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1. Raju J, Bielecki A, Caldwell D, Lok E, Taylor M, Kapal K, Curran I, Cooke GM, Bird RP, Mehta R: Soy isoflavones modulate azoxymethane-induced rat colon carcinogenesis exposed pre- and postnatally and inhibit growth of DLD-1 human colon adenocarcinoma cells by increasing the expression of estrogen receptor-beta. J Nutr; 2009 Mar;139(3):474-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Soy isoflavones modulate azoxymethane-induced rat colon carcinogenesis exposed pre- and postnatally and inhibit growth of DLD-1 human colon adenocarcinoma cells by increasing the expression of estrogen receptor-beta.
  • We studied the effects of lifetime exposure to dietary soy isoflavones in an azoxymethane (AOM)-induced rat colon cancer model.
  • After 26 wk, rats were killed and the coordinates of colon aberrant crypt foci (ACF) and tumors were determined.
  • Expression of estrogen receptor (ER)-beta was assessed in rat colon tumors and in DLD-1 human colon adenocarcinoma cells exposed to soy isoflavones.
  • Compared with the control, soy isoflavones did not affect incidences or multiplicities of colon ACF or tumors.
  • Expression of ERbeta increased in colon tumors of soy isoflavone-treated groups compared with the control.
  • Our results suggest that pre- and postnatal exposure to dietary soy isoflavones suppresses the growth of colon tumors in male rats.
  • The overexpression of ERbeta in both rat colon tumors and DLD-1 cells caused by soy isoflavones suggests that ERbeta is a critical mediator in mitigating its cancer-preventive effects.
  • [MeSH-major] Adenocarcinoma / prevention & control. Colonic Neoplasms / prevention & control. Estrogen Receptor beta / metabolism. Isoflavones / pharmacology. Soybeans / chemistry

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  • (PMID = 19141699.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Estrogen Receptor beta; 0 / Isoflavones; MO0N1J0SEN / Azoxymethane
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2. 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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  • [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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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. Adachi K, Hattori M, Kato H, Inai M, Tsukamoto M, Handharyani E, Taira E, Tsukamoto Y: Involvement of gicerin, a cell adhesion molecule, in the portal metastasis of rat colorectal adenocarcinoma cells. Oncol Rep; 2010 Dec;24(6):1427-31
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  • [Title] Involvement of gicerin, a cell adhesion molecule, in the portal metastasis of rat colorectal adenocarcinoma cells.
  • In the present study, gicerin cDNA was introduced into endogenous gicerin negative ACL-15 cells, a rat colon adenocarcinoma cell line.
  • These results suggest that gicerin might promote the interaction of tumor cells with a hepatic endothelium, thus leading to the hepatic metastasis of colon adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / pathology. Antigens, CD146 / physiology. Colorectal Neoplasms / pathology. Portal Vein. Vascular Neoplasms / secondary

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  • (PMID = 21042736.001).
  • [ISSN] 1791-2431
  • [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 / Antigens, CD146; 0 / Cell Adhesion Molecules
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5. Simmen FA, Frank JA, Wu X, Xiao R, Hennings LJ, Prior RL: Lack of efficacy of blueberry in nutritional prevention of azoxymethane-initiated cancers of rat small intestine and colon. BMC Gastroenterol; 2009 Sep 16;9:67
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  • [Title] Lack of efficacy of blueberry in nutritional prevention of azoxymethane-initiated cancers of rat small intestine and colon.
  • However, effects of BB on colon tumors and in both genders are unknown.
  • METHODS: We examined efficacy of BB in inhibition of azoxymethane (AOM)-induced colon ACF and intestine tumors in male and female Sprague-Dawley rats (outbred strain).
  • BB increased (P < 0.05) ACF numbers within the distal colon of female but not male rats.
  • There was a significant (P < 0.05) diet by gender interaction with respect to total colon ACF number.
  • Colon and duodenum tumor incidences were less in females than males at 17 weeks after AOM.
  • BB favored (P < 0.05) fewer adenocarcinomas and more adenomatous polyps (as a proportion of total tumor number) in female rat small intestine.
  • Blueberry influenced ACF occurrence in distal colon and tumor progression in duodenum, in gender-specific fashion.
  • Data indicate the potential for slowing tumor progression (adenomatous polyp to adenocarcinoma) by BB.

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  • (PMID = 19758446.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CB / N02-CB-07008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / C-Peptide; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ PMC2752457
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6. Kawamori T, Osta W, Johnson KR, Pettus BJ, Bielawski J, Tanaka T, Wargovich MJ, Reddy BS, Hannun YA, Obeid LM, Zhou D: Sphingosine kinase 1 is up-regulated in colon carcinogenesis. FASEB J; 2006 Feb;20(2):386-8
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  • [Title] Sphingosine kinase 1 is up-regulated in colon carcinogenesis.
  • The SK1/S1P pathway also plays a critical role in regulation of cyclooxygenase-2 (COX-2), a well-established pathogenic factor in colon carcinogenesis.
  • Therefore, we examined the expression of SK1 and COX-2 in rat colon tumors induced by azoxymethane (AOM) and the relationship of these two proteins in normal and malignant intestinal epithelial cells.
  • Strongly positive SK1 staining was found in 21/28 (75%) of rat colon adenocarcinomas induced by AOM, whereas no positive SK1 staining was observed in normal mucosa.
  • The increase in SK1 and COX-2 expression in AOM-induced rat colon adenocarcinoma was confirmed at the level of mRNA by real-time RT-PCR.
  • In addition, it was found that 1) down-regulation of SK1 in HT-29 human colon cancer cells by small interfering RNA (siRNA) decreases COX-2 expression and PGE2 production;.
  • 2) overexpression of SK1 in RIE-1 rat intestinal epithelial cells induces COX-2 expression; and 3) S1P stimulates COX-2 expression and PGE2 production in HT-29 cells.
  • These results suggest that the SK1/S1P pathway may play an important role in colon carcinogenesis, in part, by regulating COX-2 expression and PGE2 production.
  • [MeSH-minor] Animals. Azoxymethane / pharmacology. Cell Line, Tumor. Colon / metabolism. Cyclooxygenase 2 / metabolism. Dinoprostone / metabolism. Epithelial Cells / metabolism. Humans. Intestinal Mucosa / metabolism. Lysophospholipids / metabolism. Male. Mice. Mice, Inbred BALB C. Rats. Rats, Inbred F344. Sphingosine / analogs & derivatives. Sphingosine / metabolism

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  • (PMID = 16319132.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA102558; United States / NCI NIH HHS / CA / CA86688; United States / NCI NIH HHS / CA / P01CA097132; United States / NCRR NIH HHS / RR / P20RR017677
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lysophospholipids; 26993-30-6 / sphingosine 1-phosphate; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / sphingosine kinase; K7Q1JQR04M / Dinoprostone; MO0N1J0SEN / Azoxymethane; NGZ37HRE42 / Sphingosine
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7. 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.
  • 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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8. Ishiwata K, Liu HY, Teramoto K, Kawamura K, Oda K, Arii S: Tumor viability evaluation by positron emission tomography with [18F]FDG in the liver metastasis rat model. Ann Nucl Med; 2006 Aug;20(7):463-9
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  • [Title] Tumor viability evaluation by positron emission tomography with [18F]FDG in the liver metastasis rat model.
  • We prepared a liver metastatic tumor model by injection of rat colon adenocarcinoma cells to Fischer F344 rats through portal vein, and applied positron emission tomography (PET) using 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) ([18F]FDG-PET) to this model.

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  • (PMID = 17037278.001).
  • [ISSN] 0914-7187
  • [Journal-full-title] Annals of nuclear medicine
  • [ISO-abbreviation] Ann Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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9. Liu HY, Teramoto K, Kawamura K, Oda K, Ishiwata K, Arii S: Evaluation of tumor growth in vivo in a rat model of liver metastasis, using a newly devised index obtained by positron emission tomography with [18F] FDG. J Hepatobiliary Pancreat Surg; 2007;14(3):276-82
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  • [Title] Evaluation of tumor growth in vivo in a rat model of liver metastasis, using a newly devised index obtained by positron emission tomography with [18F] FDG.
  • METHODS: F344 rats were injected with rat colon adenocarcinoma cells (RCN-9 cell line) via the portal vein, and some of them were treated with 5-fluorouracil (5-FU).
  • [MeSH-major] Adenocarcinoma / radionuclide imaging. Fluorodeoxyglucose F18. Liver Neoplasms, Experimental / radionuclide imaging. Positron-Emission Tomography / methods. Radiopharmaceuticals

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  • (PMID = 17520203.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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10. Arimochi H, Morita K, Kataoka K, Nakanishi S, Kuwahara T, Ohnishi Y: Suppressive effect of Clostridium perfringens-produced heat-stable substance(s) on proliferation of human colon adenocarcinoma HT29 cells in culture. Cancer Lett; 2006 Sep 28;241(2):228-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppressive effect of Clostridium perfringens-produced heat-stable substance(s) on proliferation of human colon adenocarcinoma HT29 cells in culture.
  • Clostridium perfringens has been regarded as one of the intestinal bacteria increasing colon cancer risk.
  • In previous studies, we have shown that the oral administration of C. perfringens culture medium can inhibit the mutagen-induced formation of pre-neoplastic lesions in rat colon, thus proposing the existence of factor(s) preventing colon tumorigenesis in this culture medium.
  • Then, the effect of C. perfringens culture medium on human colon adenocarcinoma HT29 cells was examined.
  • These observations suggest that C. perfringens culture medium has a cytostatic action on colon tumor cells, which may be responsible for the prevention of pre-neoplastic formation in rat colon.
  • [MeSH-major] Adenocarcinoma / pathology. Clostridium perfringens / physiology. Colonic Neoplasms / pathology. Culture Media / pharmacology

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  • (PMID = 16300879.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Culture Media; 0 / Early Growth Response Protein 1
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11. 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.
  • [MeSH-major] Adenocarcinoma / pathology. Antioxidants / pharmacology. Colonic Neoplasms / pathology. Indoles / pharmacology

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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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12. He H, Zhao Y, Chen X, Zheng Y, Wu X, Wang R, Li T, Yu Q, Jing J, Ma L, Ren W, Han D, Wang G: Quantitative determination of trans-polydatin, a natural strong anti-oxidative compound, in rat plasma and cellular environment of a human colon adenocarcinoma cell line for pharmacokinetic studies. J Chromatogr B Analyt Technol Biomed Life Sci; 2007 Aug 15;855(2):145-51
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  • [Title] Quantitative determination of trans-polydatin, a natural strong anti-oxidative compound, in rat plasma and cellular environment of a human colon adenocarcinoma cell line for pharmacokinetic studies.
  • A simple, accurate, precise, specific and reproducible high-performance liquid chromatography (HPLC) method was developed for determination of trans-polydatin, a natural strong anti-oxidative compound, in rat plasma and cell suspension.
  • The described assay method was applied to pharmacokinetic studies in rats and a human colon adenocarcinoma cell line (Caco-2) successfully.
  • [MeSH-minor] Adenocarcinoma. Animals. Cell Line, Tumor. Colonic Neoplasms. Rats. Reproducibility of Results. Sensitivity and Specificity. Time Factors

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  • (PMID = 17606417.001).
  • [ISSN] 1570-0232
  • [Journal-full-title] Journal of chromatography. B, Analytical technologies in the biomedical and life sciences
  • [ISO-abbreviation] J. Chromatogr. B Analyt. Technol. Biomed. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Glucosides; 0 / Stilbenes; XM261C37CQ / polydatin
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13. Fraser A, Haines SR, Stuart EC, Scandlyn MJ, Alexander A, Somers-Edgar TJ, Rosengren RJ: Deer velvet supplementation decreases the grade and metastasis of azoxymethane-induced colon cancer in the male rat. Food Chem Toxicol; 2010 May;48(5):1288-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deer velvet supplementation decreases the grade and metastasis of azoxymethane-induced colon cancer in the male rat.
  • Since deer velvet (DV) extract promotes angiogenesis, its ability to modulate the growth and invasiveness of colon tumours was investigated.
  • Specifically, more of the tumours in the DV-treated rats were of a lower grade compared to the controls, both when all tumour sites were considered (0.91 vs. 0.66, p<0.0001), as well as those located only in the colon (0.95 vs. 0.84, p<0.03).
  • Therefore, this study can confidently conclude that DV does not increase the incidence, multiplicity, metastasis or tumour volume of AOM-induced colon cancer in the rat.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacology. Colonic Neoplasms / drug therapy. Skin / chemistry. Tissue Extracts / pharmacology

