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1. Hausott B, Greger H, Marian B: Flavaglines: a group of efficient growth inhibitors block cell cycle progression and induce apoptosis in colorectal cancer cells. Int J Cancer; 2004 May 10;109(6):933-40
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  • To assess their suitability as chemotherapeutic drugs in colorectal cancer, their cytostatic effects and the underlying mechanisms of action were analyzed in colorectal tumor cell lines.
  • Aglaiastatin was the most active flavagline, inhibiting growth and inducing apoptosis at nanomolar concentrations in SW480 and HT29/HI1 carcinoma cells, while the premalignant adenoma cell lines VACO235 and LT97 as well as the normal intestinal epithelial cell line IEC18 were 1,000 times less sensitive (IC50>10 microM).
  • [MeSH-major] Apoptosis / drug effects. Benzofurans / pharmacology. Cell Cycle / drug effects. Colorectal Neoplasms / pathology. Growth Inhibitors / pharmacology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / metabolism. Adenoma / pathology. Animals. Epithelial Cells / metabolism. Humans. Intestines / metabolism. Matrix Metalloproteinases / metabolism. Meliaceae / chemistry. Mitogen-Activated Protein Kinases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Rats. bcl-X Protein. p38 Mitogen-Activated Protein Kinases

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15027128.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, rat; 0 / Benzofurans; 0 / Growth Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.24.- / Matrix Metalloproteinases
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2. Hubina E, Nanzer AM, Hanson MR, Ciccarelli E, Losa M, Gaia D, Papotti M, Terreni MR, Khalaf S, Jordan S, Czirják S, Hanzély Z, Nagy GM, Góth MI, Grossman AB, Korbonits M: Somatostatin analogues stimulate p27 expression and inhibit the MAP kinase pathway in pituitary tumours. Eur J Endocrinol; 2006 Aug;155(2):371-9
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  • METHODS: Human pituitary adenoma cells and rat pituitary cell line (GH3) were cultured and treated in vitro with octreotide and the broad-spectrum SST agonist SOM230 (pasireotide).
  • RESULTS: We detected upregulation of p27 protein levels with SST analogue treatment in vitro in human pituitary adenoma samples. pERK1/2 was inhibited by SST analogues in both the human samples and GH3 cells.
  • SST and its analogues inhibited the proliferation of GH3 cells. p27 immunostaining was stronger in samples from patients with longer preoperative octreotide treatment (more than 6 months) than in samples from patients with shorter treatment periods.
  • More potent and broader-spectrum SST analogues are likely to play an increasing role in the treatment of tumours, where the MAP kinase pathway is overactivated.

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  • (PMID = 16868153.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 10028-17-8 / Tritium; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; RWM8CCW8GP / Octreotide; VC2W18DGKR / Thymidine
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3. Heaney AP, Fernando M, Melmed S: PPAR-gamma receptor ligands: novel therapy for pituitary adenomas. J Clin Invest; 2003 May;111(9):1381-8
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  • [Title] PPAR-gamma receptor ligands: novel therapy for pituitary adenomas.
  • In many cases, no suitable drug therapies are available, and surgical excision is currently the only effective treatment.
  • PPAR-gamma activating thiazolidinediones (TZDs) rosiglitazone and troglitazone induced G(0)-G(1) cell-cycle arrest and apoptosis in human, rat somatolactotroph, and murine gonadotroph pituitary tumor cells, and suppressed in vitro hormone secretion.
  • These results demonstrate that PPAR-gamma is an important molecular target in pituitary adenoma cells and PPAR-gamma ligands inhibit tumor cell growth and GH, PRL, and LH secretion in vitro and in vivo.
  • TZDs are proposed as novel oral medications for managing pituitary tumors.

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  • (PMID = 12727930.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA-75979
  • [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 / Antineoplastic Agents; 0 / Ligands; 0 / Nuclear Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Transcription Factors; 2295-31-0 / 2,4-thiazolidinedione
  • [Other-IDs] NLM/ PMC154441
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4. Schaaf C, Shan B, Buchfelder M, Losa M, Kreutzer J, Rachinger W, Stalla GK, Schilling T, Arzt E, Perone MJ, Renner U: Curcumin acts as anti-tumorigenic and hormone-suppressive agent in murine and human pituitary tumour cells in vitro and in vivo. Endocr Relat Cancer; 2009 Dec;16(4):1339-50
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  • Curcumin (diferuloylmethane) is the active ingredient of the spice plant Curcuma longa and has been shown to act anti-tumorigenic in different types of tumours.
  • Proliferation of lactosomatotroph GH3 and somatotroph MtT/S rat pituitary cells as well as of corticotroph AtT20 mouse pituitary cells was inhibited by curcumin in monolayer cell culture and in colony formation assay in soft agar.
  • FACS analysis with Annexin V-FITC/7-aminoactinomycin D staining demonstrated curcumin-induced early apoptosis after 3, 6, 12 and 24 h treatment and nearly no necrosis.
  • Studies in 25 human pituitary adenoma cell cultures have confirmed the anti-tumorigenic and hormone-suppressive effects of curcumin.
  • Altogether, the results described in this report suggest this natural compound as a good candidate for therapeutic use on pituitary tumours.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Pituitary Hormones / metabolism. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Caspase 3 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Cyclin-Dependent Kinase 4 / metabolism. Flow Cytometry. Humans. Male. Mice. Mice, Nude. Rats

