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1. Noguera Aguilar JF, Amengual Antich I, Morón Canis JM, Plaza Martínez A, Martínez Córcoles JA, Tortajada Collado C, Pujol Tugores JJ: Effect of rofecoxib on colon chemical carcinogenesis at colonic anastomotic area in the rat. Rev Esp Enferm Dig; 2005 Jun;97(6):405-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of rofecoxib on colon chemical carcinogenesis at colonic anastomotic area in the rat.
  • AIM: To investigate the effect of the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib on the incidence of perianastomotic colonic tumors in a model of chemical carcinogenesis in the rat.
  • The main parameter evaluated was the percentage of colonic neoplastic tissue, which relates tumor surface area to the colon's surface area.
  • RESULTS: Rofecoxib at doses of 2.5 mg/kg or 0.0058 ppm significantly reduced chemical colon carcinogenesis in rats, both in the perianastomotic area and the rest of the colon (p < 0.01).
  • CONCLUSIONS: Rofecoxib causes a reduction in chemical colon carcinogenesis in rats.
  • [MeSH-major] Adenocarcinoma / prevention & control. Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Colorectal Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Lactones / therapeutic use. Sulfones / therapeutic use

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  • (PMID = 16011415.001).
  • [ISSN] 1130-0108
  • [Journal-full-title] Revista española de enfermedades digestivas : organo oficial de la Sociedad Española de Patología Digestiva
  • [ISO-abbreviation] Rev Esp Enferm Dig
  • [Language] eng; spa
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carcinogens; 0 / Cyclooxygenase Inhibitors; 0 / Lactones; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib
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2. Maurin N, Forgue-Lafitte ME, Levy P, Zimber A, Bara J: Progression of tumors arising from large ACF is associated with the MUC5AC expression during rat colon MNNG carcinogenis. Int J Cancer; 2007 Feb 1;120(3):477-83
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  • [Title] Progression of tumors arising from large ACF is associated with the MUC5AC expression during rat colon MNNG carcinogenis.
  • Aberrant crypt foci (ACF) are microscopic lesions which have been postulated to precede the development of adenomas, precursors of colon cancer.
  • The gastric M1/MUC5AC mucin has also been described as an early marker of colon carcinogenesis in the human and in the rat.
  • This observation suggests that the expression of MUC5AC is associated with the ACF/adenoma sequence and supports the notion of large ACF as precursors of adenomas/adenocarcinomas.
  • Moreover, the expression of MUC5AC in the transitional mucosa adjacent to both rat and human colon tumors suggests that some human tumors could arise from large ACF, and reinforces the concept of the premalignant potential of these lesions.
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenoma / chemically induced. Adenoma / metabolism. Adenoma / pathology. Animals. Antibodies, Monoclonal / analysis. Antibodies, Monoclonal / immunology. Disease Progression. Immunohistochemistry. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Mucin 5AC. Rats. Rats, Wistar. Time Factors

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  • (PMID = 17066439.001).
  • [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 / Antibodies, Monoclonal; 0 / MUC5AC protein, human; 0 / Muc5ac protein, rat; 0 / Mucin 5AC; 0 / Mucins; 12H3O2UGSF / Methylnitronitrosoguanidine
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3. Femia AP, Dolara P, Giannini A, Salvadori M, Biggeri A, Caderni G: Frequent mutation of Apc gene in rat colon tumors and mucin-depleted foci, preneoplastic lesions in experimental colon carcinogenesis. Cancer Res; 2007 Jan 15;67(2):445-9

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  • [Title] Frequent mutation of Apc gene in rat colon tumors and mucin-depleted foci, preneoplastic lesions in experimental colon carcinogenesis.
  • Mucin-depleted foci (MDF) are microscopic dysplastic lesions induced in the colon of rodents by specific colon carcinogens.
  • Because Apc is a member of the Wnt pathway and the most frequent mutated gene in human colon cancer, we tested whether MDF harbor Apc mutations.
  • We screened a segment of the Apc gene comprising the region homologous to the mutation cluster region (MCR) of human APC, which frequently shows mutations in experimental colon tumors.
  • These results show that Apc mutations are present in MDF with a frequency similar to that of tumors, strengthening the evidence that they are precancerous lesions in colon carcinogenesis.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenoma / genetics. Adenoma / metabolism. Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Male. Rats. Rats, Inbred F344

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  • (PMID = 17234750.001).
  • [ISSN] 0008-5472
  • [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 / Mucins
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4. Gordon PV, Paxton JB, Fox NS: A methodology for distinguishing divergent cell fates within a common progenitor population: adenoma- and neuroendocrine-like cells are confounders of rat ileal epithelial cell (IEC-18) culture. BMC Cell Biol; 2005;6(1):2
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  • [Title] A methodology for distinguishing divergent cell fates within a common progenitor population: adenoma- and neuroendocrine-like cells are confounders of rat ileal epithelial cell (IEC-18) culture.
  • BACKGROUND: IEC-18 cells are a non-transformed, immortal cell line derived from juvenile rat ileal crypt cells.
  • The majority of IEC-18 cells in SFM alone had a loss in expression of the adenomatous polyposis coli (APC) gene at the mRNA and protein levels, consistent with adenoma-like transformation.
  • The most common fate switch that we were able to detect correlates with a down regulation of the APC gene and transformation into an adenoma-like phenotype.
  • [MeSH-minor] Adenoma / pathology. Animals. Carcinoma, Neuroendocrine / pathology. Gene Expression Profiling. Gene Expression Regulation. Genes, APC. Methods. Phenotype. Rats