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20176070.001).
  • [ISSN] 1873-6351
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tissue Extracts; MO0N1J0SEN / Azoxymethane
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14. Panchenko AV, Petrishchev NN, Kvetnoĭ IM, Anisimov VN: [Colon carcinogenesis in rat vs. variable light]. Vopr Onkol; 2008;54(3):332-7
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  • [Title] [Colon carcinogenesis in rat vs. variable light].
  • The effect of lighting and melatonin treatment on 1,2 dimethylhydrazine (DMH)-induced colon carcinogenesis was investigated in rats.
  • That presented as changes in rate of tumorigenesis, number of tumors per animal, adenocarcinoma cell differentiation grade, invasiveness and proliferative rate.
  • [MeSH-major] 1,2-Dimethylhydrazine / toxicity. Adenocarcinoma / physiopathology. Cell Differentiation / radiation effects. Colonic Neoplasms / physiopathology. Light. Photoperiod

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  • (PMID = 18652239.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Carcinogens; IX068S9745 / 1,2-Dimethylhydrazine; JL5DK93RCL / Melatonin
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15. Georges R, Adwan H, Zhivkova M, Eyol E, Bergmann F, Berger MR: Regulation of osteopontin and related proteins in rat CC531 colorectal cancer cells. Int J Oncol; 2010 Aug;37(2):249-56
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  • [Title] Regulation of osteopontin and related proteins in rat CC531 colorectal cancer cells.
  • The main aim of the study was to investigate changes which occur in CC531 rat colon adenocarcinoma cells and are instrumental to the metastatic phenotype after homing to the liver.
  • [MeSH-major] Adenocarcinoma / genetics. Colorectal Neoplasms / genetics. Osteopontin / genetics. Sialoglycoproteins / genetics

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  • (PMID = 20596651.001).
  • [ISSN] 1791-2423
  • [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 / Core Binding Factor Alpha 1 Subunit; 0 / Homeodomain Proteins; 0 / Ibsp protein, rat; 0 / Integrin-Binding Sialoprotein; 0 / Runx2 protein, rat; 0 / Sialoglycoproteins; 0 / Spp1 protein, rat; 106441-73-0 / Osteopontin; EC 3.4.24.23 / Matrix Metalloproteinase 7; EC 3.4.24.35 / Matrix Metalloproteinase 9
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16. Thome MA, Ehrlich D, Koesters R, Müller-Stich B, Unglaub F, Hinz U, Büchler MW, Gutt CN: The point of conversion in laparoscopic colonic surgery affects the oncologic outcome in an experimental rat model. Surg Endosc; 2009 Sep;23(9):1988-94
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  • [Title] The point of conversion in laparoscopic colonic surgery affects the oncologic outcome in an experimental rat model.
  • Hematogenous metastatic spread was induced in each operation group by tumor cell inoculation of a rat colon adenocarcinoma (CC 531) into the portal vein after 15 min of surgical intervention.
  • [MeSH-major] Adenocarcinoma / secondary. Cecum / surgery. Colectomy / methods. Colonic Neoplasms / pathology. Laparoscopy. Laparotomy. Liver Neoplasms / secondary. Pneumoperitoneum, Artificial / adverse effects

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  • (PMID = 18528621.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
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17. Gutt CN, Brinkmann L, Mehrabi A, Fonouni H, Müller-Stich BP, Vetter G, Stein JM, Schemmer P, Büchler MW: Dietary omega-3-polyunsaturated fatty acids prevent the development of metastases of colon carcinoma in rat liver. Eur J Nutr; 2007 Aug;46(5):279-85
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  • [Title] Dietary omega-3-polyunsaturated fatty acids prevent the development of metastases of colon carcinoma in rat liver.
  • BACKGROUND: Fish oil consisting of omega-3 polyunsaturated fatty acids (PUFA) seems to reduce the incidence of colon cancer.
  • The effect of PUFAs on metastasis of colon carcinoma is still unclear.
  • CC 531 cells, a moderately differentiated colon adenocarcinoma, were injected into the spleen of each rat.

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  • (PMID = 17593466.001).
  • [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 / Fatty Acids, Omega-3
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18. Braumann C, Schoenbeck M, Menenakos C, Kilian M, Jacobi CA: Effects of increasing doses of a bolus injection and an intravenous long-term therapy of taurolidine on subcutaneous (metastatic) tumor growth in rats. Clin Exp Metastasis; 2005;22(1):77-83
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  • METHODS: VEGF and TNFalpha levels of rat colon adenocarcinoma cells (DHD/K12/TRb) were analyzed in the supernatant undergoing treatment of increasing taurolidine doses in vitro.
  • At the beginning of the operation, 10 000 colon adenocarcinoma cells were applied subcutaneously at the back of the rats.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Antineoplastic Agents / administration & dosage. Colonic Neoplasms / drug therapy. Colonic Neoplasms / pathology. Taurine / analogs & derivatives. Thiadiazines / administration & dosage

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  • (PMID = 16132581.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Thiadiazines; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 1EQV5MLY3D / Taurine; 8OBZ1M4V3V / taurolidine
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19. Opitz I, Van der Veen H, Witte N, Braumann C, Mueller JM, Jacobi CA: Instillation of taurolidine/heparin after laparotomy reduces intraperitoneal tumour growth in a colon cancer rat model. Eur Surg Res; 2007;39(3):129-35
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  • [Title] Instillation of taurolidine/heparin after laparotomy reduces intraperitoneal tumour growth in a colon cancer rat model.
  • OBJECTIVE: To investigate whether irrigation of the abdominal cavity after laparotomy for caecum resection with taurolidine/heparin or adhesion prophylactic substances reduces intraperitoneal tumour growth or the local recurrence rate in a colon carcinoma rat model.
  • METHODS: 60 BDIX rats underwent caecum resection after intraperitoneal inoculation of 1 x 10(4) colon carcinoma cells (DHD/K12/TRb).
  • These results represent a good rationale for intraoperative adjuvant irrigation with taurolidine/heparin during resection of colon cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Anticoagulants / therapeutic use. Antineoplastic Agents / therapeutic use. Colonic Neoplasms / drug therapy. Heparin / therapeutic use. Neoplasm Recurrence, Local / prevention & control. Taurine / analogs & derivatives. Thiadiazines / therapeutic use

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  • (PMID = 17337889.001).
  • [ISSN] 0014-312X
  • [Journal-full-title] European surgical research. Europäische chirurgische Forschung. Recherches chirurgicales européennes
  • [ISO-abbreviation] Eur Surg Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antineoplastic Agents; 0 / Thiadiazines; 1EQV5MLY3D / Taurine; 8OBZ1M4V3V / taurolidine; 9005-49-6 / Heparin
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20. Davidson LA, Wang N, Shah MS, Lupton JR, Ivanov I, Chapkin RS: n-3 Polyunsaturated fatty acids modulate carcinogen-directed non-coding microRNA signatures in rat colon. Carcinogenesis; 2009 Dec;30(12):2077-84
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  • [Title] n-3 Polyunsaturated fatty acids modulate carcinogen-directed non-coding microRNA signatures in rat colon.
  • To fully understand the effects of these agents on the expression of miRNAs, Sprague-Dawley rats were fed diets containing corn oil or fish oil with pectin or cellulose and injected with azoxymethane (AOM, a colon-specific carcinogen) or saline (control).
  • These results demonstrate for the first time the utility of the rat AOM model and the novel role of fish oil in protecting the colon from carcinogen-induced miRNA dysregulation.

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  • (PMID = 19825969.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA074552-12; United States / NIEHS NIH HHS / ES / P30ES09106; United States / NCI NIH HHS / CA / CA074552-12; United States / NCI NIH HHS / CA / R01 CA059034; United States / NCI NIH HHS / CA / CA74552; United States / NCI NIH HHS / CA / CA59034; United States / NCI NIH HHS / CA / R01 CA074552; United States / NCI NIH HHS / CA / CA129444
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Fatty Acids, Unsaturated; 0 / Fish Oils; 0 / MicroRNAs; 0 / Pectins; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ PMC2792315
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21. Mitrofanova E, Unfer R, Vahanian N, Kane S, Carvour M, Link C: Effective growth arrest of human colon cancer in mice, using rat sodium iodide symporter and radioiodine therapy. Hum Gene Ther; 2005 Nov;16(11):1333-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective growth arrest of human colon cancer in mice, using rat sodium iodide symporter and radioiodine therapy.
  • We have demonstrated that the rat sodium iodide symporter (rNIS) and 131I can effectively induce growth arrest of human prostate tumor xenografts [Mitrofanova, E., Unfer, R., Vahanian, N., Daniels, W., Roberson, E., Seregina, T., Seth, P., and Link, C. (2004).
  • Rat sodium iodide symporter (rNIS) for radioiodide therapy of cancer. Clin.
  • In this work the ability of the rNIS and 131I system to inhibit the growth of relatively large (about 800 mm3 when treated with 131I) and rapidly growing colon tumors in an animal model was examined. in vitro experiments demonstrated that transduction of human colon cancer cells with Ad-rNIS resulted in a 100- to 150-fold increase in 125I uptake compared with nontransduced cells.
  • This is the first report demonstrating that rat NIS and 131I can effectively induce growth arrest of relatively large tumors in an animal model.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Division. Colorectal Neoplasms / pathology. Iodine Radioisotopes / therapeutic use. Symporters / physiology

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  • (PMID = 16259567.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Symporters; 0 / sodium-iodide symporter
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22. Brown AC, Shah C, Liu J, Pham JT, Zhang JG, Jadus MR: Ginger's (Zingiber officinale Roscoe) inhibition of rat colonic adenocarcinoma cells proliferation and angiogenesis in vitro. Phytother Res; 2009 May;23(5):640-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ginger's (Zingiber officinale Roscoe) inhibition of rat colonic adenocarcinoma cells proliferation and angiogenesis in vitro.
  • Ginger's (Zingiber officinale Roscoe) natural bioactives, specifically ginger extract and 6-gingerol, were measured for their in vitro inhibition of two key aspects of colon cancer biology--cancer cell proliferation and angiogenic potential of endothelial cell tubule formation.
  • Antiproliferation activity was assessed through tritiated thymidine ([(3)H]Tdr) incorporation studies of YYT colon cancer cells; the anti-angiogenic ability of gingerol was assessed by a Matrigel assays using MS1 endothelial cells.
  • 1) a direct effect on YYT rat cancer cell proliferation (6-1.5% ginger extract; 100-4 microM 6-gingerol);.
  • 1) direct colon cancer cell growth suppression, and 2) inhibition of the blood supply of the tumor via angiogenesis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Catechols / pharmacology. Cell Proliferation / drug effects. Colonic Neoplasms / drug therapy. Fatty Alcohols / pharmacology. Ginger / chemistry