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  • (PMID = 19726538.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pituitary Hormones; 136601-57-5 / Cyclin D1; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin
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5. Cole CD, Liu JK, Sheng X, Chin SS, Schmidt MH, Weiss MH, Couldwell WT: Hypericin-mediated photodynamic therapy of pituitary tumors: preclinical study in a GH4C1 rat tumor model. J Neurooncol; 2008 May;87(3):255-61
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  • [Title] Hypericin-mediated photodynamic therapy of pituitary tumors: preclinical study in a GH4C1 rat tumor model.
  • OBJECTIVE: Hypericin-mediated photodynamic therapy (PDT) is receiving greater interest as a potential treatment for a variety of tumors and nonmalignant disorders.
  • PDT involves systemic administration of a photosensitizer that selectively accumulates within tumor tissue followed by focal light activation.
  • The purpose of this preclinical study was to evaluate the efficacy of hypericin-mediated PDT for treatment of pituitary adenoma in a rodent model.
  • METHODS: Wistar-Furth rats were implanted with a pituitary adenoma rat cell line, GH4C1.
  • Tumor masses were allowed to develop over 28 days; rats with tumors of comparable sizes were then assigned to three treatment groups: control (neither hypericin nor light); light only; and hypericin and light.
  • Tumor size was measured up to 12 days after treatment.
  • RESULTS: Over the short interval examined, hypericin-mediated PDT was not effective against large tumors greater than 1 cm(3), but this treatment significantly slowed tumor growth for tumors less than 1 cm(3).
  • CONCLUSIONS: Hypericin-mediated PDT shows promise in its effectiveness in the treatment of residual small tumor rests.
  • [MeSH-major] Perylene / analogs & derivatives. Photochemotherapy. Pituitary Neoplasms / drug therapy. Radiation-Sensitizing Agents / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. In Situ Nick-End Labeling. Rats. Rats, Wistar

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  • (PMID = 18228116.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiation-Sensitizing Agents; 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin
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6. Brown WA, Skinner SA, Malcontenti-Wilson C, Vogiagis D, O'Brien PE: Non-steroidal anti-inflammatory drugs with activity against either cyclooxygenase 1 or cyclooxygenase 2 inhibit colorectal cancer in a DMH rodent model by inducing apoptosis and inhibiting cell proliferation. Gut; 2001 May;48(5):660-6
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  • [Title] Non-steroidal anti-inflammatory drugs with activity against either cyclooxygenase 1 or cyclooxygenase 2 inhibit colorectal cancer in a DMH rodent model by inducing apoptosis and inhibiting cell proliferation.
  • BACKGROUND: Standard non-steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of colorectal cancer by 40-60% but the mechanism by which this occurs is uncertain.
  • No study has compared the efficacy of these drugs at clinically relevant doses in a tumour model.
  • RESULTS: Test agents effectively reduced the number and volume of tumours developing in the treatment period.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenoma / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Apoptosis / drug effects. Colorectal Neoplasms / drug therapy. Cyclooxygenase Inhibitors / therapeutic use
  • [MeSH-minor] Analysis of Variance. Animals. Bromodeoxyuridine. Cell Division / drug effects. Cyclooxygenase 1. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Isoenzymes / drug effects. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / chemistry. Prostaglandin-Endoperoxide Synthases / drug effects. Rats. Rats, Sprague-Dawley. Staining and Labeling