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  • [Other-IDs] NLM/ PMC547914
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5. Wali RK, Roy HK, Kim YL, Liu Y, Koetsier JL, Kunte DP, Goldberg MJ, Turzhitsky V, Backman V: Increased microvascular blood content is an early event in colon carcinogenesis. Gut; 2005 May;54(5):654-60
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  • [Title] Increased microvascular blood content is an early event in colon carcinogenesis.
  • BACKGROUND: Increased premalignant epithelial microvascular blood content is a common theme in neoplastic transformation; however, demonstration of this phenomenon in colon carcinogenesis has been stymied by methodological limitations.
  • Finally, in a pilot study, we examined superficial blood content from the endoscopically normal mid transverse colon in 37 patients undergoing screening colonoscopy.
  • RESULTS: In the AOM treated rat model, augmentation of superficial mucosal and total mucosal/superficial submucosal blood supply preceded the appearance of aberrant crypt foci (ACF) and temporally and spatially correlated with future ACF occurrence.
  • CONCLUSION: We report, for the first time, that blood content is increased in the colonic microvasculature at the earliest stages of colon carcinogenesis.

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  • (PMID = 15831911.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1R03CA10549-01; United States / NCI NIH HHS / CA / U01 CA111257; United States / NCI NIH HHS / CA / R21 CA102750; United States / NCI NIH HHS / CA / 1U01CA11125-01; United States / NCI NIH HHS / CA / 1R21CA102750-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hemoglobins; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS2644; NLM/ PMC1262671
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6. Steele VE, Rao CV, Zhang Y, Patlolla J, Boring D, Kopelovich L, Juliana MM, Grubbs CJ, Lubet RA: Chemopreventive efficacy of naproxen and nitric oxide-naproxen in rodent models of colon, urinary bladder, and mammary cancers. Cancer Prev Res (Phila); 2009 Nov;2(11):951-6
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  • [Title] Chemopreventive efficacy of naproxen and nitric oxide-naproxen in rodent models of colon, urinary bladder, and mammary cancers.
  • Nonsteroidal anti-inflammatory drugs (NSAID) have been highly effective in preventing colon, urinary bladder, and skin cancer preclinically, and also in clinical trials of colon adenoma formation.
  • In the azoxymethane-induced rat colon aberrant crypt foci (ACF) model, naproxen administered at 200 and 400 ppm in the diet reduced mean ACFs in the colon by about 45% to 60%, respectively.
  • In the hydroxybutyl (butyl) nitrosamine rat urinary bladder cancer model, NO-naproxen was given at 183 or 550 ppm in the diet, and naproxen at 128 ppm.
  • These data show that both naproxen and NO-naproxen are effective agents against urinary bladder and colon, but not mammary, carcinogenesis.

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  • (PMID = 19892664.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CN / N01 CN043301; United States / NCI NIH HHS / CN / NCI-CN43301; United States / NCI NIH HHS / CA / N01CN53300; United States / NCI NIH HHS / CN / NCI-CN53300; United States / NCI NIH HHS / CN / N01 CN053300; United States / NCI NIH HHS / CA / N01CN43301
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carcinogens; 0 / Nitric Oxide Donors; 0 / naproxen-n-butyl nitrate; 3817-11-6 / Butylhydroxybutylnitrosamine; 57Y76R9ATQ / Naproxen; 684-93-5 / Methylnitrosourea; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS142040; NLM/ PMC2774912
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7. Barmeyer C, Ye JH, Sidani S, Geibel J, Binder HJ, Rajendran VM: Characteristics of rat downregulated in adenoma (rDRA) expressed in HEK 293 cells. Pflugers Arch; 2007 Jun;454(3):441-50
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  • [Title] Characteristics of rat downregulated in adenoma (rDRA) expressed in HEK 293 cells.
  • Studies with apical membrane vesicles have shown that two distinct and separate anion exchange processes are present in rat distal colon, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS)-sensitive CL(-)-HCO(3)(-) exchange, and DIDS-resistant Cl(-)-OH(-) exchange.
  • These studies proposed that anion exchanger (AE)-1 isoform encodes the former as both apical membrane DIDS-sensitive CL(-)-HCO(3)(-) exchange, and AE1 specific mRNA are present only in surface cells and are downregulated in Na-depleted rats, whereas downregulated in adenoma (DRA) encodes the latter as both DIDS-resistant Cl(-)-OH(-) exchange, and DRA-specific proteins are present in apical membranes of both surface and crypt cells and are not altered in Na(+)-depleted rats.
  • Studies were, therefore, initiated to identify the function of rat DRA (rDRA) in vitro. rDRA cDNA isolated from rat distal colon encodes a 757-amino-acid protein which has 96 and 81% homology with mDRA and hDRA, respectively. rDRA-specific mRNA expression was detectable only in specific segments of the digestive tract (duodenum, ileum, cecum, proximal colon, and distal colon) but not in the stomach, jejunum, or in the kidney, brain, heart, and lung.
  • Our observations that rDRA mediates DIDS-insensitive, acid pH-dependent Cl(-) uptake are consistent with prior observations that rDRA does not mediate DIDS-sensitive Cl(-)-HCO(3)(-) exchange in rat distal colon.
  • [MeSH-minor] 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / pharmacology. Amino Acid Sequence. Animals. Base Sequence. Bicarbonates / metabolism. Bicarbonates / pharmacology. Cell Line. Chlorides / metabolism. Chlorides / pharmacology. Cloning, Molecular. Colon / metabolism. DNA Primers / genetics. Fatty Acids, Volatile / pharmacology. Humans. Hydrogen-Ion Concentration. Ion Transport / drug effects. Molecular Sequence Data. Rats. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Sequence Homology, Amino Acid. Transfection

