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6. Babich JP, Klein J, Friedel DM: Endoscopic removal of a brunneroma with EUS guidance. South Med J; 2010 Mar;103(3):250-2
MedlinePlus Health Information. consumer health - Intestinal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The most common benign tumors of the small intestine are adenoma, and 25% of these occur in the duodenum.
  • Most of the literature describes their presentations as ranging from benign, nonspecific, epigastric discomfort to obstruction and intestinal bleeding.
  • We present one of the first cases of an endoscopic ultrasound (EUS) approach to the diagnosis and therapeutic removal of a brunneroma.
  • [MeSH-major] Adenoma / surgery. Brunner Glands / surgery. Duodenal Neoplasms / surgery. Duodenoscopy / methods

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  • (PMID = 20134393.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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7. Matsumoto T, Esaki M, Yanaru-Fujisawa R, Moriyama T, Yada S, Nakamura S, Yao T, Iida M: Small-intestinal involvement in familial adenomatous polyposis: evaluation by double-balloon endoscopy and intraoperative enteroscopy. Gastrointest Endosc; 2008 Nov;68(5):911-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small-intestinal involvement in familial adenomatous polyposis: evaluation by double-balloon endoscopy and intraoperative enteroscopy.
  • BACKGROUND: Small-intestinal adenoma occurs in patients with familial adenomatous polyposis (FAP).
  • OBJECTIVES: The aim was to analyze the diagnostic yield of a double-balloon endoscopy (DBE) and an intraoperative enteroscopy (IOE) for small-intestinal involvement in FAP.
  • The incidence and the endoscopic findings of adenoma were compared between the 2 procedures.
  • Phenotypes of FAP and genotypes of adenomatous polyposis coli (APC) were then compared between patients with small-intestinal adenomas and those without.
  • MAIN OUTCOME MEASUREMENT: The prevalence of adenoma.
  • RESULTS: A DBE detected small-intestinal adenomas in 9 of 12 patients (75%), as did an IOE in 15 of 29 patients (52%, P > .05).
  • In addition, a DBE detected nonpolypoid adenoma in a patient, and nodular, broad-based protrusion (advanced lesions) in 3 patients, whereas an IOE detected advanced lesions in a patient.
  • Patients with small-intestinal adenoma had more severe duodenal adenomatosis than those patients without small-intestinal adenoma (P < .001).
  • In cases in which APC was analyzed, the prevalence of small-intestinal adenoma was higher in patients with a 3' mutation (100%) than in those with a 5' mutation (44%) and with a negative mutation (42%, P < .02).
  • CONCLUSIONS: A DBE is equal to an IOE for scrutiny of small-intestinal adenomas in FAP.


8. Sale S, Tunstall RG, Ruparelia KC, Butler PC, Potter GA, Steward WP, Gescher AJ: Effects of the potential chemopreventive agent DMU-135 on adenoma development in the ApcMin+ mouse. Invest New Drugs; 2006 Nov;24(6):459-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the potential chemopreventive agent DMU-135 on adenoma development in the ApcMin+ mouse.
  • The hypothesis was tested that DMU-135 would inhibit Apc(Min/+) mouse gastrointestinal adenoma formation.
  • DMU-135 was well tolerated, induced no systemic side-effects and reduced adenoma multiplicity by 46 +/- 18.3% compared to controls (p < 0.001).
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / therapeutic use. Chalcone / analogs & derivatives. Colon / drug effects. Intestinal Neoplasms / prevention & control. Intestine, Small / drug effects. Prodrugs / therapeutic use