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  • (PMID = 11302965.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs1 protein, rat; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ PMC1728280
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7. Leung G, Tsao SW, Wong YC: The effect of flutamide and tamoxifen on sex hormone-induced mammary carcinogenesis and pituitary adenoma. Breast Cancer Res Treat; 2002 Mar;72(2):153-62
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  • [Title] The effect of flutamide and tamoxifen on sex hormone-induced mammary carcinogenesis and pituitary adenoma.
  • We have established a female Noble rat model to explore the mechanisms of hormonal mammary carcinogenesis.
  • We showed that tamoxifen could totally inhibit mammary carcinogenesis while flutamide cause a delay and reduction in tumour incidence in the 12 months treatment term.
  • Blocking effect of flutamide and tamoxifen on T + E2 (testosterone and 17beta-estradiol) short-terms treatment was demonstrated by the similar histological changes identified in the mammary glands of the T + E2 and drug treated rats to that of the age matched E2 and T controls, respectively.
  • Tamoxifen was also effective in blocking the formation of pituitary adenoma in the sex hormone treated rats.
  • Pituitary size and level of prolactin were higher in the T + E2 + flutamide group than the T + E2 group in both short-term and long-term treatments.
  • Pituitary adenomas were found in all rats that developed mammary adenocarcinoma but not vice versa suggesting that prolactin level elevation alone cannot lead to mammary tumorigenesis.
  • The animal model, in addition to mammary carcinogenesis, may be useful for investigation of anti-estrogen therapy in pituitary adenomas.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Breast / drug effects. Breast Neoplasms / prevention & control. Flutamide / pharmacology. Pituitary Gland / drug effects. Prolactinoma / prevention & control. Tamoxifen / pharmacology

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  • (PMID = 12038706.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Gonadal Steroid Hormones; 094ZI81Y45 / Tamoxifen; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 76W6J0943E / Flutamide
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8. Vigushin DM, Ali S, Pace PE, Mirsaidi N, Ito K, Adcock I, Coombes RC: Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer in vivo. Clin Cancer Res; 2001 Apr;7(4):971-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The purpose of this study was to evaluate the antiproliferative and HDAC inhibitory activity of TSA in vitro in human breast cancer cell lines and to assess its antitumor efficacy and toxicity in vivo in a carcinogen-induced rat mammary cancer model.
  • HDAC inhibitory activity of TSA was similar in all cell lines with mean +/- SD IC(50) of 2.4 +/- 0.5 nM (range, 1.5-2.9 nM), and TSA treatment resulted in pronounced histone H4 hyperacetylation.
  • In randomized controlled efficacy studies using the N-methyl-N-nitrosourea carcinogen-induced rat mammary carcinoma model, TSA had pronounced antitumor activity in vivo when administered to 16 animals at a dose of 500 microg/kg by s.c. injection daily for 4 weeks compared with 14 control animals.
  • In contrast, 19 tumors from 12 TSA-treated rats had a benign phenotype, either fibroadenoma or tubular adenoma, suggesting that the antitumor activity of TSA may be attributable to induction of differentiation.
  • CONCLUSIONS: The present studies confirm the potent dose-dependent antitumor activity of TSA against breast cancer in vitro and in vivo, strongly supporting HDAC as a molecular target for anticancer therapy in breast cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Histone Deacetylase Inhibitors. Hydroxamic Acids / therapeutic use. Mammary Neoplasms, Animal / drug therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Disease Models, Animal. Enzyme Inhibitors / pharmacology. Enzyme Inhibitors / therapeutic use. Female. Histone Deacetylases / metabolism. Humans. Methylnitrosourea. Rats. Rats, Wistar. Tumor Cells, Cultured

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  • (PMID = 11309348.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 3X2S926L3Z / trichostatin A; 684-93-5 / Methylnitrosourea; EC 3.5.1.98 / Histone Deacetylases
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9. Suzui M, Inamine M, Kaneshiro T, Morioka T, Yoshimi N, Suzuki R, Kohno H, Tanaka T: Indole-3-carbinol inhibits the growth of human colon carcinoma cells but enhances the tumor multiplicity and volume of azoxymethane-induced rat colon carcinogenesis. Int J Oncol; 2005 Nov;27(5):1391-9
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  • [Title] Indole-3-carbinol inhibits the growth of human colon carcinoma cells but enhances the tumor multiplicity and volume of azoxymethane-induced rat colon carcinogenesis.
  • We used a long-term rat model by using azoxymethane (AOM) to induce tumors (adenomas and adenocarcinomas) in the colon.
  • In the present study, we found that after AOM injection, the treatment of male F344 rats with 0.01 and 0.05% I3C caused a significant increase in the tumor multiplicity of adenocarcinomas by 2.2- (P<0.05 for 0.01% I3C) and 2.1-fold (P<0.0002 for 0.05% I3C) respectively, when compared to the control rats.
  • In addition, the tumor multiplicity of adenoma plus adenocarcinoma and the volume of adenocarcinoma were also increased by 2.0- (P<0.00001) and 2.1-fold (P<0.05) respectively, compared to the control.
  • These results suggest that I3C inhibits the growth of human colon carcinoma cells, at least in part, by inducing p27KIP1 and p21CIP1-mediated G1 cell-cycle arrest but dietary I3C promotes AOM-induced rat colon carcinogenesis by inhibiting the apoptosis of colon tumors.
  • Therefore, the present study may provide further evidence for the ambivalent modulatory activity of I3C and this information may be useful when including I3C in cancer chemoprevention and/or extensive clinical therapy trials.
  • [MeSH-minor] Administration, Oral. Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cell Transformation, Neoplastic. Chemoprevention. Humans. Male. Rats. Rats, Inbred F344. Tumor Cells, Cultured