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  • (PMID = 17492310.001).
  • [ISSN] 0031-6768
  • [Journal-full-title] Pflugers Archiv : European journal of physiology
  • [ISO-abbreviation] Pflugers Arch.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF337809
  • [Grant] United States / NIDDK NIH HHS / DK / DK60069; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antiporters; 0 / Bicarbonates; 0 / Chlorides; 0 / DNA Primers; 0 / Fatty Acids, Volatile; 0 / Recombinant Proteins; 0 / Slc26a3 protein, rat; Q1O6DSW23R / 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
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8. 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.
  • The purpose of this study was to examine the effects of I3C on colon carcinogenesis, cell proliferation, cell-cycle progression and apoptosis, and on the levels of expression of several cell-cycle control molecules.
  • We used a long-term rat model by using azoxymethane (AOM) to induce tumors (adenomas and adenocarcinomas) in the colon.
  • 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.
  • I3C significantly increased the proliferating cell nuclear antigen labeling index (PCNA LI) (P<0.008) and decreased the apoptotic index (P<0.05) of the colon adenocarcinoma.
  • In contrast, in HCT 116 and HT29 human colon carcinoma cells, I3C inhibited growth and induced G1-phase cell-cycle arrest and apoptosis.
  • 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.

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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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9. Che TC, François S, Bouchet S, Chapel A, Forgue-Lafitte ME: Early lesions induced in rat colon epithelium by N-methyl-N'-nitro-N-nitrosoguanidine. Tissue Cell; 2010 Jun;42(3):190-4
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  • [Title] Early lesions induced in rat colon epithelium by N-methyl-N'-nitro-N-nitrosoguanidine.
  • The development of ACF (aberrant crypt foci), adenoma and cancer following intrarectal administration of the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) has been described.
  • These lesions protrude slightly over the epithelial lining of the colon, with a micropolyp-like appearance.
  • The epithelium lining the cysts and the distorted crypts shows expression of gastric mucin M1/MUC5AC, an early marker of colonic carcinogenesis which is not present in normal colon.
  • [MeSH-major] Colon / drug effects. Colon / pathology. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Methylnitronitrosoguanidine / toxicity

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20493508.001).
  • [ISSN] 1532-3072
  • [Journal-full-title] Tissue & cell
  • [ISO-abbreviation] Tissue Cell
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Muc5ac protein, rat; 0 / Mucin 5AC; 12H3O2UGSF / Methylnitronitrosoguanidine
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10. Saini MK, Sharma P, Kaur J, Sanyal SN: The cyclooxygenase-2 inhibitor etoricoxib is a potent chemopreventive agent of colon carcinogenesis in the rat model. J Environ Pathol Toxicol Oncol; 2009;28(1):39-46
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  • [Title] The cyclooxygenase-2 inhibitor etoricoxib is a potent chemopreventive agent of colon carcinogenesis in the rat model.
  • Cyclooxygenase-2 (COX-2), an inducible prostaglandin G/H synthase, is overexpressed in several human cancers, including colon cancer, and therefore the potential ability of a selective COX-2 inhibitor, etoricoxib, is considered in the prevention of the 1,2-dimethyl hydrazine (DMH)-induced colon carcinogenesis in the rat model.
  • The results showed that DMH produced a very high number of multiple plaque lesions (MPLs), putative neoplastic biomarkers, localized throughout the colon, whereas considerable regression was observed with etoricoxib treatment.
  • Because all these changes were clearly reversed by etoricoxib in DMH-treated animals, and the use of etoricoxib alone did not produce a neoplastic effect per se, it appears that etoricoxib, a selective COX-2 inhibitor, might be a safe and potentially chemopreventive agent in colon cancer.
  • [MeSH-minor] 1,2-Dimethylhydrazine. Adenoma / chemically induced. Adenoma / pathology. Adenoma / prevention & control. Animals. Apoptosis. Biomarkers / analysis. Disease Models, Animal. Immunohistochemistry. In Situ Nick-End Labeling. Male. Rats. Rats, Sprague-Dawley