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  • (PMID = 19117330.001).
  • [ISSN] 1099-1573
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Phytogenic; 0 / Catechols; 0 / Fatty Alcohols; 0 / Plant Extracts; 925QK2Z900 / gingerol
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23. Lee YM, Wu TH: Effects of 5-methoxypsoralen (5-MOP) on arylamine N-acetyltransferase activity in the stomach and colon of rats and human stomach and colon tumor cell lines. In Vivo; 2005 Nov-Dec;19(6):1061-9
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  • [Title] Effects of 5-methoxypsoralen (5-MOP) on arylamine N-acetyltransferase activity in the stomach and colon of rats and human stomach and colon tumor cell lines.
  • The main objective of this study was to document the effects of 5-MOP on the modulation of NAT activities in the stomach and colon of rats and human stomach and colon tumor cell lines.
  • MATERIALS AND METHODS: N-Acetylation of 2-aminofluorene (AF) to 2-acetylaminofluorene (AAF) by NAT in the stomach and colon of Sprague-Dawley (SD) rats and in human stomach (SC-M1) and colon (COLO 205) tumor cell lines was investigated.
  • RESULTS: The data show that the metabolic activity of NAT in the rat colon was higher than that in the rat stomach, and the further metabolism of AAF was slower in the stomach than in the colon.
  • 5-MOP increased the activity of NATand also increased the further metabolism of AAF at 24 h in the rat stomach.
  • In the rat colon, no statistically significant changes caused by 5-MOP were observed in NAT activity, but 5-MOP increased the further metabolism of AAF at 24 to 72 h. 5-MOP decreased the activity of NAT only at 72-h incubation in SC-M1 cells.
  • CONCLUSION: The metabolic activity of NAT in the rat colon was higher than that in the rat stomach, and the results also showed a high degree of correspondence with SC-M1 cells and COLO 205 cells.
  • 5-MOP more efficiently inhibited NAT activity in human stomach and colon tumor cell lines than in the stomach and colon of rats.
  • [MeSH-major] Arylamine N-Acetyltransferase / metabolism. Colon / enzymology. Colonic Neoplasms / enzymology. Methoxsalen / analogs & derivatives. Stomach / enzymology. Stomach Neoplasms / enzymology
  • [MeSH-minor] 2-Acetylaminofluorene / metabolism. Acetylation. Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Cytosol / chemistry. Dose-Response Relationship, Drug. Enzyme Inhibitors / administration & dosage. Enzyme Inhibitors / pharmacology. Fluorenes / metabolism. Humans. Kinetics. Male. Rats. Rats, Sprague-Dawley

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  • (PMID = 16277023.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Fluorenes; 3A69OS195N / 2-aminofluorene; 4FVK84C92X / 5-methoxypsoralen; 9M98QLJ2DL / 2-Acetylaminofluorene; EC 2.3.1.5 / Arylamine N-Acetyltransferase; U4VJ29L7BQ / Methoxsalen
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24. Terai K, Sakamoto K, Goto M, Matsuda M, Kasamaki S, Shinmura K, Takita N, Kamano T: Greater development of 1,2-dimethylhydrazine-induced colon cancer in a rat model of type 2 diabetes mellitus. J Int Med Res; 2006 Jul-Aug;34(4):385-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Greater development of 1,2-dimethylhydrazine-induced colon cancer in a rat model of type 2 diabetes mellitus.
  • Several clinical cohort and case-control studies have suggested a link between diabetes and colon cancer.
  • The relationship between type 2 diabetes mellitus and colon cancer was examined in these rats.
  • The number of colon cancers per rat was significantly greater in the diabetic than in the non-diabetic rats.
  • Type 2 diabetes mellitus may enhance the generation and growth of colon cancer.
  • [MeSH-major] 1,2-Dimethylhydrazine / toxicity. Adenocarcinoma / complications. Carcinogens / toxicity. Cocarcinogenesis. Colonic Neoplasms / complications. Diabetes Mellitus, Type 2 / complications

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  • (PMID = 16989494.001).
  • [ISSN] 0300-0605
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Carcinogens; IX068S9745 / 1,2-Dimethylhydrazine
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25. Sanyal SN, Kaur J: Induction of apoptosis as a potential chemopreventive effect of dual cycloxygenase inhibitor, diclofenac, in early colon carcinogenesis. J Environ Pathol Toxicol Oncol; 2010;29(1):41-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of apoptosis as a potential chemopreventive effect of dual cycloxygenase inhibitor, diclofenac, in early colon carcinogenesis.
  • We evaluated the role of diclofenac, a dual cycloxygenase inhibitor, in chemoprevention of 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rat model.
  • Because ACF can be accepted as reliable prognostic biomarkers in colon carcinogenesis, its inhibition and also the induction of the apoptosis process may favorably indicate the preclinical promise for chemoprevention of colon cancer as demonstrated in the initiation phase of carcinogenesis.
  • [MeSH-major] Adenocarcinoma / prevention & control. Apoptosis / drug effects. Colonic Neoplasms / prevention & control. Cyclooxygenase Inhibitors / pharmacology. Diclofenac / pharmacology. Precancerous Conditions / prevention & control
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Blotting, Western. Chemoprevention. Colon / drug effects. Colon / pathology. Cyclooxygenase 2 / metabolism. Disease Models, Animal. Immunohistochemistry. In Situ Nick-End Labeling. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Male. Rats. Rats, Sprague-Dawley

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  • (PMID = 20528746.001).
  • [ISSN] 2162-6537
  • [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 / Biomarkers, Tumor; 0 / Cyclooxygenase Inhibitors; 144O8QL0L1 / Diclofenac; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs2 protein, rat
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26. Bobrich E, Braumann C, Opitz I, Menenakos C, Kristiansen G, Jacobi CA: Influence of intraperitoneal application of taurolidine/heparin on expression of adhesion molecules and colon cancer in rats undergoing laparoscopy. J Surg Res; 2007 Jan;137(1):75-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of intraperitoneal application of taurolidine/heparin on expression of adhesion molecules and colon cancer in rats undergoing laparoscopy.
  • BACKGROUND: Recent experimental studies have shown that intraperitoneal administration of taurolidine/heparin causes a reduction of local tumor growth after laparoscopy in rat models.
  • MATERIALS AND METHODS: Following a 10,000 colon adenocarcinoma cells' (DHD/K12/TRb) intraperitoneal application a cecum resection and a partial parietal peritoneum resection (1 x 1 cm) were performed using a three trocar technique in 30 BD IX rats.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / surgery. Antineoplastic Agents / pharmacology. Cell Adhesion Molecules / genetics. Colonic Neoplasms / drug therapy. Colonic Neoplasms / surgery. Taurine / analogs & derivatives. Thiadiazines / pharmacology

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  • (PMID = 17109891.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antigens, CD29; 0 / Antigens, CD44; 0 / Antineoplastic Agents; 0 / Cadherins; 0 / Cell Adhesion Molecules; 0 / Thiadiazines; 1EQV5MLY3D / Taurine; 8OBZ1M4V3V / taurolidine; 9005-49-6 / Heparin
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27. Xu B, Cai WS, Xiao HQ, Li SH, Xia JT, Zhu GH, Weng JF: [Influence of liver regeneration after partial hepatectomy on the development of liver metastasis of colon cancer in rats]. Zhonghua Wai Ke Za Zhi; 2009 Mar 1;47(5):369-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Influence of liver regeneration after partial hepatectomy on the development of liver metastasis of colon cancer in rats].
  • OBJECTIVE: To investigate the stimulated effect of liver regeneration on colon cancer cells in remnant liver in rats.
  • METHODS: Rat models with liver metastases or retro-peritoneal metastases of colon cancer were established: animals underwent 37% or 70% liver resection and were compared with a sham laparotomy (15, 25, 15 cases, respectively).
  • The human colon adenocarcinoma cell line Lovo was cultured in the presence of portal serum withdrawn 24 hours and 14 days after partial hepatectomy (PH).

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  • (PMID = 19595017.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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28. Nakayama Y, Inoue Y, Minagawa N, Onitsuka K, Nagata J, Shibao K, Hirata K, Sako T, Nagata N, Yamaguchi K: Chemopreventive effect of 4-[3,5-Bis(trimethylsilyl) benzamido] benzoic acid (TAC-101) on MNU-induced colon carcinogenesis in a rat model. Anticancer Res; 2009 Jun;29(6):2059-65
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  • [Title] Chemopreventive effect of 4-[3,5-Bis(trimethylsilyl) benzamido] benzoic acid (TAC-101) on MNU-induced colon carcinogenesis in a rat model.
  • The chemopreventive effect and the mechanism of action of TAC-101 were investigated using a rat chemical colon carcinogenesis model.
  • MATERIALS AND METHODS: Colon tumors were induced using intra-rectal instillation of N-methyl-N-nitrosourea (MNU) in F344 rats.
  • After the large bowels were resected at 20 weeks, the number of aberrant crypt foci (ACF) and tumors in the colon were counted.
  • CONCLUSION: TAC-101 might inhibit MNU induced colon carcinogenesis via a decrease of ACF.
  • [MeSH-major] Adenocarcinoma / prevention & control. Alkylating Agents / toxicity. Benzoates / therapeutic use. Colonic Neoplasms / prevention & control. Methylnitrosourea / toxicity. Trimethylsilyl Compounds / therapeutic use

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  • (PMID = 19528465.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Antigens, CD95; 0 / Benzoates; 0 / Proliferating Cell Nuclear Antigen; 0 / TAC 101; 0 / Tnfrsf6 protein, rat; 0 / Trimethylsilyl Compounds; 684-93-5 / Methylnitrosourea
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29. Chu QD, Sun L, Li J, Byrnes K, Chervenak D, DeBenedetti A, Mathis JM, Li BD: Rat adenocarcinoma cell line infected with an adenovirus carrying a novel herpes-simplex virus-thymidine kinase suicide gene construct dies by apoptosis upon treatment with ganciclovir. J Surg Res; 2007 Nov;143(1):189-94
Hazardous Substances Data Bank. GANCICLOVIR .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rat adenocarcinoma cell line infected with an adenovirus carrying a novel herpes-simplex virus-thymidine kinase suicide gene construct dies by apoptosis upon treatment with ganciclovir.
  • This protein has been found in elevated quantities in breast, colon, and head and neck cancers.
  • In this study, we investigated the in vitro activity of this suicide gene therapy against the rat Mat BIII breast adenocarcinoma cell line, and assessed whether apoptosis was the responsible mechanism of cell killing.
  • CONCLUSION: Suicide gene therapy targeting the overexpression of eIF4E induces apoptosis and cell death in rat Mat BIII mammary adenocarcinoma cells.
  • [MeSH-major] Adenocarcinoma / therapy. Apoptosis / drug effects. Eukaryotic Initiation Factor-4E / metabolism. Ganciclovir / pharmacology. Genes, Transgenic, Suicide. Mammary Neoplasms, Animal / therapy

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  • (PMID = 17950092.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Eukaryotic Initiation Factor-4E; 0 / Fluorescent Dyes; EC 2.7.1.21 / Thymidine Kinase; I223NX31W9 / Fluorescein-5-isothiocyanate; P9G3CKZ4P5 / Ganciclovir
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30. Elias D, Glehen O, Pocard M, Quenet F, Goéré D, Arvieux C, Rat P, Gilly F, Association Française de Chirurgie: A comparative study of complete cytoreductive surgery plus intraperitoneal chemotherapy to treat peritoneal dissemination from colon, rectum, small bowel, and nonpseudomyxoma appendix. Ann Surg; 2010 May;251(5):896-901

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparative study of complete cytoreductive surgery plus intraperitoneal chemotherapy to treat peritoneal dissemination from colon, rectum, small bowel, and nonpseudomyxoma appendix.
  • OBJECTIVE: To report a large number of patients with peritoneal carcinomatosis (PC) treated with complete cytoreductive (CCR-0) plus intraperitoneal chemotherapy, and to compare the results according to the origin of the primary: colon, rectum, small bowel, and appendix (excluding peritoneal pseudomyxoma).
  • Primary sites were: colon (n=341), rectum (n=27), appendix (n=41), and small bowel (n=31).
  • The 5-year overall survival rates were not statistically different for the colon (29.7%), rectum (37.9%), nor the small bowel (33.8%), but was higher (P=0.01) for appendix adenocarcinoma (63.2%).
  • CONCLUSION: Cytoreductive surgery plus intraperitoneal chemotherapy yields satisfying and similar survival results in the treatment of PC from colon, rectum, and small bowel adenocarcinomas.
  • Results were better for appendix adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / secondary. Appendiceal Neoplasms / pathology. Colonic Neoplasms / pathology. Intestinal Neoplasms / pathology. Peritoneal Neoplasms / secondary. Peritoneal Neoplasms / surgery. Rectal Neoplasms / pathology