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  • (PMID = 16505954.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0100874
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3,4-methylenedioxy-3',4',5'-trimethoxy chalcone; 0 / Antineoplastic Agents; 0 / Prodrugs; 5S5A2Q39HX / Chalcone; EC 2.7.10.1 / Protein-Tyrosine Kinases
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9. Schulz AC, Bojarski C, Buhr HJ, Kroesen AJ: Occurrence of adenomas in the pouch and small intestine of FAP patients after proctocolectomy with ileoanal pouch construction. Int J Colorectal Dis; 2008 Apr;23(4):437-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Occurrence of adenomas in the pouch and small intestine of FAP patients after proctocolectomy with ileoanal pouch construction.
  • In our patient population, we observed the postoperative development of adenomas not only in the pouch but also in the remaining small intestine.
  • The exact incidence of these ileal polyps is still unknown, since the diagnostic possibilities of examining the small intestine are limited.
  • METHODS: We performed wireless capsule endoscopy (CE) in patients who developed postoperative pouch adenomas (PA) to record the simultaneous occurrence of small bowel adenomas and PA.
  • Eight PA patients (all with PA) also had adenomas in the small intestine diagnosed by CE.
  • [MeSH-major] Adenoma / epidemiology. Adenomatous Polyposis Coli / surgery. Colonic Pouches / adverse effects. Intestine, Small / pathology. Proctocolectomy, Restorative / adverse effects
  • [MeSH-minor] Adult. Biopsy. Capsule Endoscopy. Female. Follow-Up Studies. Humans. Incidence. Intestinal Neoplasms / diagnosis. Intestinal Neoplasms / epidemiology. Intestinal Neoplasms / etiology. Male. Middle Aged. Prognosis. Prospective Studies. Time Factors

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  • (PMID = 18193239.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
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10. Lingohr P, Knoefel WT, Kleimann E, Rheinwalt KP: [Laparoscopic coincidental finding in a case of incomplete ileus: adenocarcinoma of the small intestine as first manifestation of Crohn's disease]. Zentralbl Chir; 2007 Dec;132(6):564-8
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  • [Title] [Laparoscopic coincidental finding in a case of incomplete ileus: adenocarcinoma of the small intestine as first manifestation of Crohn's disease].
  • The case-study reminds of adenocarcinoma of the small intestine as a rare complication of Crohn's disease.
  • Epidemiological studies concerning small bowel carcinoma showed consumption of sugar and carbohydrates as pathogenetic factors, other conditions like ileostoma, ileumconduit, Crohn's disease and coeliac disease have been identified to some extent.
  • An adenoma-carcinoma sequence as in large intestine carcinoma has been discussed.
  • Diagnosis of early stages of adenocarcinoma of the small intestine is very difficult and thus might be impossible to differentiate from exacerbation or progressive stenosis of preexisting Crohn's disease.
  • If non-invasive diagnostic measures (ultrasound, small bowel enema, CT-scan, intestinoscopy, radiography, NMR-Sellink, capsule-endoscopy) fail to clear the situation a diagnostic laparoscopy or even laparotomy should not be delayed.
  • [MeSH-minor] Aged. Appendectomy. Cell Transformation, Neoplastic / pathology. Cholecystectomy, Laparoscopic. Cholelithiasis / diagnosis. Cholelithiasis / surgery. Diagnosis, Differential. Female. Humans. Ileum / pathology. Ileum / surgery. Intestinal Mucosa / pathology. Intestinal Mucosa / surgery. Neoplasm Invasiveness

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  • (PMID = 18098087.001).
  • [ISSN] 0044-409X
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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11. Svendsen C, Husøy T, Glatt H, Paulsen JE, Alexander J: 5-Hydroxymethylfurfural and 5-sulfooxymethylfurfural increase adenoma and flat ACF number in the intestine of Min/+ mice. Anticancer Res; 2009 Jun;29(6):1921-6
Hazardous Substances Data Bank. FURFURAL .