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  • (PMID = 19392653.001).
  • [ISSN] 0731-8898
  • [Journal-full-title] Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
  • [ISO-abbreviation] J. Environ. Pathol. Toxicol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Biomarkers; 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyridines; 0 / Sulfones; 202409-33-4 / etoricoxib; IX068S9745 / 1,2-Dimethylhydrazine
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11. Begleiter A, Sivananthan K, Lefas GM, Maksymiuk AW, Bird RP: Inhibition of colon carcinogenesis by post-initiation induction of NQO1 in Sprague-Dawley rats. Oncol Rep; 2009 Jun;21(6):1559-65
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  • [Title] Inhibition of colon carcinogenesis by post-initiation induction of NQO1 in Sprague-Dawley rats.
  • Phase II detoxifying enzymes may play a significant role in preventing carcinogen-induced colon cancer at the initiation and post-initiation stage, but the contribution of NAD(P) H:quinone oxidoreductase 1 (NQO1) to this effect remains unclear.
  • Using the carcinogen-induced colon cancer Sprague-Dawley rat model, we previously showed that oltipraz selectively induces NQO1 in the colons of these rats without inducing other phase II detoxifying enzymes.
  • We demonstrated that selective induction of NQO1 in the rat colon prior to treatment with a carcinogen significantly inhibited the formation of aberrant crypt foci (ACF).
  • Using the same rat model, we found that rats fed oltipraz containing diet following treatment with the colon carcinogen, azoxymethane (AOM), had 60% fewer ACF after 12 weeks compared with rats fed a control diet.
  • In addition, rats fed oltipraz containing diet after AOM treatment developed 40% fewer colon adenomas and fewer colon tumors than rats fed a control diet.
  • Together, these results suggest that NQO1 can contribute to inhibition of colon carcinogenesis at the post-initiation stage.
  • Thus, NQO1 may be an important target for chemoprevention of colon cancer.
  • [MeSH-major] Adenoma / prevention & control. Anticarcinogenic Agents / pharmacology. Cell Transformation, Neoplastic / drug effects. Colon / drug effects. Colonic Neoplasms / prevention & control. NAD(P)H Dehydrogenase (Quinone) / biosynthesis. Precancerous Conditions / prevention & control. Pyrazines / pharmacology

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  • (PMID = 19424637.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Pyrazines; 6N510JUL1Y / oltipraz; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, rat; EC 2.4.1.17 / Glucuronosyltransferase; EC 2.5.1.18 / Glutathione Transferase; MO0N1J0SEN / Azoxymethane
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12. Babyatsky M, Lin J, Yio X, Chen A, Zhang JY, Zheng Y, Twyman C, Bao X, Schwartz M, Thung S, Lawrence Werther J, Itzkowitz S: Trefoil factor-3 expression in human colon cancer liver metastasis. Clin Exp Metastasis; 2009;26(2):143-51
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  • [Title] Trefoil factor-3 expression in human colon cancer liver metastasis.
  • Trefoil factor-3 (TFF3) is expressed by normal intestinal epithelial cells and its expression is maintained throughout the colon adenoma-carcinoma sequence.
  • Our previous work demonstrated a correlation between TFF3 expression and metastatic potential in an animal model of colon cancer.
  • The aim of this study was to determine whether TFF3 is expressed in human colon cancer liver metastasis (CCLM) and whether inhibiting TFF3 expression in colon cancer cells would alter their invasive potential in vitro.
  • Two highly metastatic rat colon cancer cell lines that either natively express TFF3 (LN cells) or were transfected with TFF3 (LPCRI-2 cells), were treated with two rat TFF3 siRNA constructs (si78 and si365), and analyzed in an in vitro invasion assay.
  • At the mRNA and protein level, TFF3 was expressed in 17/17 (100%) CCLMs and 10/11 (91%) primary colon cancers, but not in normal liver tissue.
  • These results provide further evidence that TFF3 contributes to the malignant behavior of colon cancer cells.

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  • (PMID = 18979216.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA109189
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Neuropeptides; 0 / Peptides; 0 / TFF3 protein, human; 0 / TFF3 protein, rat; 0 / Trefoil Factor-3
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13. Aparicio T, Kotelevets L, Tsocas A, Laigneau JP, Sobhani I, Chastre E, Lehy T: Leptin stimulates the proliferation of human colon cancer cells in vitro but does not promote the growth of colon cancer xenografts in nude mice or intestinal tumorigenesis in Apc(Min/+) mice. Gut; 2005 Aug;54(8):1136-45
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  • [Title] Leptin stimulates the proliferation of human colon cancer cells in vitro but does not promote the growth of colon cancer xenografts in nude mice or intestinal tumorigenesis in Apc(Min/+) mice.
  • BACKGROUND AND AIMS: Leptin, the product of the ob gene, has been suggested to increase the risk of colon cancer.
  • However, we have shown that although leptin stimulates epithelial cell proliferation it reduces the development of carcinogen induced preneoplastic lesions in the rat colon.
  • Here, we explored the effect of leptin in vitro on proliferation of human colon cancer cells, and in vivo on the growth of HT-29 xenografts in nude mice and the development of intestinal tumours in Apc(Min/+) mice.
  • CONCLUSIONS: Leptin acts as a growth factor on colon cancer cells in vitro but does not promote tumour growth in vivo in the two models tested.
  • [MeSH-minor] Adenoma / genetics. Adenoma / pathology. Adenoma / physiopathology. Animals. Apoptosis / physiology. Cell Division / physiology. Cell Line, Tumor. Colon / pathology. Colon / physiopathology. DNA, Neoplasm / biosynthesis. Humans. Intestinal Mucosa / pathology. Intestinal Mucosa / physiopathology. Male. Mice. Mice, Inbred BALB C. Mice, Nude