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  • (PMID = 20395843.001).
  • [ISSN] 1528-1140
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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31. Alain T, Wong JF, Endersby R, Urbanski SJ, Lee PW, Muruve DA, Johnston RN, Forsyth PA, Beck PL: Reovirus decreases azoxymethane-induced aberrant crypt foci and colon cancer in a rodent model. Cancer Gene Ther; 2007 Oct;14(10):867-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reovirus decreases azoxymethane-induced aberrant crypt foci and colon cancer in a rodent model.
  • In this study, we investigated the effectiveness of reovirus against aberrant crypt foci (ACF) and colon cancer induced by the carcinogen azoxymethane (AOM) in an immunocompetent rat model.
  • Two weeks after completion of reovirus therapy, animals were examined for tumor burden in the colon and other tissues.
  • Fewer obstructing tumors in the colon (P=0.07) and duodenum (P=0.03) and reduced hepatic metastases were also noted.
  • Our results show that repeated rectal reovirus administration had some efficacy in the treatment and prevention of AOM-induced ACFs, colon cancers and metastases.
  • [MeSH-major] Adenocarcinoma / prevention & control. Azoxymethane / toxicity. Carcinogens / toxicity. Colonic Neoplasms / prevention & control. Orthoreovirus / physiology. Precancerous Conditions / prevention & control

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  • (PMID = 17627293.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; MO0N1J0SEN / Azoxymethane
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32. Cheng KC, Li YC, Yu CS, Yu FS, Lee JH, Lin ML, Yang JS, Chung JG: Ketoprofen-inhibited N-acetyltransferase activity and gene expression in human colon tumor cells. Anticancer Res; 2006 Mar-Apr;26(2A):1105-11
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  • [Title] Ketoprofen-inhibited N-acetyltransferase activity and gene expression in human colon tumor cells.
  • The activation of ketoprofen, which inhibits the outgrowth of azoxymethane-induced aberrant crypt foci in the rat colon, on the inhibition of arylamine N-acetyltransferase (NAT) activity (N-acetylation of substrates), gene expression (mRNA NAT) and 2-aminofluorene (AF)-DNA adduct formation was studied in a human colon tumor (adenocarcinoma) cell line (colo 205).
  • Cellular cytosols (9000 xg supernatant) and intact colon tumor cells were used.
  • Based on the results from PCR, it was shown that ketoprofen affected mRNA NAT expression in human colon colo 205 cells.
  • This report is the first to demonstrate that ketoprofen inhibits human colon tumor cell NAT activity, gene expression and DNA adduct formation.

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  • (PMID = 16619513.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 2-aminofluorene-DNA complex; 0 / DNA Adducts; 0 / Fluorenes; 0 / RNA, Messenger; 0 / para-Aminobenzoates; 04Z20NMK31 / Acedoben; 90Y4QC304K / Ketoprofen; 9M98QLJ2DL / 2-Acetylaminofluorene; EC 2.3.1.5 / Arylamine N-Acetyltransferase; TL2TJE8QTX / 4-Aminobenzoic Acid
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33. Barault L, Charon-Barra C, Jooste V, de la Vega MF, Martin L, Roignot P, Rat P, Bouvier AM, Laurent-Puig P, Faivre J, Chapusot C, Piard F: Hypermethylator phenotype in sporadic colon cancer: study on a population-based series of 582 cases. Cancer Res; 2008 Oct 15;68(20):8541-6
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  • [Title] Hypermethylator phenotype in sporadic colon cancer: study on a population-based series of 582 cases.
  • In our study, we defined three different subgroups of methylation (No-CIMP, CIMP-Low, and CIMP-High) and evaluated the prognostic significance of methylation status on a population-based series of sporadic colon cancers.
  • A total of 582 colon adenocarcinomas were evaluated using methylation-specific PCR for 5 markers (hMLH1, P16, MINT1, MINT2, and MINT31).
  • Methylation is an independent prognostic factor in MSS colon cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Colonic Neoplasms / genetics. CpG Islands. DNA Methylation

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  • (PMID = 18922929.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
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34. Hill M, Mazal D, Biron VA, Pereira L, Ubillos L, Berriel E, Ahmed H, Freire T, Rondán M, Vasta GR, Liu FT, Iglesias MM, Osinaga E: A novel clinically relevant animal model for studying galectin-3 and its ligands during colon carcinogenesis. J Histochem Cytochem; 2010 Jun;58(6):553-65

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel clinically relevant animal model for studying galectin-3 and its ligands during colon carcinogenesis.
  • To better understand the role of Gal-3 and its ligands during colon carcinogenesis, we studied its expression in tumors induced in rats treated with 1,2-dimethylhydrazine (DMH) and in human tissues.
  • Normal colon from untreated rats showed no staining using two specific monoclonal antibodies.
  • In contrast, morphologically normal colon from DMH-treated rats and dysplastic aberrant crypt foci were strongly stained, indicating that increased Gal-3 expression is an early event during the neoplastic transformation in colon cells.
  • Overall, the Gal-3 expression pattern observed in the DMH rat model closely resembles that displayed by human colon stained with the same antibodies.
  • We also found that Gal-3 phosphorylation diminishes in serines while increasing in tyrosines during rat colon carcinogenesis.
  • Finally, we showed that Gal-3-ligands expression is strikingly similar in rat and human malignant colon and in non-malignant tissues.
  • In conclusion, the DMH-induced rat colon cancer model displays expression patterns of Gal-3 and its ligands very similar to those observed in human samples.
  • This animal model should contribute to clarifying the role of Gal-3 in colon carcinogenesis and also to finding effective preventive cancer agents based on Gal-3 targeting.
  • [MeSH-major] Adenocarcinoma / metabolism. Colonic Neoplasms / metabolism. Galectin 3 / metabolism
  • [MeSH-minor] Animals. Colon / metabolism. Female. Humans. Immunohistochemistry. Ligands. Models, Animal. Phosphorylation. Polymerase Chain Reaction. RNA Splicing. RNA, Messenger / genetics. Rats. Rats, Wistar

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  • (PMID = 20197492.001).
  • [ISSN] 1551-5044
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Galectin 3; 0 / Ligands; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2874187
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35. Nestler G, Schulz HU, Tautenhahn J, Kuhn R, Krüger S, Lippert H, Pross M: Effects of the angiogenesis inhibitor angiostatin on the growth of CC531 colon carcinoma cells in vitro and in a laparoscopic animal model of peritoneal carcinomatosis. Int J Colorectal Dis; 2006 May;21(4):314-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the angiogenesis inhibitor angiostatin on the growth of CC531 colon carcinoma cells in vitro and in a laparoscopic animal model of peritoneal carcinomatosis.
  • We investigated the cytotoxic, anti-adhesive, and anti-invasive effects of angiostatin in vitro and on intraperitoneal tumor growth in a laparoscopic rat model of peritoneal carcinomatosis using CC531 colon adenocarcinoma cells.
  • In in vivo experiments, CC531 adenocarcinoma cells were intraperitoneally given to Wistar Albino Glaxo rats after the establishment of a pneumoperitoneum.
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Cell Adhesion / drug effects. Cell Line, Tumor / drug effects. Colonic Neoplasms / pathology. Disease Models, Animal. Dose-Response Relationship, Drug. Injections, Intraperitoneal. Injections, Subcutaneous. Laparoscopy. Male. Neoplasm Transplantation. Pneumoperitoneum, Artificial. Random Allocation. Rats. Rats, Wistar

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  • (PMID = 16205930.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 86090-08-6 / Angiostatins
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36. Tai JH, Tessier J, Ryan AJ, Hoffman L, Chen X, Lee TY: Assessment of acute antivascular effects of vandetanib with high-resolution dynamic contrast-enhanced computed tomographic imaging in a human colon tumor xenograft model in the nude rat. Neoplasia; 2010 Sep;12(9):697-707
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of acute antivascular effects of vandetanib with high-resolution dynamic contrast-enhanced computed tomographic imaging in a human colon tumor xenograft model in the nude rat.
  • In the present study, we used 200-microm in-plane high-resolution dynamic contrast-enhanced computed tomography (DCE-CT) to noninvasively assess the immediate antivascular effects of vandetanib in a subcutaneous human colon cancer (LoVo) xenograft model in nude rats and to investigate correlation between changes in CT perfusion parameters and tumor volume or immunohistochemical end points.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiography. Colonic Neoplasms / drug therapy. Colonic Neoplasms / radiography. Neovascularization, Pathologic / drug therapy. Piperidines / therapeutic use. Quinazolines / therapeutic use. Tomography, X-Ray Computed / methods

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  • (PMID = 20824046.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Contrast Media; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Quinazolines
  • [Other-IDs] NLM/ PMC2933690
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37. Brown AC, Reitzenstein JE, Liu J, Jadus MR: The anti-cancer effects of poi (Colocasia esculenta) on colonic adenocarcinoma cells In vitro. Phytother Res; 2005 Sep;19(9):767-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The anti-cancer effects of poi (Colocasia esculenta) on colonic adenocarcinoma cells In vitro.
  • Soluble extracts of poi were incubated at 100 mg/mL in vitro for antiproliferative activity against the rat YYT colon cancer cell line. (3)H-thymidine incorporation studies were conducted to demonstrate that the poi inhibited the proliferation of these cancer cells in a dose-dependent manner.
  • The greatest suppression of YYT colon cancer growth occurred when 25% concentration was used.
  • Although numerous factors can contribute to the risk of colon cancer, perhaps poi consumption may contribute to the lower colon cancer rates among Hawaiians by two distinct mechanisms.
  • First, by inducing apoptosis within colon cancer cells; second, by non-specifically activating lymphocytes, which in turn can lyse cancerous cells.
  • [MeSH-minor] Adenocarcinoma / prevention & control. Animals. Cell Line, Tumor / drug effects. Colonic Neoplasms / prevention & control. Flow Cytometry. Hawaii. In Vitro Techniques. Medicine, Traditional. Rats

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  • [Copyright] Copyright 2005 John Wiley & Sons, Ltd.
  • (PMID = 16220568.001).
  • [ISSN] 0951-418X
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Plant Extracts
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38. Barault L, Veyrie N, Jooste V, Lecorre D, Chapusot C, Ferraz JM, Lièvre A, Cortet M, Bouvier AM, Rat P, Roignot P, Faivre J, Laurent-Puig P, Piard F: Mutations in the RAS-MAPK, PI(3)K (phosphatidylinositol-3-OH kinase) signaling network correlate with poor survival in a population-based series of colon cancers. Int J Cancer; 2008 May 15;122(10):2255-9
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  • [Title] Mutations in the RAS-MAPK, PI(3)K (phosphatidylinositol-3-OH kinase) signaling network correlate with poor survival in a population-based series of colon cancers.
  • We evaluated the clinicopathological features and the prognosis of patients with activated-network colon cancers in a population-based study.
  • A total of 586 colon adenocarcinomas were evaluated using sequencing for mutations of KRAS and PI3KCA, and allelic discrimination for mutation of BRAF.
  • Our study is the first report to underline the potential role of RAS-MAPK, PI (3)K network mutations on survival in colon cancers.
  • [MeSH-major] Adenocarcinoma / genetics. Colonic Neoplasms / genetics. Mitogen-Activated Protein Kinases / genetics. Mutation / genetics. Phosphatidylinositol 3-Kinases / genetics. Proto-Oncogene Proteins / genetics. ras Proteins / genetics

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18224685.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.2 / ras Proteins
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39. Sako T, Nakayama Y, Minagawa N, Inoue Y, Onitsuka K, Katsuki T, Tsurudome Y, Shibao K, Hirata K, Nagata N, Ohie S, Kohno K, Itoh H: 4-[3,5-Bis(trimethylsilyl)benzamido] benzoic acid (TAC-101) induces apoptosis in colon cancer partially through the induction of Fas expression. In Vivo; 2005 Jan-Feb;19(1):125-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 4-[3,5-Bis(trimethylsilyl)benzamido] benzoic acid (TAC-101) induces apoptosis in colon cancer partially through the induction of Fas expression.
  • Apoptotic induction by TAC-101 was investigated using a rat hepatic metastatic model of rat RCN-9 colon cancer cells in vivo and FACScan analysis with the DLD-1 human colon cancer cell line in vitro.
  • Moreover, evaluation of apoptosis by TAC-101 in vitro using FACScan analysis was performed in the DLD-1 human colon cancer cell line.
  • CONCLUSION: These findings suggest that TAC-101 inhibits hepatic metastasis of colon cancer and induces apoptosis partially through enhanced Fas expression.
  • [MeSH-major] Adenocarcinoma / metabolism. Antigens, CD95 / metabolism. Apoptosis / drug effects. Benzoates / pharmacology. Colonic Neoplasms / metabolism. Trimethylsilyl Compounds / pharmacology