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  • [Title] 5-Hydroxymethylfurfural and 5-sulfooxymethylfurfural increase adenoma and flat ACF number in the intestine of Min/+ mice.
  • MATERIALS AND METHODS: Three to six days after birth, multiple intestinal neoplasia (Min/+) mice were given a single subcutaneous injection of either 500 mg/kg body weight (bw) HMF, 25 mg/kg bw SMF or vehicle (0.9 % NaCl), and were euthanised at 12 weeks of age.
  • The number and size of adenomas and flat aberrant crypt foci (ACF) were counted in the intestine.
  • RESULTS: HMF increased the number of small intestinal adenomas (p=0.033), whereas SMF increased the flat ACF number in the large intestine (p=0.025).
  • CONCLUSION: These results show that both HMF and SMF are weak intestinal carcinogens in Min/+ mice.
  • [MeSH-major] Adenoma / chemically induced. Adenomatous Polyposis Coli Protein / physiology. Carcinogens / toxicity. Furaldehyde / analogs & derivatives. Intestinal Neoplasms / chemically induced. Intestinal Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 19528448.001).
  • [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 / 5-sulfooxymethylfurfural; 0 / Adenomatous Polyposis Coli Protein; 0 / Carcinogens; 70ETD81LF0 / 5-hydroxymethylfurfural; DJ1HGI319P / Furaldehyde
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12. Simon J, de Petriconi R, Meilinger M, Hautmann RE, Bartsch G Jr: Optimized haemostasis in nephron-sparing surgery using small-intestine submucosa. BMC Urol; 2008;8:8
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  • [Title] Optimized haemostasis in nephron-sparing surgery using small-intestine submucosa.
  • To prevent this, we prospectively studied the effect of application of small-intestine submucosa (SIS) over the renal defect.
  • RESULTS: The final pathology revealed clear-cell and papillary carcinoma, papillary adenoma, oncocytoma, and angiomyolipoma in 39 (70.9%), 6 (10.9), 1 (1.8%), 2 (3.6%) and 7 (12.7%) patients, respectively.
  • [MeSH-major] Hemostasis, Surgical / methods. Intestinal Mucosa. Intestine, Small. Kidney Neoplasms / surgery. Nephrectomy / methods

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  • (PMID = 18445250.001).
  • [ISSN] 1471-2490
  • [Journal-full-title] BMC urology
  • [ISO-abbreviation] BMC Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biocompatible Materials
  • [Other-IDs] NLM/ PMC2386496
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13. Osifo OD, Akhiwu W, Efobi CA: Small intestinal tubulovillous adenoma--case report and literature review. Niger J Clin Pract; 2009 Jun;12(2):205-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small intestinal tubulovillous adenoma--case report and literature review.
  • Benign small intestinal tumour, though rare, have been reported.
  • We report a case of sessile and extensive tubulovillous adenoma in a 13-year-old girl.
  • Erect and supine plain abdominal x-rays revealed features of partial intestinal obstruction and abdominal ultrasound scan revealed dilated and hypertrophied bowel segment but could not say the bowel segment affected.
  • The affected segment was found to be a 55cm portion of terminal ileum at operation which was resected due to hypertrophied proximal and collapsed distal segments, features in keeping with chronic intestinal obstruction, and ileo-ileal anastomosis done.
  • Histology report was that of benign tubulovillous adenoma and the girl has enjoyed stable health for more than a year on close follow up in surgical outpatient clinic.
  • This case highlights the unusual presentation and unusual gross nature of this small intestinal adenoma, which was found to be a benign adenoma on histological examination.
  • [MeSH-major] Adenoma, Villous / diagnosis. Intestinal Neoplasms / diagnosis

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  • (PMID = 19764676.001).
  • [ISSN] 1119-3077
  • [Journal-full-title] Nigerian journal of clinical practice
  • [ISO-abbreviation] Niger J Clin Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Nigeria
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4. Yao T: [Clinicopathological features of small intestinal tumors]. Gan To Kagaku Ryoho; 2010 Aug;37(8):1436-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathological features of small intestinal tumors].
  • Small intestinal neoplasms are rare, accounting for only 1-2% of all gastrointestinal neoplasms.
  • Variable neoplasms are recognized in the small intestine.
  • The prognosis of small intestinal cancer is poor, because preoperative diagnosis is difficult and it is usually discovered at the advanced stage.
  • In addition, it is thought that there are few small intestinal cancers of an adenoma origin, but dysplasia is considered to be associated with that complicated by Crohn's disease.
  • Among malignant lymphomas of the small intestine, the incidence of MALT lymphoma is lower, and those of T cell and follicular ones are higher than in the stomach.
  • Lymphomas with minimal cellular atypia are often encountered, and in such cases biopsy diagnosis is difficult.
  • The prognosis of small intestinal lymphoma is better than for small intestinal cancer.
  • It must be recalled that multiple GIST occurs in specific disorders such as von Recklinghausen's disease and familial disease among small intestinal GIST, although very rarely.
  • The prognosis of malignant small intestinal disease will improve through early diagnosis with the recent progress in the procedures for detecting small intestinal disease.
  • [MeSH-major] Intestinal Neoplasms / pathology. Intestine, Small / pathology