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  • (PMID = 16211236.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Indoles; C11E72455F / indole-3-carbinol
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10. Lafferty JS, Kamendulis LM, Kaster J, Jiang J, Klaunig JE: Subchronic acrylamide treatment induces a tissue-specific increase in DNA synthesis in the rat. Toxicol Lett; 2004 Dec 1;154(1-2):95-103
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  • [Title] Subchronic acrylamide treatment induces a tissue-specific increase in DNA synthesis in the rat.
  • Chronic treatment with acrylamide results in increased incidence of adrenal (pheochromocytoma), testicular (mesotheliomas) and thyroid (adenoma) neoplasia in male rats.
  • While acrylamide has been demonstrated to be DNA reactive, the tissue pattern of neoplasm induction by acrylamide suggests other mechanisms in addition to DNA reactivity may be involved in the carcinogenesis of this compound.
  • The present studies were performed to determine whether acrylamide or an acrylamide metabolite altered cell growth in the neoplastic target tissues in the rat.
  • Acrylamide increased DNA synthesis in the target tissues for tumor development (thyroid, testicular mesothelium, adrenal medulla) in both rat species.
  • In contrast, cell growth was not altered in the liver and adrenal cortex (non-target tissues for acrylamide carcinogenesis).
  • No changes in apoptosis or mitosis were observed in any of the tissues examined.
  • In summary, acrylamide produced a selective increase in DNA synthesis that correlates with the previously reported tumor target tissues.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bromodeoxyuridine / metabolism. Cell Division / drug effects. Dose-Response Relationship, Drug. Drug Therapy, Combination. Male. Mitosis / drug effects. Rats. Rats, Inbred F344. Rats, Sprague-Dawley. Triazoles / pharmacology

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  • (PMID = 15475183.001).
  • [ISSN] 0378-4274
  • [Journal-full-title] Toxicology letters
  • [ISO-abbreviation] Toxicol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Environmental Pollutants; 0 / Triazoles; 1614-12-6 / 1-aminobenzotriazole; 20R035KLCI / Acrylamide; 9007-49-2 / DNA; G34N38R2N1 / Bromodeoxyuridine
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11. Ren SG, Kim S, Taylor J, Dong J, Moreau JP, Culler MD, Melmed S: Suppression of rat and human growth hormone and prolactin secretion by a novel somatostatin/dopaminergic chimeric ligand. J Clin Endocrinol Metab; 2003 Nov;88(11):5414-21

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  • [Title] Suppression of rat and human growth hormone and prolactin secretion by a novel somatostatin/dopaminergic chimeric ligand.
  • The selective SSTR2 agonist, BIM-23023 (50% effective dose, 0.42), and the DAR2 agonist, BIM-53097 (50% effective dose, 22.1), dose- dependently inhibited GH secretion in cultured primary rat and human fetal as well as in human pituitary tumor cells derived from GH-secreting adenomas.
  • The combination of individual SSTR2 and DAR2 agonists was additive for suppressing GH secretion in both rat and human pituitary cells.
  • BIM-23A387 (50% effective dose, 0.16 for SSTR2 and 24.5 for DAR2), displayed similar efficacy in suppressing GH secretion from rat pituitary cells as the combination of the two individual agonists.
  • In contrast, the chimeric molecule was more potent than individual selective analogs in suppressing GH secretion by human fetal pituitary and GH-secreting adenoma cells (P < 0.05).
  • The SRIF/DA chimeric molecule, BIM-23A387, represents a novel tool for effective drug treatment of acromegaly and for prolactinomas otherwise resistant to dopaminergic therapy.
  • [MeSH-minor] Animals. Humans. Ligands. Peptides, Cyclic / pharmacology. Pituitary Gland / cytology. Pituitary Gland / drug effects. Pituitary Neoplasms. Prolactinoma. Rats. Receptors, Dopamine D2 / agonists. Recombinant Fusion Proteins / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / secretion