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  • (PMID = 15796164.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Benzoates; 0 / TAC 101; 0 / Trimethylsilyl Compounds
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40. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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-major] 1,2-Dimethylhydrazine / toxicity. Adenocarcinoma / prevention & control. Benzenesulfonates / therapeutic use. Carcinogens / toxicity. Colonic Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / antagonists & inhibitors. Oxazoles / therapeutic use

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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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41. Jalil YA, Ritz V, Jakimenko A, Schmitz-Salue C, Siebert H, Awuah D, Kotthaus A, Kietzmann T, Ziemann C, Hirsch-Ernst KI: Vesicular localization of the rat ATP-binding cassette half-transporter rAbcb6. Am J Physiol Cell Physiol; 2008 Feb;294(2):C579-90
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  • [Title] Vesicular localization of the rat ATP-binding cassette half-transporter rAbcb6.
  • Rat Abcb6 (rAbcb6) is a membrane-situated half-transporter belonging to the ABC protein superfamily.
  • To investigate rAbcb6 subcellular distribution, the human colon adenocarcinoma line LoVo, which we found to be devoid of endogenous human ABCB6 mRNA, was employed for heterologous expression of rAbcb6 bearing a COOH-terminal epitope tag (rAbcb6-V5).
  • Vesicular distribution in LoVo cells was consistent with localization of endogenous rAbcb6 expressed in rat primary hepatocyte cultures or in liver sections, as revealed by overlap of rat Lamp1 with rAbcb6 in double immunofluorescence analyses.

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  • (PMID = 18160489.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Abcb6 protein, rat; 0 / Glycoproteins; 0 / Lamp1 protein, rat; 0 / Lysosome-Associated Membrane Glycoproteins; 0 / Metals; 0 / Metals, Heavy; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 147336-22-9 / Green Fluorescent Proteins
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42. Rong M, Rossi EA, Zhang J, McNeer RR, van den Brande JM, Yasin M, Weed DT, Carothers Carraway CA, Thompson JF, Carraway KL: Expression and localization of Muc4/sialomucin complex (SMC) in the adult and developing rat intestine: implications for Muc4/SMC function. J Cell Physiol; 2005 Jan;202(1):275-84
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and localization of Muc4/sialomucin complex (SMC) in the adult and developing rat intestine: implications for Muc4/SMC function.
  • Muc4/sialomucin complex (SMC) is a high molecular mass heterodimeric membrane mucin, encoded by a single gene, and originally discovered in a highly metastatic ascites rat mammary adenocarcinoma.
  • Immunoblot and immunofluorescence analyses demonstrated that Muc4/SMC expression in the rat small intestine increases from proximal to distal regions and is located predominantly in cells at the base of the crypts.
  • Muc4/SMC expression was higher in the rat colon than small intestine and was abundantly present in colonic goblet cells, but not in goblet cells in the small intestine.
  • Biochemical analyses indicated that rat colonic Muc4/SMC is primarily the soluble form of the membrane mucin.
  • Analyses of Muc4/SMC during development of the rat gastrointestinal tract showed its appearance at embryonic day 14 of the esophagus and at day 15 at the surface of the undifferentiated stratified epithelium at the gastroduodenal junction, then later at cell surfaces in the more distal regions of the differentiated epithelium of the small intestine, culminating in expression as an intracellular form in the crypts of the small intestine at about day 21.
  • Limited expression in the colon was observed during development before birth at cell surfaces, with expression as an intracellular form in the goblet cells arising during the second week after birth.
  • These results suggest that membrane mucin Muc4/SMC serves different functions during development of the intestine in the rat, but is primarily a secreted product in the adult animal.
  • [MeSH-major] Colon / metabolism. Intestinal Mucosa / metabolism. Intestine, Small / metabolism. Mucins / metabolism

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 15389518.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA52498
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MUC4 protein, human; 0 / Muc4 protein, rat; 0 / Mucin-4; 0 / Mucins
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43. Tamagawa K, Horiuchi T, Uchinami M, Doi K, Yoshida M, Nakamura T, Sasaki H, Taniguchi M, Tanaka K: Hepatic ischemia-reperfusion increases vascular endothelial growth factor and cancer growth in rats. J Surg Res; 2008 Aug;148(2):158-63
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  • We hypothesized that I/R-induced VEGF expression could enhance growth of microscopic tumor via VEGF receptors on tumor cells, thus promoting liver metastasis in a rat model.
  • Other rats given an intrasplenic inoculation of a rat colon adenocarcinoma cell line (RCH-H4) were divided 3 days later into three groups: group A, untreated; group B, sham operation; group C, 70% I/R for 60 min.
  • CONCLUSION: Hepatic ischemia reperfusion leads to induction of VEGF and this is associated with increased tumor burden in an animal model of colon cancer metastasis.
  • [MeSH-major] Adenocarcinoma / pathology. Colonic Neoplasms / pathology. Liver Neoplasms / physiopathology. Liver Neoplasms / secondary. Reperfusion Injury / physiopathology. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18468635.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; EC 2.7.10.1 / Flt1 protein, rat; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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44. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Here, we performed genome-wide scanning of male (ACI/SegHsd x Wistar-Furth)F2 (AWF2) rats to map susceptibility genes influencing the evolution of early colorectal lesions to adenocarcinoma following 1,2-dimethylhydrazine administration.
  • 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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45. Yokooji T, Murakami T, Yumoto R, Nagai J, Takano M: Site-specific bidirectional efflux of 2,4-dinitrophenyl-S-glutathione, a substrate of multidrug resistance-associated proteins, in rat intestine and Caco-2 cells. J Pharm Pharmacol; 2007 Apr;59(4):513-20
Hazardous Substances Data Bank. 1-CHLORO-2,4-DINITROBENZENE .

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  • [Title] Site-specific bidirectional efflux of 2,4-dinitrophenyl-S-glutathione, a substrate of multidrug resistance-associated proteins, in rat intestine and Caco-2 cells.
  • The site-specific function of multidrug-resistance-associated proteins (MRPs), especially MRP2 and MRP3, was examined in rat intestine and human colon adenocarcinoma (Caco-2) cells.
  • The expression of rat and human MRP2 and MRP3 was analysed by Western blotting.
  • The rat jejunum exhibited a higher apical MRP2 and a lower basolateral MRP3 expression than ileum.
  • In conclusion, the efflux of DNP-SG from enterocytes mediated by MRPs exhibited a significant regional difference in rat intestine, indicating possible variability in intestinal bioavailabilities of MRP substrates, depending on their absorption sites along the intestine.

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  • (PMID = 17430634.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Transport Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / multidrug resistance-associated protein 2; 0 / multidrug resistance-associated protein 3; 26289-39-4 / S-(2,4-dinitrophenyl)glutathione; GAN16C9B8O / Glutathione; GE3IBT7BMN / Dinitrochlorobenzene; PO572Z7917 / Probenecid
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46. de Heer P, Sandel MH, Guertens G, de Boeck G, Koudijs MM, Nagelkerke JF, Junggeburt JM, de Bruijn EA, van de Velde CJ, Kuppen PJ: Celecoxib inhibits growth of tumors in a syngeneic rat liver metastases model for colorectal cancer. Cancer Chemother Pharmacol; 2008 Oct;62(5):811-9
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  • [Title] Celecoxib inhibits growth of tumors in a syngeneic rat liver metastases model for colorectal cancer.
  • The present study was designed to evaluate the inhibitory effects of the COX-2 inhibitor celecoxib on the growth of colorectal cancer liver metastases in a syngeneic rat model, CC531.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Antineoplastic Agents. Colorectal Neoplasms / pathology. Cyclooxygenase 2 Inhibitors / pharmacology. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Pyrazoles / pharmacology. Sulfonamides / pharmacology

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  • (PMID = 18247029.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Prostaglandins; 0 / Pyrazoles; 0 / Sulfonamides; EC 3.4.22.- / Caspase 3; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ PMC2516537
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47. Doi K, Hagihara A, Wei M, Yunoki T, Fukushima S, Wanibuchi H: Altered gene expression in rat colonic adenocarcinomas induced in an azoxymethane plus 2-amino-1-methyl-6-phenylimidazo[4,5-b]- pyridine initiation-promotion model. Oncology; 2007;73(3-4):252-60
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  • [Title] Altered gene expression in rat colonic adenocarcinomas induced in an azoxymethane plus 2-amino-1-methyl-6-phenylimidazo[4,5-b]- pyridine initiation-promotion model.
  • 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), the most abundant food-derived mutagenic/carcinogenic heterocyclic amine (HCA), has attracted particular attention as a probable human colon carcinogen.
  • Some studies have shown that PhIP administered in the post-initiation phase is able to enhance rat colon carcinogenesis remarkably.
  • To determine whether this genotoxicant leaves a DNA footprint in colon carcinogenesis, 6-week-old male F344 rats were first subcutaneously injected with azoxymethane (AOM) and then continuously treated with various doses (0-200 ppm) of PhIP added to their diet.
  • In summary, overexpression of Stat1, VEGF and other genes could be involved in PhIP-enhanced colon tumorigenesis in the post-initiation phase.
  • [MeSH-major] Adenocarcinoma / genetics. Azoxymethane / toxicity. Carcinogens / toxicity. Colonic Neoplasms / genetics. Gene Expression Regulation, Neoplastic / drug effects. Imidazoles / toxicity. STAT1 Transcription Factor / genetics. Vascular Endothelial Growth Factor A / genetics

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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18424890.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Imidazoles; 0 / STAT1 Transcription Factor; 0 / Stat1 protein, mouse; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 909C6UN66T / 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine; MO0N1J0SEN / Azoxymethane
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48. Liu L, Sun H, Valji WY, Pang KS: Transporters, enzymes, and enalapril removal in a rat (CC531-induced) liver metastatic model. Am J Physiol Gastrointest Liver Physiol; 2007 Nov;293(5):G1078-88
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  • [Title] Transporters, enzymes, and enalapril removal in a rat (CC531-induced) liver metastatic model.
  • Temporal changes in physiological spaces, protein expression of transporters and enzymes, and enalapril removal were appraised in the metastatic liver tumor model developed from male Wag/Rij rats after the intraportal injection of CC531 colon adenocarcinoma cells; sham-operated preparations received PBS.

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  • (PMID = 17855765.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzymes; 0 / Neoplasm Proteins; 69PN84IO1A / Enalapril
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49. Tanaka T, Yasui Y, Tanaka M, Tanaka T, Oyama T, Rahman KM: Melatonin suppresses AOM/DSS-induced large bowel oncogenesis in rats. Chem Biol Interact; 2009 Jan 27;177(2):128-36
Hazardous Substances Data Bank. MELATONIN .