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  • (PMID = 15857934.001).
  • [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 / DNA, Neoplasm; 0 / Leptin
  • [Other-IDs] NLM/ PMC1774895
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14. Corpet DE, Pierre F: How good are rodent models of carcinogenesis in predicting efficacy in humans? A systematic review and meta-analysis of colon chemoprevention in rats, mice and men. Eur J Cancer; 2005 Sep;41(13):1911-22
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  • [Title] How good are rodent models of carcinogenesis in predicting efficacy in humans? A systematic review and meta-analysis of colon chemoprevention in rats, mice and men.
  • Tumours in rodent and human colon share many histological and genetic features.
  • To know if rodent models of colon carcinogenesis are good predictors of chemopreventive efficacy in humans, we conducted a meta-analysis of aspirin, beta-carotene, calcium, and wheat bran studies.
  • Controlled intervention studies of adenoma recurrence in human volunteers were compared with chemoprevention studies of carcinogen-induced tumours in rats, and of polyps in Min (Apc(+/-)) mice: 6714 volunteers, 3911 rats and 458 mice were included in the meta-analyses.
  • A closer look showed that carcinogen-induced rat studies matched human trials for aspirin, calcium, carotene, and were compatible for wheat bran.
  • Based on three cases only, the carcinogen-induced rat model seems better than the Min mouse model.

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  • (PMID = 16084718.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 01YAE03M7J / beta Carotene; R16CO5Y76E / Aspirin; SY7Q814VUP / Calcium
  • [Number-of-references] 108
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15. Grijelmo C, Rodrigue C, Svrcek M, Bruyneel E, Hendrix A, de Wever O, Gespach C: Proinvasive activity of BMP-7 through SMAD4/src-independent and ERK/Rac/JNK-dependent signaling pathways in colon cancer cells. Cell Signal; 2007 Aug;19(8):1722-32
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  • [Title] Proinvasive activity of BMP-7 through SMAD4/src-independent and ERK/Rac/JNK-dependent signaling pathways in colon cancer cells.
  • Recent data indicate that the Bone Morphogenetic Protein BMP-7 exhibits mucosal protection against experimental colitis in rats, suggesting that this cytokine exerts direct actions in intestinal epithelial cells during inflammatory bowel diseases and other precancerous lesions of the colon.
  • In this study, we investigated the functional expression of BMP-7 and its receptors in normal human colon crypts, aberrant crypt foci (ACF) in sigmoiditis and colorectal tumors, and their derived cancer cell lines.
  • The cytokine was identified by immunohistochemistry in surface epithelial cells and crypts in the normal colon mucosa, ACF in sigmoiditis, sporadic high grade dysplastic adenoma, and in 9 of 16 colon carcinomas (56.2%).
  • In addition, the conditioned medium collected from the adenoma PC/AA/C1 and carcinoma HCT8/S11 and SW48 cell lines in culture contained significant levels of BMP-7 ranging from 0.17 to 0.38 ng/ml.
  • We found that BMP-7 induced scattering and proinvasive responses (EC50=1 ng/ml) in kidney and colon cancer cell lines through SMAD4 and src -independent pathways and signaling cascades using FAK phosphorylation at Y925 and activation of ERK1/2, Rac1 and JNK.
  • Taken together, our findings suggest that BMP-7 exerts divergent effects in the colon mucosa, one counteracting transient inflammatory situations and the other linked to pejorative functions during chronic ulcerative diseases and the neoplastic progression.