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  • (PMID = 14602782.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIM 23023; 0 / Dopamine Agonists; 0 / Ligands; 0 / Peptides, Cyclic; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 0 / somatostatin receptor 2; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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12. Vogiagis D, Brown W, Glare EM, O'Brien PE: Rat colorectal tumours treated with a range of non-steroidal anti-inflammatory drugs show altered cyclooxygenase-2 and cyclooxygenase-1 splice variant mRNA expression levels. Carcinogenesis; 2001 Jun;22(6):869-74
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  • [Title] Rat colorectal tumours treated with a range of non-steroidal anti-inflammatory drugs show altered cyclooxygenase-2 and cyclooxygenase-1 splice variant mRNA expression levels.
  • Non-steroidal anti-inflammatory drugs (NSAIDs) reduce tumour mass by increasing the rate of tumour cell apoptosis and decreasing cell proliferation.
  • In the rat, the COX-1 gene expresses an alternatively spliced mRNA COX-1 splice variant (SV) which may, at best, code for a truncated COX-1 protein.
  • In addition, we immunolocalized COX-1 and COX-2 in the same tumour and normal colonic tissue.
  • The expression of COX-1 mRNA remained unchanged in all tissues examined.
  • However, COX-1SV mRNA levels were elevated in colorectal tumours and reduced after NSAID treatment to the levels observed in normal colonic mucosa.
  • [MeSH-major] Alternative Splicing / drug effects. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Colorectal Neoplasms / enzymology. Colorectal Neoplasms / genetics. Isoenzymes / genetics. Prostaglandin-Endoperoxide Synthases / genetics
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Adenoma / drug therapy. Adenoma / enzymology. Adenoma / genetics. Animals. Carcinogens. Cyclooxygenase 1. Cyclooxygenase 2. Dimethylhydrazines. Gene Expression Regulation, Neoplastic / drug effects. Immunohistochemistry. Membrane Proteins. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats

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  • (PMID = 11375891.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carcinogens; 0 / Dimethylhydrazines; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs1 protein, rat
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13. Pushkar' DIu, belousov IuB, Dukhanin AS, Maneshina OA, Govorov AV, Kurdzhiev MA: [Interaction of omnic (tamsulozine) and its generic analogues with alpha-adrenoreceptors]. Urologiia; 2009 Sep-Oct;(5):36-40
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  • In current practice of pharmacotherapy of prostatic adenoma alpha1-adrenoblockers are first-line drugs the efficacy and safety of which have been proved in many randomized studies.
  • Because of the appearance of a large amount of generic analogues of tamsulozine on the market we studied the ability of tamsulozine analogues to bind with alpha-adrenoreceptors on rat and human prostate affected by adenoma.
  • [MeSH-major] Adenoma / metabolism. Adenoma / microbiology. Adrenergic alpha-Antagonists / pharmacokinetics. Drugs, Generic / pharmacokinetics. Prostate / metabolism. Receptors, Adrenergic, alpha / metabolism. Sulfonamides / pharmacokinetics

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  • (PMID = 20209868.001).
  • [ISSN] 1728-2985
  • [Journal-full-title] Urologii︠a︡ (Moscow, Russia : 1999)
  • [ISO-abbreviation] Urologiia
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Adrenergic alpha-Antagonists; 0 / Drugs, Generic; 0 / Receptors, Adrenergic, alpha; 0 / Sulfonamides; G3P28OML5I / tamsulosin
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14. Howarth GS, Xian CJ, Read LC: Predisposition to colonic dysplasia is unaffected by continuous administration of insulin-like growth factor-I for twenty weeks in a rat model of chronic inflammatory bowel disease. Growth Factors; 2000;18(2):119-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predisposition to colonic dysplasia is unaffected by continuous administration of insulin-like growth factor-I for twenty weeks in a rat model of chronic inflammatory bowel disease.
  • BACKGROUND: Insulin-like growth factor-I (IGF-I) is currently under evaluation for the treatment of a variety of chronic disease conditions.
  • We investigated the safety of long-term IGF-I administration in a rat model of inflammatory bowel disease which predisposes to the development of dysplasia.
  • [MeSH-major] Colonic Neoplasms / etiology. Dextran Sulfate / pharmacology. Inflammatory Bowel Diseases / drug therapy. Insulin-Like Growth Factor I / therapeutic use
  • [MeSH-minor] Adenoma / pathology. Animals. Blood Glucose / analysis. Cecum / pathology. Chronic Disease. Disease Models, Animal. Disease Susceptibility. Dose-Response Relationship, Drug. Insulin / blood. Insulin-Like Growth Factor Binding Proteins / blood. Male. Organ Size. Rats. Rats, Sprague-Dawley