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  • The inhibitory effects of exogenous melatonin (MEL) on colon oncogenesis were investigated using an azoxymethane (AOM)/dextran sodium sulfate (DSS) rat model.
  • At week 20, the development of colonic adenocarcinoma was significantly inhibited by the administration with MEL dose-dependently.
  • These results may indicate the beneficial effects of MEL on colitis-related colon carcinogenesis and a potential application for inhibiting colorectal cancer development in the inflamed colon.
  • [MeSH-major] Adenocarcinoma / prevention & control. Antineoplastic Agents / pharmacology. Colonic Neoplasms / prevention & control. Melatonin / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Azoxymethane / toxicity. Biomarkers, Tumor / metabolism. Colon / drug effects. Colon / metabolism. Colon / pathology. Dextran Sulfate / toxicity. Dose-Response Relationship, Drug. Drinking. Immunohistochemistry. Injections, Intraperitoneal. Interleukin-1beta / metabolism. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Mitotic Index. NF-kappa B / metabolism. Rats. Rats, Inbred F344. STAT3 Transcription Factor / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 19028472.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Interleukin-1beta; 0 / NF-kappa B; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, rat; 0 / Tumor Necrosis Factor-alpha; 9042-14-2 / Dextran Sulfate; JL5DK93RCL / Melatonin; MO0N1J0SEN / Azoxymethane
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50. Nylander-Koski O, Kiviluoto T, Puolakkainen P, Kivilaakso E, Mustonen H: The effect of nitric oxide, growth factors, and estrogen on gastric cell migration. J Surg Res; 2007 Dec;143(2):230-7
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  • MATERIAL AND METHODS: Isolated primary cultured rabbit gastric epithelial cells, rat gastric mucosal cells, human gastric adenocarcinoma cells, and human colon adenocarcinoma cells (WiDr) were cultured to confluency in appropriate media (5% CO2, 37 degrees C).
  • The more profound decrease in migration speed of gastric adenocarcinoma cell line may suggest that estrogen might be one of the protective factor against female gastric adenocarcinoma before menopausal age.
  • [MeSH-minor] Adenocarcinoma. Animals. Caspase 3 / metabolism. Cell Line. Cell Survival / drug effects. Fibroblast Growth Factor 7 / pharmacology. Hepatocyte Growth Factor / pharmacology. Humans. Nitric Oxide / metabolism. Rabbits. Rats. Receptors, Estrogen / metabolism. Stomach Neoplasms. Transforming Growth Factor alpha / pharmacology. Tumor Cells, Cultured

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  • (PMID = 17950324.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Nitric Oxide Donors; 0 / Receptors, Estrogen; 0 / Transforming Growth Factor alpha; 126469-10-1 / Fibroblast Growth Factor 7; 169D1260KM / Nitroprusside; 31C4KY9ESH / Nitric Oxide; 4TI98Z838E / Estradiol; 67256-21-7 / Hepatocyte Growth Factor; EC 3.4.22.- / Caspase 3
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51. 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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  • 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.
  • On histological examination, we found 10 colonic adenocarcinomas (the first being observed at Week 22) and 7 adenocarcinoma in the small bowel.
  • In total, seven colon adenomas were found in five rats, six of which expressed high-grade dysplasia.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / radionuclide imaging. Colonic Neoplasms / metabolism. Colonic Neoplasms / radionuclide imaging. Disease Models, Animal. Fluorodeoxyglucose F18 / pharmacokinetics

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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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52. Borrelli F, Capasso R, Aviello G, Di Carlo G, Izzo AA, Mascolo N, Capasso F: Senna and the formation of aberrant crypt foci and tumors in rats treated with azoxymethane. Phytomedicine; 2005 Jun;12(6-7):501-5; discussion 505
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  • These results suggest that a chronic SE use does not predispose to colon cancer.
  • By contrast, SE might exert an anti-tumoral activity on rat colon carcinogenesis.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anticarcinogenic Agents / pharmacology. Colonic Neoplasms / prevention & control. Phytotherapy. Senna Extract / pharmacology. Senna Plant

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  • (PMID = 16008128.001).
  • [ISSN] 0944-7113
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cathartics; 8013-11-4 / Senna Extract; MO0N1J0SEN / Azoxymethane
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53. Ziliotto L, Pinheiro F, Barbisan LF, Rodrigues MA: Screening for in vitro and in vivo antitumor activities of the mushroom Agaricus blazei. Nutr Cancer; 2009;61(2):245-50
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  • We have investigated the in vitro antitumor activity of the mushroom Agaricus blazei Murill on human cancer cell lines as well as its potential anticancer activity in a model of rat colon carcinogenesis.
  • In the in vivo analysis, crude A. blazei was given orally after carcinogen treatment in a rat medium-term study (20 weeks) of colon carcinogenesis using aberrant crypt foci (ACF) as biomarker.
  • No differences in tumor incidence in the colon were observed among the DMH-treated groups.
  • Our results indicate that employing A. blazei in the diet does not have a suppressive effect on colon carcinogenesis.
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / pathology. Adenocarcinoma / prevention & control. Animals. Cell Division / drug effects. Cell Line, Tumor. Colonic Neoplasms / chemically induced. Colonic Neoplasms / pathology. Colonic Neoplasms / prevention & control. Female. Humans. Male. Rats. Rats, Wistar

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  • (PMID = 19235041.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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54. Rao CV, Steele VE, Swamy MV, Patlolla JM, Guruswamy S, Kopelovich L: Inhibition of azoxymethane-induced colorectal cancer by CP-31398, a TP53 modulator, alone or in combination with low doses of celecoxib in male F344 rats. Cancer Res; 2009 Oct 15;69(20):8175-82
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  • The present study explores the effects of p53-modulating agent CP-31398 alone and combined with celecoxib on azoxymethane-induced aberrant crypt foci (ACF) and colon adenocarcinomas in F344 rats.
  • ACF and colon adenocarcinomas were determined at 8 and 48 weeks after azoxymethane treatment, respectively.
  • Dietary CP-31398 was shown to suppress mean colonic total ACF by 43% and multicrypt ACF by 63%; dietary CP-31398 at 150 and 300 ppm suppressed adenocarcinoma incidence by 30.4% (P < 0.02) and 44% (P < 0.005), respectively, and adenocarcinoma multiplicity by 51% (P < 0.005) and 65% (P < 0.0001), respectively.
  • Dietary celecoxib suppressed colon adenocarcinoma incidence (60%; P < 0.0003) and multiplicity (70%; P < 0.0001).
  • Importantly, combination of low-dose CP-31398 and celecoxib suppressed colon adenocarcinoma incidence by 78% and multiplicity by 90%.
  • These observations show, for the first time, that CP-31398 possesses significant dose-dependent chemopreventive activity in a well-established colon cancer model and that a combination of low-dose CP-31398 and celecoxib significantly enhanced colon cancer chemopreventive efficacy.

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  • (PMID = 19826045.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-25114; United States / NCI NIH HHS / CA / N01CN53300; United States / NCI NIH HHS / CA / R01 CA094962; United States / NCI NIH HHS / CA / R01 CA109247-05; United States / NCI NIH HHS / CA / R01 CA109247; United States / NCI NIH HHS / CA / CA094962-06; United States / NCI NIH HHS / CA / CA-94962; United States / NCI NIH HHS / CA / R01 CA094962-06; United States / NCI NIH HHS / CN / N01 CN053300; United States / NCI NIH HHS / CN / N01-CN-53300
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CP 31398; 0 / Carcinogens; 0 / Cdkn1a protein, rat; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclooxygenase Inhibitors; 0 / Membrane Proteins; 0 / Pyrazoles; 0 / Pyrimidines; 0 / Sulfonamides; 0 / Tumor Suppressor Protein p53; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs1 protein, rat; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS141657; NLM/ PMC2792897
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55. Tejeda M, Gaal D, Hullán L, Csuka O, Schwab R, Szokoloczi O, Kéri GY: Continuous administration of the somatostatin structural derivative /TT-232/ by subcutaneously implanted osmotic pump improves the efficacy and potency of antitumor therapy in different mouse and human tumor models. Anticancer Res; 2008 Sep-Oct;28(5A):2769-74

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  • This somatostatin structural derivative has no GH release inhibitory or antisecretory activity and does not bind to rat pituitary or the cortex, where all the known somatostatin receptor subtypes are expressed.
  • -inserted Alzet osmotic minipump, and on different types of transplantable rodent (S-180 sarcoma, P-388sc lymphoid leukemia, Colon-26 adenocarcinoma, MXT breast carcinoma, B-16 melanoma) and human tumor models (HT-18 lymphoid melanoma, T-47/D breast carcinoma, A-431 epidermoid carcinoma).
  • In the aggressive Colon-26 adenocarcinoma and MXT breast carcinoma models, the infusion treatment resulted in 52%-75% tumor growth inhibition.

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  • (PMID = 19035308.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Peptides, Cyclic; 0 / TT2-32; 51110-01-1 / Somatostatin
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56. Ceelen W, Boterberg T, Smeets P, Van Damme N, Demetter P, Zwaenepoel O, Cesteleyn L, Houtmeyers P, Peeters M, Pattyn P: Recombinant human erythropoietin alpha modulates the effects of radiotherapy on colorectal cancer microvessels. Br J Cancer; 2007 Mar 12;96(5):692-700
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  • The purpose of the present study was to examine the modulation of radiotherapy (RT) effects on tumour microvessels by rhEPO in a rat colorectal cancer model.
  • [MeSH-major] Adenocarcinoma / drug therapy. Colorectal Neoplasms / drug therapy. Erythropoietin / pharmacology. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / radiotherapy

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  • (PMID = 17299396.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Erythropoietin; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin
  • [Other-IDs] NLM/ PMC2360077
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57. Ibarz G, Oiry C, Carnazzi E, Crespy P, Escrieut C, Fourmy D, Galleyrand JC, Gagne D, Martinez J: Cholecystokinin 1 receptor modulates the MEKK1-induced c-Jun trans-activation: structural requirements of the receptor. Br J Pharmacol; 2006 Apr;147(8):951-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In cells overexpressing active MEKK1 to enhance c-Jun trans-activation, expression of rat cholecystokinin 1 receptor increased the activity of c-Jun while in the same experimental conditions overexpression of mouse cholecystokinin 1 receptor repressed it.
  • This differential behaviour was also detected in a human colon adenocarcinoma cell-line naturally producing high levels of endogenous MEKK1.
  • Two amino acids (Val43 and Phe50 in the mouse cholecystokinin 1 receptor, replaced by Leu43 and Ileu50 in the rat cholecystokinin 1 receptor) localized in the first transmembrane domain were found to play a crucial role in this differential behaviour.
  • MEKK1 probably activates a transcriptional partner of c-Jun whose activity is maintained or increased in the presence of the rat cholecystokinin 1 receptor but repressed in the presence of the mouse cholecystokinin 1 receptor.

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  • (PMID = 16491099.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Cholecystokinin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinase 1
  • [Other-IDs] NLM/ PMC1760718
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58. Antunes IF, Haisma HJ, Elsinga PH, Dierckx RA, de Vries EF: Synthesis and evaluation of [18F]-FEAnGA as a PET Tracer for beta-glucuronidase activity. Bioconjug Chem; 2010 May 19;21(5):911-20
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  • [(18)F]-FEAnGA is about 10-fold more hydrophilic than the cleavage product [(18)F]-FEA, and it is stable in PBS and rat plasma for at least 3 h.
  • Incubation of CT26 murine colon adenocarcinoma cells or the genetically engineered CT26mbetaGUS cells, which expressed membrane-anchored GUS on the outer cell membrane, with the tracer, resulted in a 3-fold higher uptake into GUS-expressing cells as compared to control cells.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Animals. Cattle. Cell Line, Tumor. Colonic Neoplasms / diagnosis. Colonic Neoplasms / metabolism. Escherichia coli / enzymology. Glioma / diagnosis. Glioma / metabolism. Humans. Mice. Rats

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  • (PMID = 20415436.001).
  • [ISSN] 1520-4812
  • [Journal-full-title] Bioconjugate chemistry
  • [ISO-abbreviation] Bioconjug. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-fluoroethylamine; 0 / Ethylamines; 0 / Radiopharmaceuticals; 8A5D83Q4RW / Glucuronic Acid; EC 3.2.1.31 / Glucuronidase
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59. Nishiumi S, Yabushita Y, Fukuda I, Mukai R, Yoshida K, Ashida H: Molokhia (Corchorus olitorius L.) extract suppresses transformation of the aryl hydrocarbon receptor induced by dioxins. Food Chem Toxicol; 2006 Feb;44(2):250-60
Hazardous Substances Data Bank. ETHANOL .

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  • In this study, we demonstrated that ethanolic extract from molokhia, known as Egyptian spinach, showed the strongest suppressive effect on AhR transformation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in cell-free system using rat hepatic cytosol among 41 kinds of extracts from vegetables and fruits.
  • The molokhia extract also suppressed TCDD-induced AhR transformation in mouse hepatoma Hepa-1c1c7 cells and in intestinal permeability system constructed with human colon adenocarcinoma Caco-2 cells and human hepatoma HepG2 cells.
  • The molokhia extract-administered rat liver showed a tolerance to TCDD-induced AhR transformation by ex vivo experiment.