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  • (PMID = 17478078.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMP7 protein, human; 0 / Bmp7 protein, rat; 0 / Bone Morphogenetic Protein 7; 0 / Bone Morphogenetic Proteins; 0 / SMAD4 protein, human; 0 / Smad4 Protein; 0 / Transforming Growth Factor beta; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.6.5.2 / rac GTP-Binding Proteins
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16. Femia AP, Caderni G, Vignali F, Salvadori M, Giannini A, Biggeri A, Gee J, Przybylska K, Cheynier V, Dolara P: Effect of polyphenolic extracts from red wine and 4-OH-coumaric acid on 1,2-dimethylhydrazine-induced colon carcinogenesis in rats. Eur J Nutr; 2005 Mar;44(2):79-84
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  • [Title] Effect of polyphenolic extracts from red wine and 4-OH-coumaric acid on 1,2-dimethylhydrazine-induced colon carcinogenesis in rats.
  • BACKGROUND: Total polyphenolic extracts from red wine protect against azoxymethane (AOM)-induced colon carcinogenesis in rats.
  • AIM OF THE STUDY: We investigated the effect of high molecular weight polyphenols (HMWP), low molecular weight polyphenols (LMWP) and total polyphenolic extracts from red wine (WE) on colon carcinogenesis.
  • RESULTS: WE treated rats had significantly fewer (p < 0.05) colorectal adenomas than controls, while rats in other treatment groups did not differ significantly from controls (colorectal adenomas/rat were: 2.2 +/- 0.3; 1.4 +/- 0.2; 2.9 +/- 0.5; 2.6 +/- 0.4; 2.3 +/- 0.3; in controls, WE, HMWP, LMWP and 4-OH-coumaric acid groups, respectively; means +/- SE).
  • The mean number of colorectal carcinomas per rat was similar among all experimental groups.
  • Proliferative activity in the normal colon mucosa did not vary among experimental groups.
  • CONCLUSIONS: Total polyphenolic extracts (WE) from red wine, but neither the HMWP nor the LMWP, have some inhibitory effect on the process of colon carcinogenesis by DMH reducing the number of adenomas.
  • [MeSH-major] Adenoma / epidemiology. Colonic Neoplasms / epidemiology. Colorectal Neoplasms / epidemiology. Coumaric Acids / pharmacology. Flavonoids / pharmacology. Phenols / pharmacology. Wine

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  • (PMID = 15309424.001).
  • [ISSN] 1436-6207
  • [Journal-full-title] European journal of nutrition
  • [ISO-abbreviation] Eur J Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Carcinogens; 0 / Coumaric Acids; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; IX068S9745 / 1,2-Dimethylhydrazine
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17. Wei M, Morimura K, Wanibuchi H, Shen J, Salim EI, Moku M, Hakoi K, Fukushima S: JTE-522, a selective cyclooxygenase-2 inhibitor, inhibits induction but not growth and invasion of 1,2-dimethylhydrazine-induced tubular adenocarcinomas of colon in rats. Int J Cancer; 2005 Jan 20;113(3):354-8
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  • [Title] JTE-522, a selective cyclooxygenase-2 inhibitor, inhibits induction but not growth and invasion of 1,2-dimethylhydrazine-induced tubular adenocarcinomas of colon in rats.
  • We have previously demonstrated that JTE-522, a selective cyclooxygenase-2 (COX-2) inhibitor, inhibited development of aberrant crypt foci (ACF) in rats, a putative preneoplastic lesion in colon, and suggested its inhibitory potential in rat colon carcinogenesis.
  • To evaluate the chemopreventive properties of JTE-522, the present study was design to evaluate the inhibitory effects of JTE-522 on rat colon tumorigenesis induced by 1,2-dimethylhydrazine (DMH).
  • Forty weeks after the start of the experiment, administration of 150 ppm JTE-522 during both initiation and postinitiation stages significantly inhibited the incidences of tubular adenocarcinomas and total carcinomas, as well as total tumors in the colon.
  • These findings suggest that JTE-522 possesses chemopreventive activity against induction but not progression of tubular adenocarcinomas in rat colon.
  • In view of the significant inhibitory effects of JTE-522 on ACF, its major anticancer action may occur in the postinitiation stage but before the malignant conversion stage of DMH-induced colon carcinogenesis.
  • [MeSH-minor] Adenoma / chemically induced. Adenoma / enzymology. Adenoma / prevention & control. Animals. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Disease Progression. Gene Expression Profiling. Male. Oligonucleotide Array Sequence Analysis. Prostaglandin-Endoperoxide Synthases / metabolism. Rats. Rats, Inbred F344

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  • (PMID = 15455344.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide; 0 / Benzenesulfonates; 0 / Biomarkers, Tumor; 0 / Carcinogens; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Oxazoles; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; IX068S9745 / 1,2-Dimethylhydrazine
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18. Kobunai T, Watanabe T, Yamamoto Y, Eshima K: The frequency of KRAS mutation detection in human colon carcinoma is influenced by the sensitivity of assay methodology: a comparison between direct sequencing and real-time PCR. Biochem Biophys Res Commun; 2010 Apr 23;395(1):158-62
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  • [Title] The frequency of KRAS mutation detection in human colon carcinoma is influenced by the sensitivity of assay methodology: a comparison between direct sequencing and real-time PCR.
  • PURPOSE: Kirsten rat sarcoma (KRAS) gene mutations occur early in the progression of colorectal adenoma to carcinoma.