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  • (PMID = 20716865.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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15. Alrefai WA, Wen X, Jiang W, Katz JP, Steinbrecher KA, Cohen MB, Williams IR, Dudeja PK, Wu GD: Molecular cloning and promoter analysis of downregulated in adenoma (DRA). Am J Physiol Gastrointest Liver Physiol; 2007 Nov;293(5):G923-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular cloning and promoter analysis of downregulated in adenoma (DRA).
  • Downregulated in adenoma (DRA), also referred to as SLC26A3, is an intestinal anion transporter essential for intestinal chloride absorption.
  • We also demonstrated a reduction in DRA promoter activity in Caco-2 cells by IFN-gamma, suggesting that regulation of DRA promoter by IFN-gamma may contribute to the pathophysiology of intestinal inflammation.
  • Furthermore, we showed that the DRA promoter fragment is sufficient to drive human growth hormone transgene expression specifically in villus epithelial cells of the small intestine and in differentiated upper crypt and surface epithelial cells of the colon.
  • Our studies provide evidence for the involvement of HNF-4, YY1, and GATA transcription factors in DRA expression in intestinal differentiated epithelial cells.
  • [MeSH-minor] Adenoma / genetics. Adenoma / immunology. Animals. Base Sequence. Cell Line, Tumor. Chloride-Bicarbonate Antiporters. Cloning, Molecular. Gene Expression Regulation, Neoplastic. Genes, Reporter. Human Growth Hormone / genetics. Humans. Intestinal Mucosa / physiology. Mice. Mice, Transgenic. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics

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  • (PMID = 17761837.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK39368; United States / NIDDK NIH HHS / DK / DK47318; United States / NIDDK NIH HHS / DK / DK54016; United States / NIDDK NIH HHS / DK / DK54893; United States / NIDDK NIH HHS / DK / DK64730; United States / NIDDK NIH HHS / DK / DK68324; United States / NIDDK NIH HHS / DK / DK71596
  • [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 / Antiporters; 0 / Chloride-Bicarbonate Antiporters; 0 / SLC26A3 protein, human; 0 / Transcription Factors; 12629-01-5 / Human Growth Hormone
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16. Umeno J, Matsumoto T, Esaki M, Kukita Y, Tahira T, Yanaru-Fujisawa R, Nakamura S, Arima H, Hirahashi M, Hayashi K, Iida M: Impact of group IVA cytosolic phospholipase A2 gene polymorphisms on phenotypic features of patients with familial adenomatous polyposis. Int J Colorectal Dis; 2010 Mar;25(3):293-301
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Rs12749354 C allele was more frequently found in patients with small intestinal adenoma (OR, 7.0; 95% CI, 1.5-30.4; p = 0.008).

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  • (PMID = 19795129.001).
  • [ISSN] 1432-1262
  • [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 / Adenomatous Polyposis Coli Protein; EC 3.1.1.4 / Group IV Phospholipases A2; EC 3.1.1.4 / PLA2G4A protein, human
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17. Hinoi T, Akyol A, Theisen BK, Ferguson DO, Greenson JK, Williams BO, Cho KR, Fearon ER: Mouse model of colonic adenoma-carcinoma progression based on somatic Apc inactivation. Cancer Res; 2007 Oct 15;67(20):9721-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse model of colonic adenoma-carcinoma progression based on somatic Apc inactivation.
  • Existing mouse intestinal tumor models display mainly small intestinal lesions and carcinomas are rare.
  • The predominantly distal colon and rectal distribution of tumors seen in mice where one Apc allele was inactivated in epithelial cells from distal ileum to rectum suggests that regional differences in the intestinal tract in the frequency and nature of secondary genetic and epigenetic events associated with adenoma outgrowth have a contributing role in determining where adenomas develop.
  • The presence of large numbers of small intestine tumors seemed to inhibit colorectal tumor development in the mouse, and gender-specific effects on tumor multiplicity in the distal mouse colon and rectum mimic the situation in humans where males have a larger number of advanced adenomas and carcinomas in the distal colon and rectum than females.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. Genes, APC. Homeodomain Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 17942902.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA082223; United States / NCI NIH HHS / CA / CA085463; United States / NCI NIH HHS / CA / CA46592
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Nuclear Localization Signals; 0 / Transcription Factors; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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18. Zhang FW, Cheng HC, Jiang CD, Deng CY, Xiong YZ, Li FE, Lei MG: Imprinted status of pleomorphic adenoma gene-like I and paternal expression gene 10 genes in pigs. J Anim Sci; 2007 Apr;85(4):886-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imprinted status of pleomorphic adenoma gene-like I and paternal expression gene 10 genes in pigs.
  • In this study, the polymorphism-based approach was used to detect the expression patterns of the porcine pleomorphic adenoma gene-like I (PLAGL1) and paternal expression gene 10 (PEG10) genes.
  • Imprinting analysis indicated that the PLAGL1 and PEG10 genes were both paternally expressed in all tissues tested (heart, liver, spleen, lung, kidney, stomach, small intestine, skeletal muscle, fat, uterus, and ovary).