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  • (PMID = 11019783.001).
  • [ISSN] 0897-7194
  • [Journal-full-title] Growth factors (Chur, Switzerland)
  • [ISO-abbreviation] Growth Factors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Insulin-Like Growth Factor Binding Proteins; 67763-96-6 / Insulin-Like Growth Factor I; 9042-14-2 / Dextran Sulfate
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15. Imai T, Onose J, Hasumura M, Ueda M, Takizawa T, Hirose M: Sequential analysis of development of invasive thyroid follicular cell carcinomas in inflamed capsular regions of rats treated with sulfadimethoxine after N-bis(2-hydroxypropyl)nitrosamine-initiation. Toxicol Pathol; 2004 Mar-Apr;32(2):229-36
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  • A number of goitrogens are known to strongly promote carcinogenesis, and the carcinomas often originate adjacent to the thyroid capsule and show invasive growth into the capsule or adjacent tissues.
  • In DHPN-SDM-treated rats, multiple focal hyperplasias and adenomas developed in thyroid follicular parenchyma at weeks 4 to 6.
  • Focal hyperplasias/adenomas adjacent to the capsule progressively developed to invasive carcinomas at weeks 6 to 10.
  • With SDM-treatment alone, although no neoplastic lesions were observed, capsular thickening with inflammation and epithelial migration resulted in intracapsular residual follicles.
  • [MeSH-major] Adenocarcinoma, Follicular / chemically induced. Carcinogens / toxicity. Nitrosamines / toxicity. Sulfadimethoxine / toxicity. Thyroid Gland / drug effects. Thyroid Neoplasms / chemically induced
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / pathology. Administration, Oral. Animals. Biomarkers, Tumor. Cytoskeletal Proteins / metabolism. Drug Therapy, Combination. Hyperplasia. Injections, Subcutaneous. Male. Neoplasm Invasiveness. Rats. Rats, Inbred F344. Trans-Activators / metabolism. Water Supply. beta Catenin

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  • (PMID = 15200161.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol 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 / Carcinogens; 0 / Ctnnb1 protein, rat; 0 / Cytoskeletal Proteins; 0 / Nitrosamines; 0 / Trans-Activators; 0 / beta Catenin; 30CPC5LDEX / Sulfadimethoxine; 4J072HB2ND / diisopropanolnitrosamine
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16. Rossmanith W, Chabicovsky M, Grasl-Kraupp B, Peter B, Schausberger E, Schulte-Hermann R: Follistatin overexpression in rodent liver tumors: a possible mechanism to overcome activin growth control. Mol Carcinog; 2002 Sep;35(1):1-5
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  • The activin-follistatin system is a potent growth regulatory system of liver tissue homeostasis.
  • Using RNase protection analysis, we studied the expression of follistatin in rat and mouse liver tumors as a possible mechanism to overcome activin growth control.
  • Approximately 40% of the tumors (nine of 24 each), most of them hepatocellular carcinomas, displayed increased levels of follistatin mRNA when compared to tumor-surrounding liver tissue.
  • The degree of overexpression was highly variable but independent of the carcinogen treatment that animals had received.
  • It was also independent from the histological stage of malignancy and further found in rat liver adenomas.
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / genetics. Adenoma / pathology. Alternative Splicing. Animals. Blotting, Western. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / pathology. Cell Division / genetics. Diethylnitrosamine / pharmacology. Follistatin. Humans. Male. Mice. Mice, Inbred Strains. Nafenopin / pharmacology. Phenobarbital / pharmacology. RNA, Messenger / analysis. Rats. Reference Values. Transforming Growth Factor alpha / genetics. Transforming Growth Factor alpha / metabolism. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12203361.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Follistatin; 0 / RNA, Messenger; 0 / Transforming Growth Factor alpha; 093W78U96W / Nafenopin; 104625-48-1 / Activins; 3IQ78TTX1A / Diethylnitrosamine; YQE403BP4D / Phenobarbital
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17. Ning S, Knox SJ, Harsh GR, Culler MD, Katznelson L: Lanreotide promotes apoptosis and is not radioprotective in GH3 cells. Endocr Relat Cancer; 2009 Sep;16(3):1045-55
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  • Somatostatin analogs are a mainstay of medical therapy in patients with GH producing human pituitary tumors, and it has been suggested that somatostatin analogs may be radioprotective.
  • We utilized GH secreting rat GH3 cells to investigate whether a somatostatin analog may limit the effects of radiation on proliferation and apoptosis in vitro and on tumor growth in vivo.
  • Treatment with lanreotide alone at doses of either 100 or 1000 nM for 48 h reduced clonogenic survival by 5-10%.
  • In a mouse GH3 tumor xenograft model, lanreotide 10 mg/kg moderately inhibited the growth of GH3 tumors, with a 4x tumor growth delay (TGD) time that ranged from 4.5 to 8.3 days.
  • The combination of lanreotide, either antecedent to or concurrent, with radiation of 250, 200 or 150 cGy/fraction for 5 days inhibited tumor growth and produced the TGD times that were similar to radiation alone (P>0.05).
  • [MeSH-major] Adenoma / pathology. Apoptosis / drug effects. Growth Hormone-Secreting Pituitary Adenoma / pathology. Peptides, Cyclic / pharmacology. Radiation Tolerance / drug effects. Somatostatin / analogs & derivatives. Somatotrophs / pathology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Dose-Response Relationship, Drug. Gamma Rays. Male. Mice. Mice, Nude. Radiation Dosage. Radiation-Protective Agents / pharmacology. Rats. Xenograft Model Antitumor Assays