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20361930.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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19. Zoghbi S, Drouin E, Claustre J, Bara J, Scoazec JY, Plaisancié P: Intestinal MUC2 and gastric M1/MUC5AC in preneoplastic lesions induced by 1,2-dimethylhydrazine in rat: a sequential analysis. Int J Oncol; 2007 Feb;30(2):489-97
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  • [Title] Intestinal MUC2 and gastric M1/MUC5AC in preneoplastic lesions induced by 1,2-dimethylhydrazine in rat: a sequential analysis.
  • Our study was performed to sequentially analyze the expression of the intestinal mucin MUC2 and of the gastric mucin MUC5AC as indicators during progression of preneoplastic biomarkers in rat colon.
  • [MeSH-minor] Adenoma / metabolism. Animals. Carcinoma / metabolism. Cell Line, Tumor. Colon / metabolism. Humans. Male. Mucin 5AC. Mucin-2. Precancerous Conditions. Rats. Rats, Inbred F344. beta Catenin / metabolism

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  • (PMID = 17203232.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Carcinogens; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Muc2 protein, rat; 0 / Muc5ac protein, rat; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucins; 0 / beta Catenin; IX068S9745 / 1,2-Dimethylhydrazine
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20. De Miglio MR, Virdis P, Calvisi DF, Mele D, Muroni MR, Frau M, Pinna F, Tomasi ML, Simile MM, Pascale RM, Feo F: Identification and chromosome mapping of loci predisposing to colorectal cancer that control Wnt/beta-catenin pathway and progression of early lesions in the rat. Carcinogenesis; 2007 Nov;28(11):2367-74
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  • [Title] Identification and chromosome mapping of loci predisposing to colorectal cancer that control Wnt/beta-catenin pathway and progression of early lesions in the rat.
  • Linkage analysis of 138 AWF2 rats identified three loci on chromosomes 4, 15 and 18 in significant linkage with lesion multiplicity that were identified as rat Colon cancer resistance (rCcr) 1, rCcr2 and rCcr3, respectively.
  • Seven other loci on chromosomes 5, 6, 15, 17, 18 and 20 were in suggestive linkage with adenoma/adenocarcinoma multiplicity/surface area.
  • However, influence of susceptibility/resistance genes on Wnt/beta-catenin pathway was shown by defective beta-catenin inactivation in WF but not in ACI and AWF1 rat adenocarcinomas.

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  • (PMID = 17510081.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NIAAA NIH HHS / AA / F32 AA020150
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
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21. Naishiro Y, Yamada T, Idogawa M, Honda K, Takada M, Kondo T, Imai K, Hirohashi S: Morphological and transcriptional responses of untransformed intestinal epithelial cells to an oncogenic beta-catenin protein. Oncogene; 2005 Apr 28;24(19):3141-53
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  • A rat intestinal epithelial cell line IEC6 became elongated, extended protrusions at cell periphery, and increased stress fibers and focal contacts upon the induction of beta-catenin protein stabilized by deletion of the N-terminal glycogen synthase kinase-3beta (GSKbeta) phosphorylation sites (beta-catenin DeltaN89).
  • [MeSH-minor] Adenoma / metabolism. Animals. Cell Adhesion. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cells, Cultured. Chromatin Immunoprecipitation. Colon / metabolism. Colorectal Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Extracellular Matrix / metabolism. Genes, Reporter. Glycogen Synthase Kinase 3 / metabolism. HeLa Cells. Humans. Immunohistochemistry. Intercellular Signaling Peptides and Proteins / metabolism. Intestine, Small / metabolism. Luciferases / metabolism. Lymphoid Enhancer-Binding Factor 1. Male. Mice. Mice, Inbred C57BL. Microscopy, Fluorescence. Oligonucleotide Array Sequence Analysis. Protein Structure, Tertiary. Rats. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Time Factors. Transcription Factors / metabolism. Wnt Proteins. beta Catenin

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  • (PMID = 15735679.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Ctnnb1 protein, rat; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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22. van Kouwen MC, Laverman P, van Krieken JH, Oyen WJ, Nagengast FM, Drenth JP: Noninvasive monitoring of colonic carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model. Nucl Med Biol; 2006 Feb;33(2):245-8

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  • At present, it is unknown at which stage FDG accumulation occurs during the adenoma carcinoma sequence.
  • To address this issue, we studied the FDG uptake in AOM-induced rat colorectal adenocarcinoma (CRC) and correlated this with histopathological findings.
  • RESULTS: Macroscopic examination revealed 21 tumors (7 located in the small bowel and 14 in the colon) in 19 rats.
  • In total, seven colon adenomas were found in five rats, six of which expressed high-grade dysplasia.

