarian carcinoma using paclitaxel-loaded ultrasound microbubbles.
  • RATIONALE AND OBJECTIVES: The aim of this study was to explore the antitumor effects on mice xenografted ovarian carcinoma using the technique of ultrasound-mediated drug release from paclitaxel-loaded lipid microbubbles (PLMs).
  • MATERIALS AND METHODS: Twenty-five ovarian cancer-bearing nude mice were randomly divided into five groups of five mice each.
  • Each group received a unique kind of treatment once a day.
  • These treatments were PLMs combined with ultrasound, intravenous paclitaxel administration, non-drug-loaded microbubbles combined with ultrasound, intravenous PLM administration, and normal saline administration (the control group).
  • After 7 days of consecutive treatment, all mice were sacrificed, and their tumors were harvested to measure volumes and weights.
  • The tumor inhibition rate was calculated by weight.
  • Expressions of vascular endothelial growth factor (VEGF) and p53 in tumor tissues were detected by immunohistochemical staining.
  • RESULTS: Mean tumor volume and weight were the lowest in the first group (PLMs combined with ultrasound), so this group's tumor inhibition rate was the highest (P < .05).
  • CONCLUSION: Ultrasound irradiation mediates PLM destruction so that the drug is released from the vehicles at the same time.
  • It helps achieve targeted chemotherapy in tumor tissues.
  • This technique has potential to be adopted as a novel tool for ovarian cancer chemotherapy.
  • [MeSH-major] Drug Carriers / administration & dosage. Drug Carriers / radiation effects. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / pathology. Paclitaxel / administration & dosage. Paclitaxel / chemistry. Sonication
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Mice. Mice, Nude. Microbubbles. Treatment Outcome

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  • (PMID = 19000874.001).
  • [ISSN] 1878-4046
  • [Journal-full-title] Academic radiology
  • [ISO-abbreviation] Acad Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Carriers; P88XT4IS4D / Paclitaxel
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24. Rudginsky S, Siders W, Ingram L, Marshall J, Scheule R, Kaplan J: Antitumor activity of cationic lipid complexed with immunostimulatory DNA. Mol Ther; 2001 Oct;4(4):347-55
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  • [Title] Antitumor activity of cationic lipid complexed with immunostimulatory DNA.
  • We previously reported that treatment of intraperitoneal tumors with complexes of cationic lipid and noncoding plasmid DNA leads to the development of a specific, cytotoxic T-cell response correlating with the rejection of established tumor cells as well as subsequent tumor re-challenge.
  • Here, focusing on an intraperitoneal AB12 mesothelioma model, we show that the anticancer effects of the lipid:DNA complex are associated with DNA containing immunostimulatory CpG motifs.
  • Complexes prepared with cationic lipid and bacterial plasmid DNA, Escherichia coli genomic DNA fragments, or synthetic immunostimulatory CpG oligodeoxynucleotides provided a substantial survival benefit, whereas eukaryotic DNA and methylated bacterial DNA had little or no therapeutic activity.
  • Alternative inflammatory stimuli such as thioglycolate, poly(I:C), and incomplete or complete Freund's adjuvant failed to reproduce the antitumor activity obtained with the lipid:DNA complex.
  • The innate immune response triggered by lipid:DNA complexes led to the development of a systemic immune response against tumor cells that allowed animals to reject tumors not only at the intraperitoneal treatment site, but also at a distal subcutaneous site.
  • These data demonstrate that immunostimulatory DNA complexed with cationic lipid is a potent inducer of innate and adaptive immune responses against tumor cells and represents a potentially useful tool in the immunotherapy of cancers for which tumor-associated antigens have not been identified.
  • [MeSH-major] DNA, Bacterial / immunology. DNA, Bacterial / therapeutic use. Drug Carriers / therapeutic use. Lipids / chemistry. Lipids / pharmacology. Mesothelioma / genetics. Mesothelioma / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / chemistry. Antineoplastic Agents / immunology. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. CpG Islands / genetics. CpG Islands / immunology. Cytokines / immunology. Cytokines / metabolism. DNA Methylation. Disease Models, Animal. Female. Freund's Adjuvant / immunology. Freund's Adjuvant / pharmacology. Genetic Therapy / methods. Humans. Immunity, Cellular / drug effects. Immunity, Cellular / immunology. Immunity, Innate / drug effects. Immunity, Innate / immunology. Inflammation / chemically induced. Injections, Intraperitoneal. Melanoma / genetics. Melanoma / therapy. Mice. Neoplasm Transplantation. Ovarian Neoplasms / genetics. Ovarian Neoplasms / therapy. Rats. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 11592838.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / DNA, Bacterial; 0 / Drug Carriers; 0 / Lipids; 9007-81-2 / Freund's Adjuvant
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25. Li W, Xu RJ, Lin ZY, Zhuo GC, Zhang HH: Effects of a cyclooxygenase-1-selective inhibitor in a mouse model of ovarian cancer, administered alone or in combination with ibuprofen, a nonselective cyclooxygenase inhibitor. Med Oncol; 2009;26(2):170-7
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  • [Title] Effects of a cyclooxygenase-1-selective inhibitor in a mouse model of ovarian cancer, administered alone or in combination with ibuprofen, a nonselective cyclooxygenase inhibitor.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to be potent inhibitors of the cyclooxygenases.
  • The present study was designed to investigate the effects of a cyclooxygenase (COX)-1 inhibitor, SC-560, administered alone or in combination with ibuprofen on the growth inhibition of s.c. human ovarian SKOV-3 carcinoma and on angiogenesis.
  • The effects of SC-560 and ibuprofen on tumor growth inhibition have been examined in mouse ovarian cancer models.
  • Prostaglandin E(2) (PGE(2)) levels in tumor tissues of mice were also determined by ELISA.
  • In combination therapy with SC-560 and ibuprofen, tumor volumes were significantly reduced compared with that of control group (P < 0.05).
  • In treatment groups, both COX inhibitors significantly reduced intratumor PGE(2) levels (all P < 0.01).
  • Microvessel density (MVD) in tumor tissues were significantly decreased from 80.90 +/- 5.14 in vehicle-treated to 40.70 +/- 10.45 and 38.90 +/- 8.41 in SC-560 group alone and combination ibuprofen therapy (all P < 0.01).
  • Ibuprofen was similar to the cyclooxygenase-1-selective inhibitor SC-560 in its ability to suppress the values of MVD of tumor tissues.
  • These studies demonstrate synergism between two COX inhibitors and that antiangiogenic therapy can be used to inhibit ovarian cancer growth.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Ibuprofen / therapeutic use. Ovarian Neoplasms / drug therapy. Pyrazoles / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclooxygenase 1 / metabolism. Dinoprostone / metabolism. Disease Models, Animal. Female. Humans. Mice. Mice, Nude. Microvessels / drug effects. Neovascularization, Pathologic / drug therapy. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18988002.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / SC 560; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / PTGS1 protein, human; K7Q1JQR04M / Dinoprostone; WK2XYI10QM / Ibuprofen
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