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  • (PMID = 19528243.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptides, Cyclic; 0 / Radiation-Protective Agents; 118992-92-0 / lanreotide; 51110-01-1 / Somatostatin
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18. Yamagishi M, Natsume M, Osakabe N, Nakamura H, Furukawa F, Imazawa T, Nishikawa A, Hirose M: Effects of cacao liquor proanthocyanidins on PhIP-induced mutagenesis in vitro, and in vivo mammary and pancreatic tumorigenesis in female Sprague-Dawley rats. Cancer Lett; 2002 Nov 28;185(2):123-30
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  • For determination of the influence on initiation and subsequent development of lesions, CLPr (0.025% or 0.25%) were fed during the period of PhIP application (100 mg/kg given to rats via gastric tubes eight times over 4 weeks), or thereafter until the termination at 48 weeks.
  • CLPr treatments did not affect body or organ weights.
  • These results indicate that CLPr inhibit in vitro mutagenicity of PhIP, as well as rat pancreatic carcinogenesis in the initiation stage, but not mammary carcinogenesis induced by PhIP.
  • [MeSH-major] Adenocarcinoma / prevention & control. Adenoma / drug therapy. Anthocyanins / pharmacology. Anticarcinogenic Agents / pharmacology. Antineoplastic Agents, Phytogenic / therapeutic use. Cacao / chemistry. Flavonoids. Mammary Neoplasms, Experimental / prevention & control. Mutagenesis / drug effects. Pancreatic Neoplasms / prevention & control. Phytotherapy. Plant Extracts / pharmacology. Proanthocyanidins
  • [MeSH-minor] Animals. Biotransformation. Carcinogens / toxicity. Catechin / isolation & purification. Catechin / pharmacology. Catechin / therapeutic use. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Female. Imidazoles / toxicity. Microsomes, Liver / metabolism. Mutagenicity Tests. Organ Specificity. Phenols / isolation & purification. Phenols / pharmacology. Phenols / therapeutic use. Polymers / isolation & purification. Polymers / pharmacology. Polymers / therapeutic use. Rats. Rats, Sprague-Dawley. Salmonella typhimurium / drug effects