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  • (PMID = 16546679.001).
  • [ISSN] 0969-8051
  • [Journal-full-title] Nuclear medicine and biology
  • [ISO-abbreviation] Nucl. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; MO0N1J0SEN / Azoxymethane
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23. Worrell RT, Best A, Crawford OR, Xu J, Soleimani M, Matthews JB: Apical ammonium inhibition of cAMP-stimulated secretion in T84 cells is bicarbonate dependent. Am J Physiol Gastrointest Liver Physiol; 2005 Oct;289(4):G768-78
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  • However, apical NH(4)(+) inhibition of current was prevented by 10 min of pretreatment of the apical surface with 500 microM DIDS, 100 microM 4,4'-dinitrostilbene-2,2'-disulfonic acid (DNDS), or 25 microM niflumic acid, suggesting a role for NH(4)(+) action through an apical anion exchanger. mRNA and protein for the apical anion exchangers SLC26A3 [downregulated in adenoma (DRA)] and SLC26A6 [putative anion transporter (PAT1)] were detected in T84 cells by RT-PCR and Northern and Western blots.
  • [MeSH-major] Bicarbonates / metabolism. Colon / metabolism. Cyclic AMP / antagonists & inhibitors. Cyclic AMP / pharmacology. Quaternary Ammonium Compounds / pharmacology

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  • (PMID = 16002564.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-051630; United States / NIDDK NIH HHS / DK / DK-62809
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiporters; 0 / Bicarbonates; 0 / Carbonic Anhydrase Inhibitors; 0 / Chloride Channels; 0 / Membrane Transport Proteins; 0 / Muscarinic Agonists; 0 / Quaternary Ammonium Compounds; 0 / SLC26A6 protein, human; 0 / Slc26a3 protein, rat; 0 / Stilbenes; 128-42-7 / 4,4'-dinitro-2,2'-stilbenedisulfonic acid; 8Y164V895Y / Carbachol; E0399OZS9N / Cyclic AMP; Q1O6DSW23R / 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
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24. Mustafi R, Cerda S, Chumsangsri A, Fichera A, Bissonnette M: Protein Kinase-zeta inhibits collagen I-dependent and anchorage-independent growth and enhances apoptosis of human Caco-2 cells. Mol Cancer Res; 2006 Sep;4(9):683-94
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  • The expression level of PKC-zeta, an atypical PKC isoform, increases from the crypt base to the luminal surface and parallels crypt cell differentiation in normal colon.
  • In prior studies in the azoxymethane model of colon cancer, we showed that PKC-zeta was down-regulated in rat colonic tumors.
  • In this study, we showed that PKC-zeta is expressed predominantly in colonic epithelial and not stromal cells, and loss of PKC-zeta occurs as early as the adenoma stage in human colonic carcinogenesis.
  • To assess the regulation of growth and differentiation by PKC-zeta, we altered this isoform in human Caco-2 colon cancer cells using stable constitutive or inducible expression vectors, specific peptide inhibitors or small interfering RNA.
  • Taken together, these studies indicate that PKC-zeta inhibits colon cancer cell growth and enhances differentiation and apoptosis, while inhibiting the transformed phenotype of these cells.

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  • (PMID = 16940160.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA36745; United States / NIDDK NIH HHS / DK / P30DK42086
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / RNA, Small Interfering; EC 2.7.11.1 / protein kinase C zeta; EC 2.7.11.13 / Protein Kinase C
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25. Xiao H, Hao X, Simi B, Ju J, Jiang H, Reddy BS, Yang CS: Green tea polyphenols inhibit colorectal aberrant crypt foci (ACF) formation and prevent oncogenic changes in dysplastic ACF in azoxymethane-treated F344 rats. Carcinogenesis; 2008 Jan;29(1):113-9
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  • In order to prepare for a human trial on the inhibition of colon carcinogenesis, we conducted a study with green tea polyphenols as the preventive agent in an azoxymethane (AOM)-induced rat colon cancer model using aberrant crypt foci (ACF) as an end point.
  • Dietary PPE administration was found to significantly and dose dependently decrease the total number of ACF per rat and the total number of aberrant crypt per rat.
  • Retinoid X receptor (RXR)alpha expression was reduced in high-grade dysplastic ACF, adenoma and adenocarcinoma during AOM-induced colon carcinogenesis, and the PPE treatment partially prevented the loss of RXRalpha expression in high-grade dysplastic ACF.
  • Taken together, our results strongly suggest the colon cancer-preventive activity of PPE and identified possible molecular markers for future colon cancer prevention studies.

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  • (PMID = 17893236.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES005022
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / Tea; MO0N1J0SEN / Azoxymethane
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26. Chakravarti B, Dwivedi SK, Mithal A, Chattopadhyay N: Calcium-sensing receptor in cancer: good cop or bad cop? Endocrine; 2009 Jun;35(3):271-84
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  • One situation is loss of CaR expression, resulting in loss of growth suppressing effects of elevated extracellular Ca(2+) by CaR, reported in parathyroid adenoma and in colon carcinoma.
  • CaR signaling and effects have been studied in several cancers including ovarian cancers, gastrinomas, and gliomas in addition to comparatively detailed studies in breast, prostate, and colon cancers.
  • Studies on H-500 rat Leydig cells, a xenotransplantable model of humoral hypercalcemia of malignancy has shed much light on the mechanisms of CaR-induced cancer cell growth and survival.
  • Pharmacological agonists and antagonists of CaR hold therapeutic promise depending on whether activation of CaR is required such as in case of colon cancer or inactivating the receptor is required as in the case of breast- and prostate tumors.

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  • (PMID = 19011996.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Calcium-Sensing
  • [Number-of-references] 203
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