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  • (PMID = 16115717.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dioxins; 0 / Plant Extracts; 0 / Receptors, Aryl Hydrocarbon; 0 / Solvents; 0 / Teratogens; 3K9958V90M / Ethanol; DO80M48B6O / Tetrachlorodibenzodioxin; EC 1.14.14.1 / Cytochrome P-450 CYP1A1
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60. Cho NL, Lin CI, Whang EE, Carothers AM, Moore FD Jr, Ruan DT: Sulindac reverses aberrant expression and localization of beta-catenin in papillary thyroid cancer cells with the BRAFV600E mutation. Thyroid; 2010 Jun;20(6):615-22
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  • Nonsteroidal antiinflammatory drugs reverse aberrant beta-catenin expression and localization in colon cancer.
  • PCCL3 rat thyroid cells that conditionally overexpress either BRAF(V600E) or RET/PTC were also treated with sulindac.
  • [MeSH-minor] Adenocarcinoma, Papillary / genetics. Adenocarcinoma, Papillary / metabolism. Animals. Cell Line, Tumor. Humans. Mutation. Proto-Oncogene Proteins B-raf / genetics. Rats. Thyroid Gland / drug effects. Thyroid Gland / metabolism


61. Sureban SM, May R, George RJ, Dieckgraefe BK, McLeod HL, Ramalingam S, Bishnupuri KS, Natarajan G, Anant S, Houchen CW: Knockdown of RNA binding protein musashi-1 leads to tumor regression in vivo. Gastroenterology; 2008 May;134(5):1448-58
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  • Msi-1 expression is increased during rat brain development and in APC(min/+) mice tumors.
  • METHODS: Msi-1 small interfering RNA (siRNA) was administered as a liposomal preparation to HCT116 colon adenocarcinoma xenografts in athymic nude mice and tumor volume was measured.
  • [MeSH-major] Adenocarcinoma / pathology. Colorectal Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Nerve Tissue Proteins / genetics. RNA, Neoplasm / genetics. RNA-Binding Proteins / genetics

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  • (PMID = 18471519.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK-52574; United States / NIDDK NIH HHS / DK / DK-002822; United States / NIDDK NIH HHS / DK / K08 DK002822; United States / NIDDK NIH HHS / DK / DK-066161; United States / NIDDK NIH HHS / DK / P30 DK052574
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MSI1 protein, human; 0 / Msi1h protein, mouse; 0 / Nerve Tissue Proteins; 0 / RNA, Neoplasm; 0 / RNA-Binding Proteins
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62. Etcheverry SB, Ferrer EG, Naso L, Rivadeneira J, Salinas V, Williams PA: Antioxidant effects of the VO(IV) hesperidin complex and its role in cancer chemoprevention. J Biol Inorg Chem; 2008 Mar;13(3):435-47
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  • When tested on two tumoral cell lines in culture (one of them derived from a rat osteosarcoma UMR106 and the other from human colon adenocarcinoma Caco-2), the complex enhanced the antiproliferative effects of the free ligand, and this effect correlated with the morphological alterations toward apoptosis.

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  • (PMID = 18097692.001).
  • [ISSN] 0949-8257
  • [Journal-full-title] Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry
  • [ISO-abbreviation] J. Biol. Inorg. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Vanadium Compounds; E750O06Y6O / Hesperidin; EC 1.15.1.1 / Superoxide Dismutase; EC 3.1.3.1 / Alkaline Phosphatase
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63. Koehl GE, Wagner F, Stoeltzing O, Lang SA, Steinbauer M, Schlitt HJ, Geissler EK: Mycophenolate mofetil inhibits tumor growth and angiogenesis in vitro but has variable antitumor effects in vivo, possibly related to bioavailability. Transplantation; 2007 Mar 15;83(5):607-14
Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .

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  • METHODS: Mouse CT26 colon adenocarcinoma, B16 melanoma, and human TMK1 gastric adenocarcinoma cells were tested for in vitro growth in the presence of MMF.
  • In vitro angiogenesis was tested with a rat aortic-ring assay.
  • [MeSH-minor] Adenocarcinoma. Animals. Aorta. Biological Availability. Cell Line, Tumor. Colonic Neoplasms. Endothelium, Vascular / drug effects. Endothelium, Vascular / physiology. Humans. Melanoma, Experimental. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Muscle, Smooth, Vascular / drug effects. Muscle, Smooth, Vascular / physiology. Stomach Neoplasms. Umbilical Veins

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  • (PMID = 17353782.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid
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64. Miliaras S, Anogeianaki A, Meditskou S, Kefala V, Koutsonikolas D, Liangouris J, Anogianakis G, Miliaras D: Effects of rich-in-fat diets and highly selective COX-2 inhibitors on 7,12-dimethylbenz-(A)-anthracene-induced tumor growth. Int J Immunopathol Pharmacol; 2009 Apr-Jun;22(2):323-32
Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .

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  • At the same time there is substantial, but not conclusive, evidence that the risk of breast and colon cancer correlates with total fat intake rather than a specific type of fat.
  • 7,12-Dimethylbenz-(a)-anthracene (DMBA) has been used for a long time to induce carcinogenesis in a number of rat animal models.
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Adenocarcinoma / chemically induced. Adenocarcinoma / enzymology. Adenocarcinoma / prevention & control. Animals. Celecoxib. Cell Transformation, Neoplastic / chemically induced. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / metabolism. Female. Mammary Neoplasms, Animal / chemically induced. Mammary Neoplasms, Animal / enzymology. Mammary Neoplasms, Animal / prevention & control. Rats. Rats, Sprague-Dawley. Sarcoma / chemically induced. Sarcoma / enzymology. Sarcoma / prevention & control. Time Factors

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  • (PMID = 19505386.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Dietary Fats; 0 / Pyrazoles; 0 / Sulfonamides; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs2 protein, rat; JCX84Q7J1L / Celecoxib
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65. Yeung EY, Sueyoshi T, Negishi M, Chang TK: Identification of Ginkgo biloba as a novel activator of pregnane X receptor. Drug Metab Dispos; 2008 Nov;36(11):2270-6
Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827858673 for PMID:18725505 [PharmGKB] .

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  • Treatment of primary cultures of rat hepatocytes with G. biloba extract increases the mRNA expression of CYP3A23, which is a target gene for rat PXR.
  • To determine whether G. biloba extract induces hPXR target gene expression, cultured LS180 human colon adenocarcinoma cells were treated for 72 h with the extract. G. biloba extract at 200, 400, and 800 microg/ml increased CYP3A4 mRNA expression by 1.7-, 2.4-, and 2.5-fold, respectively.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Cell Line, Tumor. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic / drug effects. Gene Targeting. Humans. Mice. Plant Extracts / isolation & purification. Plant Extracts / pharmacology. Plant Leaves / physiology. Tumor Cells, Cultured

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  • (PMID = 18725505.001).
  • [ISSN] 1521-009X
  • [Journal-full-title] Drug metabolism and disposition: the biological fate of chemicals
  • [ISO-abbreviation] Drug Metab. Dispos.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 ES999999
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Receptors, Steroid; 0 / pregnane X receptor
  • [Other-IDs] NLM/ NIHMS75380; NLM/ PMC2626634
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66. Ohsawa I, Murakami T, Uemoto S, Kobayashi E: In vivo luminescent imaging of cyclosporin A-mediated cancer progression in rats. Transplantation; 2006 Jun 15;81(11):1558-67
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  • METHODS: The metastatic fate of luciferase-expressing rat metastatic colon cancer cells (luc-RCN-H4) injected intravenously into the liver of syngeneic and allogeneic rats was examined in the presence of the immunosuppressant cyclosporin A (CsA) by in vivo luminescent technique.
  • [MeSH-major] Adenocarcinoma / pathology. Colonic Neoplasms / pathology. Cyclosporine / adverse effects. Cyclosporine / pharmacology. Image Processing, Computer-Assisted / methods

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  • (PMID = 16770245.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0 / Benzamides; 0 / Dioxoles; 0 / Receptors, Chemokine; 0 / Tgfb1 protein, rat; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 83HN0GTJ6D / Cyclosporine
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67. Yamada HY, Rao CV: BRD8 is a potential chemosensitizing target for spindle poisons in colorectal cancer therapy. Int J Oncol; 2009 Nov;35(5):1101-9
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  • Normal-appearing rat colonic mucosa and azoxymethane (AOM)-induced colorectal adenocarcinoma tissue expressed a barely detectable amount of BRD8 protein, but aggressive colon tumors induced with AOM and dextran sodium sulfate expressed BRD8 at a significantly higher level, suggesting that BRD8 expression is associated with tumor progression toward advanced stages and may aid to gain growth advantage.
  • [MeSH-major] Adenocarcinoma / enzymology. Antineoplastic Agents / pharmacology. Colorectal Neoplasms / enzymology. Drug Resistance, Neoplasm / genetics. Receptors, Thyroid Hormone / genetics

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  • (PMID = 19787264.001).
  • [ISSN] 1791-2423
  • [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; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BRD8 protein, human; 0 / Biomarkers, Tumor; 0 / RNA, Small Interfering; 0 / Receptors, Thyroid Hormone
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68. Bonin AM, Yáñez JA, Fukuda C, Teng XW, Dillon CT, Hambley TW, Lay PA, Davies NM: Inhibition of experimental colorectal cancer and reduction in renal and gastrointestinal toxicities by copper-indomethacin in rats. Cancer Chemother Pharmacol; 2010 Sep;66(4):755-64
Hazardous Substances Data Bank. COPPER, ELEMENTAL .

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  • PURPOSE: To evaluate, for the first time, the efficacy of copper-indomethacin in the inhibition of aberrant crypt foci formation using the azoxymethane-induced adenocarcinoma model, to examine cell viability in the HCT-116 colorectal cancer cell line, gastrointestinal permeability, mitochondrial oxidative damage, and renal toxicity in rat models.
  • METHODS: Azoxymethane-induced adenocarcinoma rats were dosed with indomethacin and copper-indomethacin for 28 days and aberrant crypt foci were evaluated.
  • CONCLUSIONS: Copper-indomethacin has both gastrointestinal and renal sparing properties while maintaining efficacy in experimental adenocarcinoma.
  • [MeSH-minor] Acetylglucosaminidase / metabolism. Animals. Azoxymethane. Carcinogens. Cecum / metabolism. Cell Line, Tumor. Colon / pathology. DNA, Mitochondrial / metabolism. Drug Combinations. Duodenal Ulcer / chemically induced. Duodenal Ulcer / pathology. Electrolytes / urine. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Haptoglobins / metabolism. Hemoglobins / metabolism. Intestinal Mucosa / metabolism. Male. Permeability. Rats. Rats, Sprague-Dawley. Stomach Ulcer / chemically induced. Stomach Ulcer / pathology

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  • (PMID = 20035423.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carcinogens; 0 / DNA, Mitochondrial; 0 / Drug Combinations; 0 / Electrolytes; 0 / Haptoglobins; 0 / Hemoglobins; 789U1901C5 / Copper; EC 3.2.1.52 / Acetylglucosaminidase; MO0N1J0SEN / Azoxymethane; XXE1CET956 / Indomethacin
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69. Aalbers AG, ten Kate M, van Grevenstein WM, Hofland LJ, Wiemer EA, Jeekel J, van Eijck CH: A small mammal model of tumour implantation, dissemination and growth factor expression after partial hepatectomy. Eur J Surg Oncol; 2008 Apr;34(4):469-75
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  • CC531 rat colon carcinoma cells were inoculated i.v.
  • Rat serum was obtained at different time-points after phX and added to in vitro CC531 cell cultures.
  • No growth stimulation of tumour cells after incubation with rat serum, obtained at different time-points after phX, could be detected in vitro.
  • [MeSH-major] Adenocarcinoma / immunology. Colorectal Neoplasms / surgery. Liver Neoplasms / surgery. Lung Neoplasms / immunology

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  • (PMID = 17442529.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Receptors, Growth Factor
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70. Arrambide G, Barrio DA, Etcheverry SB, Gambino D, Baran EJ: Spectroscopic behavior and biological activity of K2[VO(O2)NTA].2H2O. Biol Trace Elem Res; 2010 Aug;136(2):241-8
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  • The bioactivity of the complex on the cell proliferation was tested on three cell lines in culture (UMR106 rat osteosarcoma-derived cells, Caco-2 derived from a human colon adenocarcinoma, and RAW 264.7, a macrophage murine cell line).