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  • (PMID = 12169385.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Anthocyanins; 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Carcinogens; 0 / Flavonoids; 0 / Imidazoles; 0 / Phenols; 0 / Plant Extracts; 0 / Polymers; 0 / Proanthocyanidins; 18206-61-6 / proanthocyanidin; 8R1V1STN48 / Catechin; 909C6UN66T / 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine
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19. Stepień H, Lawnicka H, Mucha S, Wagrowska-Danilewicz M, Stepień B, Siejka A, Komorowski J: Inhibitory effect of thalidomide on the growth, secretory function and angiogenesis of estrogen-induced prolactinoma in Fischer 344 rats. Life Sci; 2006 Sep 27;79(18):1741-8
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  • Thalidomide [(alpha-(N-phthalimido)-glutarimide] is known to be a potent immunomodulatory drug with antiangiogenic properties, but its effect on lactotroph cell secretory function and pituitary prolactinoma formation has not been described yet.
  • The purpose of this study was to examine the effects of thalidomide on secretion of prolactin (PRL) and vascular endothelial growth factor (VEGF), cell proliferation, apoptosis and angiogenesis within the anterior pituitary gland in long-term diethylstilboestrol (DES)-treated male F344 rats in vivo and in vitro.
  • It was found that DES sharply increased serum PRL and VEGF levels.
  • On the other hand, simultaneous treatment of F344 rats with thalidomide for the last 15 days of the experiment attenuated the stimulatory effect of DES on PRL and VEGF secretion.
  • It also diminished prolactin cell proliferation evaluated as the number of proliferating cell nuclear antigen (PCNA)-positive stained cell nuclei and increased the number of apoptotic bodies determined by the terminal deoxynucleotidyl-mediated dUTP nick-end labeling (TUNEL) method in sections of the DES-induced pituitary prolactinoma.
  • The density of pituitary microvessels evaluated by microscopic counting of CD-31-positive blood vessels was also diminished by the tested drug.
  • In addition, thalidomide (10(-4) to 10(-6) M) inhibited cell proliferation, prolactin and VEGF secretion from rat pituitary prolactinoma cells cultured in vitro.
  • In conclusion, our results provide strong evidence for the antiprolactin and antitumor activity of thalidomide in experimentally DES-induced pituitary adenoma.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neovascularization, Pathologic / drug therapy. Pituitary Neoplasms / drug therapy. Prolactin / metabolism. Prolactinoma / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Animals. Antigens, CD31 / analysis. Apoptosis. Cell Nucleus / chemistry. Cell Proliferation / drug effects. Diethylstilbestrol / toxicity. Estrogens / toxicity. Pituitary Gland / chemistry. Pituitary Gland / pathology. Proliferating Cell Nuclear Antigen / analysis. Rats. Rats, Inbred F344. Vascular Endothelial Growth Factor A

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  • (PMID = 16846617.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Estrogens; 0 / Proliferating Cell Nuclear Antigen; 0 / Vascular Endothelial Growth Factor A; 4Z8R6ORS6L / Thalidomide; 731DCA35BT / Diethylstilbestrol; 9002-62-4 / Prolactin
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20. Liddle RA, Toskes PP, Horrow J, Ghali J, Dachman A, Stong D: Lack of trophic pancreatic effects in humans with long-term administration of ximelagatran. Pancreas; 2006 Mar;32(2):205-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CCK1 receptors are abundant in rat pancreas but are either absent or present at very low levels in human pancreas.
  • METHODS: One hundred thirty patients requiring anticoagulation treatment for atrial fibrillation randomly received, in a double-blind fashion, either 36 mg oral ximelagatran twice daily or warfarin dose adjusted to an international normalized ratio of 2.0 to 3.0.
  • Before enrollment and after 12 months of treatment, computed tomography scans of the pancreas were performed, and pancreas volumes were quantified using the summation-of-areas technique.
  • Three months after the initiation of drug treatment, plasma CCK concentrations were measured by radioimmunoassay 120 minutes after the patients drank 240 mL of a mixed liquid meal (Ensure).
  • RESULTS: After 3 months of treatment, plasma CCK concentrations did not differ between the ximelagatran and warfarin groups, 15 +/- 18 and 11 +/- 17 pmol/L (X +/- SD; P = 0.22), respectively.
  • The initial average pancreas volumes were 82 +/- 31 and 88 +/- 28 mL in the ximelagatran and warfarin groups, respectively, and decreased to 70 +/- 25 and 75 +/- 28 mL, respectively, after 12 months of treatment.
  • Although the decrease in pancreas volume with time was significant in each group (P = 0.0001), the magnitude of the volume reduction was similar in the 2 groups.
  • CONCLUSION: In contrast to rats, in which long-term oral administration of ximelagatran stimulates pancreatic growth and adenoma formation, in humans, ximelagatran does not increase plasma CCK concentrations and has no demonstrable trophic effect on the human pancreas.
  • [MeSH-major] Anticoagulants / therapeutic use. Atrial Fibrillation / drug therapy. Azetidines / therapeutic use. Benzylamines / therapeutic use. Pancreas / anatomy & histology
  • [MeSH-minor] Aged. Body Mass Index. Body Weight. Cholecystokinin / blood. Double-Blind Method. Humans. Tomography, X-Ray Computed. Warfarin / therapeutic use

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  • (PMID = 16552342.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-064213; United States / NIDDK NIH HHS / DK / DK-38626
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Azetidines; 0 / Benzylamines; 49HFB70472 / ximelagatran; 5Q7ZVV76EI / Warfarin; 9011-97-6 / Cholecystokinin
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