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  • (PMID = 19841872.001).
  • [ISSN] 1559-0720
  • [Journal-full-title] Biological trace element research
  • [ISO-abbreviation] Biol Trace Elem 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 / Vanadium Compounds
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71. Kaur Saini M, Kaur J, Sharma P, Nath Sanyal S: Chemopreventive response of diclofenac, a non-steroidal anti-inflammatory drug in experimental carcinogenesis. Nutr Hosp; 2009 Nov-Dec;24(6):717-23
The Lens. Cited by Patents in .

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  • The chemopreventive response was evaluated of nonsteroidal anti-inflammatory drug, Diclofenac, a preferential cyclooxygenase-2 (COX-2) inhibitor in 1,2-dimethyhydrazine (DMH)-induced colon cancer in rat model.
  • The results suggest that Diclofenac could be an effective chemopreventive agent in colon cancer, where perhaps apoptosis plays a very dominant end effect in cancer cell killings.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Anticarcinogenic Agents / therapeutic use. Colonic Neoplasms / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Diclofenac / therapeutic use

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  • (PMID = 20049376.001).
  • [ISSN] 0212-1611
  • [Journal-full-title] Nutrición hospitalaria
  • [ISO-abbreviation] Nutr Hosp
  • [Language] eng
  • [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 / Anticarcinogenic Agents; 0 / Cyclooxygenase Inhibitors; 144O8QL0L1 / Diclofenac; IX068S9745 / 1,2-Dimethylhydrazine
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72. Final report on the safety assessment of capsicum annuum extract, capsicum annuum fruit extract, capsicum annuum resin, capsicum annuum fruit powder, capsicum frutescens fruit, capsicum frutescens fruit extract, capsicum frutescens resin, and capsaicin. Int J Toxicol; 2007;26 Suppl 1:3-106
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  • Adenocarcinoma of the abdomen was observed in 7/20 mice fed 100 mg red chilies per day for 12 months; no tumors were seen in control animals.
  • Neoplastic changes in the liver and intestinal tumors were observed in rats fed red chili powder at 80 mg/kg day-1 for 30 days, intestinal and colon tumors were seen in rats fed red chili powder and 1,2-dimethyl hydrazine, but no tumors were observed in controls.
  • In vitro percutaneous absorption of Capsaicin has been demonstrated in human, rat, mouse, rabbit, and pig skin.

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  • (PMID = 17365137.001).
  • [ISSN] 1091-5818
  • [Journal-full-title] International journal of toxicology
  • [ISO-abbreviation] Int. J. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cosmetics; 0 / Plant Extracts; 0 / Resins, Plant; S07O44R1ZM / Capsaicin
  • [Number-of-references] 462
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73. Wang XP, Li ZJ, Magnusson J, Brunicardi FC: Tissue MicroArray analyses of pancreatic duodenal homeobox-1 in human cancers. World J Surg; 2005 Mar;29(3):334-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In previous studies, we demonstrated that rat insulin promoter (RIP)-driven gene therapy successfully targeted human pancreatic tumor PANC-1 cells and mouse insulinoma NIT-1 cells, which are both pancreatic duodenal homeobox-1 (PDX-1)-positive.
  • The custom-designed Tissue MicroArray of human tumor specimens consists of human cancer specimens from different origins, such as the pancreas, breast, colon, prostate, kidney, liver, lung, and ovary.
  • PDX-1 expression intensity was elevated in both benign and malignant tissues from the same patient with pancreas, breast, colon, prostate, and kidney cancers, whereas normal human tissues from control subjects without cancer did not express PDX-1.
  • [MeSH-major] Adenocarcinoma / metabolism. Homeodomain Proteins / metabolism. Pancreatic Neoplasms / metabolism. Trans-Activators / metabolism

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  • (PMID = 15706433.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA95731
  • [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 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein
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74. Huang L, Song M, Yang HS, Zhang YG, Hu HZ: [Cloning, expression, distribution and subcellular localization of AK078438 gene]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2007 Jun;24(3):271-4
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  • At mRNA expressing levels semi-quantitative RT-PCR was employed for the investigation of its distribution in normal rat tissues, tumor cell and mesenchymal stem cell (MSC) lines.
  • RESULTS: The full open reading frame of AK078438 gene with 1065 bp, 355aa were identified. mRNA of the gene distributed in brain, uterus, colon, bone marrow, testis and kidney, but not in stomach, liver, the lung, spleen and heart.
  • Murine colon adenocarcinoma C26, melanoma B16, Lewis lung carcinoma LL/2 and MSC had the gene and mouse myeloma cell line NS-1 and Hepa mouse hepatoma cell line had no the gene.

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  • (PMID = 17557235.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Proteins; 0 / RNA, Messenger
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75. Gibson RJ, Bowen JM, Keefe DM: Palifermin reduces diarrhea and increases survival following irinotecan treatment in tumor-bearing DA rats. Int J Cancer; 2005 Sep 1;116(3):464-70
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  • Palifermin pretreatment did not prevent apoptosis that peaked at 6 hr in the jejunum or colon, but prevented apoptosis at 96 hr in the small intestine.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / veterinary. Animals. Female. Fibroblast Growth Factor 7. Keratinocytes. Mammary Neoplasms, Animal / drug therapy. Rats. Survival Analysis

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  • (PMID = 15800945.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / Fgf7 protein, rat; 126469-10-1 / Fibroblast Growth Factor 7; 62031-54-3 / Fibroblast Growth Factors; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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76. Li J, Ji C, Zheng H, Fei X, Zheng M, Dai J, Gu S, Xie Y, Mao Y: Molecular cloning and characterization of a novel human gene containing 4 ankyrin repeat domains. Cell Mol Biol Lett; 2005;10(1):185-93
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  • It displays a high degree of homology with rat low-density lipoprotein receptor-related protein 2-binding protein (Lrp2bp), and was therefore was named hLrp2bp (human Lrp2bp).
  • RT-PCR revealed that hLrp2bp was mainly expressed in the human testis, small intestine, colon and blood leukocytes, and in human pancreatic adenocarcinoma cells.

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  • (PMID = 15809689.001).
  • [ISSN] 1425-8153
  • [Journal-full-title] Cellular & molecular biology letters
  • [ISO-abbreviation] Cell. Mol. Biol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / LRP2BP protein, human; 0 / Low Density Lipoprotein Receptor-Related Protein-2
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77. Vallejo M, Castro MA, Medarde M, Macias RI, Romero MR, El-Mir MY, Monte MJ, Briz O, Serrano MA, Marin JJ: Novel bile acid derivatives (BANBs) with cytostatic activity obtained by conjugation of their side chain with nitrogenated bases. Biochem Pharmacol; 2007 May 1;73(9):1394-404

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  • Using several cell lines - HepG2 (human hepatoblastoma), LS 174T and Caco-2 (human colon adenocarcinoma), Hepa 1-6 (mouse hepatoma), McA-RH7777 (rat hepatoma), CCRF S-180 II (mouse sarcoma) and CHO (Chinese hamster ovary) - their effect on cell viability was measured with the formazan test after drug exposure for 6h (cytotoxic effect) or 72h (cytostatic effect).
  • A weak cytostatic effect of BANB-1, BANB-2 and BANB-3 was detected even in CHO cells stably transfected with rat bile acid transporters (Ntcp and Oatp1/1a1).

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  • (PMID = 17257589.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bile Acids and Salts
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78. 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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79. Lo YL, Ho CT, Tsai FL: Inhibit multidrug resistance and induce apoptosis by using glycocholic acid and epirubicin. Eur J Pharm Sci; 2008 Sep 2;35(1-2):52-67
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  • We evaluated the effects and mechanisms of glycocholic acid (GC), a bile acid, on inhibiting pump and non-pump resistance, and increasing the chemosensitivity of epirubicin in human colon adenocarcinoma Caco-2 cells and rat intestine.
  • GC increased the cytotoxicity of epirubicin, significantly increased the intracellular accumulation of epirubicin in Caco-2 cells and the absorption of epirubicin in rat small intestine, and intensified epirubicin-induced apoptosis.

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  • (PMID = 18606222.001).
  • [ISSN] 0928-0987
  • [Journal-full-title] European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
  • [ISO-abbreviation] Eur J Pharm Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Chromatin; 0 / DNA, Neoplasm; 0 / P-Glycoproteins; 3Z8479ZZ5X / Epirubicin; EC 1.13.12.- / Luciferases; G59NX3I3RT / Glycocholic Acid
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80. Femia AP, Luceri C, Toti S, Giannini A, Dolara P, Caderni G: Gene expression profile and genomic alterations in colonic tumours induced by 1,2-dimethylhydrazine (DMH) in rats. BMC Cancer; 2010;10:194
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  • BACKGROUND: Azoxymethane (AOM) or 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rats shares many phenotypical similarities with human sporadic colon cancer and is a reliable model for identifying chemopreventive agents.
  • Genetic mutations relevant to human colon cancer have been described in this model, but comprehensive gene expression and genomic analysis have not been reported so far.
  • Therefore, we applied genome-wide technologies to study variations in gene expression and genomic alterations in DMH-induced colon cancer in F344 rats.
  • METHODS: For gene expression analysis, 9 tumours (TUM) and their paired normal mucosa (NM) were hybridized on 4 x 44K Whole rat arrays (Agilent) and selected genes were validated by semi-quantitative RT-PCR.
  • Array-comparative genomic hybridization (a-CGH) was performed on 10 paired TUM-NM samples hybridized on Rat genome arrays 2 x 105K (Agilent) and the results were analyzed by CGH Analytics (Agilent).
  • The fact that many of the molecular alterations described in this study are documented in human colon tumours confirms the relevance of DMH-induced cancers as a powerful tool for the study of colon carcinogenesis and chemoprevention.
  • [MeSH-major] Adenocarcinoma / genetics. Cell Transformation, Neoplastic / genetics. Colonic Neoplasms / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic

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  • (PMID = 20459814.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] IX068S9745 / 1,2-Dimethylhydrazine
  • [Other-IDs] NLM/ PMC2877689
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81. Bock KW, Köhle C: UDP-glucuronosyltransferase 1A6: structural, functional, and regulatory aspects. Methods Enzymol; 2005;400:57-75
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  • UGT1A6 is the founding member of the rat and human UGT1 family.
  • UGT1A6 is also involved in conjugation of the drug paracetamol (acetaminophen) and of phenolic metabolites of benzo[a]pyrene (together with rat UGT1A7 and human UGT1A9).
  • However, marked differences have been noted in the expression of rat and human UGT1A6.
  • Regulatory factors have been studied in detail in the human Caco-2 colon adenocarcinoma cell model.

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  • (PMID = 16399343.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 126548-29-6 / Hepatocyte Nuclear Factor 1; 333DO1RDJY / Serotonin; EC 2.4.1.- / UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.17 / Glucuronosyltransferase
  • [Number-of-references] 80
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82. Yoo J, Kim HR, Lee YJ: Hyperthermia enhances tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human cancer cells. Int J Hyperthermia; 2006 Dec;22(8):713-28

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  • METHODS: Human prostate adenocarcinoma DU-145, human pancreatic carcinoma MIA PaCa-2 and BxPC-3, human colon fibroblast CCD-33Co and rat prostate endothelial YPEN-1 cells were treated with various concentrations of TRAIL (0-200 ngml(-1)) with hyperthermia (40-42 degrees C).

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  • (PMID = 17391000.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA121395; United States / NCI NIH HHS / CA / CA95191; United States / NCI NIH HHS / CA / CA96989
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.36 / Caspase 1
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