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  • (PMID = 17178803.001).
  • [ISSN] 1525-3163
  • [Journal-full-title] Journal of animal science
  • [ISO-abbreviation] J. Anim. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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19. Oikarinen S, Heinonen SM, Nurmi T, Adlercreutz H, Mutanen M: No effect on adenoma formation in Min mice after moderate amount of flaxseed. Eur J Nutr; 2005 Aug;44(5):273-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] No effect on adenoma formation in Min mice after moderate amount of flaxseed.
  • The present work aims to evaluate the effect of flaxseed on tumour formation in multiple intestinal neoplasia (Min) mice, a model for colon tumorigenesis.
  • RESULTS: The total number of adenomas or their size in the small intestine was not different in the flaxseed and control groups.
  • Gender and genotype based differences were found in the intestinal ENL levels.
  • When compared to Min females, Min males in the flaxseed group had several fold higher ENL levels in the small intestine (Min males 125 +/- 124.5 nmol/g vs. females 22.8 +/- 16.0 nmol/g, P = 0.048) and caecum (47.6 +/- 31.6 nmol/g vs. females 14.5 +/- 6.6 nmol/g, P = 0.001).
  • Presence of adenomas in the gut influences the intestinal lignan metabolism.
  • Min mice had less intestinal END and ENL as compared with the wild-type mice (P < 0.05).
  • The plasma ENL level did not correlate with adenoma number in the small intestine and colon.
  • CONCLUSION: The number of intestinal adenomas in the Min mouse model is not related to ENL level in plasma nor is it associated with the levels of intestinal lignans.
  • [MeSH-major] Adenoma / prevention & control. Flax. Intestinal Neoplasms / prevention & control. Lignans / pharmacology. Phytoestrogens / pharmacology

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  • (PMID = 15278371.001).
  • [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 / Lignans; 0 / Phytoestrogens; 76543-16-3 / 2,3-bis(3'-hydroxybenzyl)butane-1,4-diol
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20. Alferez DG, Ryan AJ, Goodlad RA, Wright NA, Wilkinson RW: Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model. Int J Oncol; 2010 Oct;37(4):767-72
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  • [Title] Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
  • The Apc(MIN/+) mouse is a well-characterised model of intestinal tumourigenesis in which animals develop macroscopically detectable adenomas.
  • However, most of the adenomas are formed in the small intestine and resolution of events in the colon, the most relevant site for human disease, is limited.
  • Eight-week old Apc(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for adenoma formation in the intestines.
  • Vandetanib treatment significantly reduced adenoma formation in the small intestine by 68% (P=0.001) and the colon by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated Apc(MIN/+) mice.
  • In the Apc(MIN/+) group, vandetanib also reduced the mean number of adenomas in the small intestine by 76% (P<0.001) and in the colon by 60% (from 3.9 to 1.5, P=0.1).
  • Moreover these preclinical data provide a rationale for studying the effects of vandetanib in early stages of intestinal cancer in the clinic.
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced. Colonic Neoplasms / prevention & control. Dextran Sulfate. Genes, APC. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Intestine, Small / drug effects. Intestine, Small / enzymology. Intestine, Small / pathology. Mice. Mice, Inbred C57BL. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / metabolism. beta Catenin / metabolism

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  • (PMID = 20811697.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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21. Cai H, Marczylo TH, Teller N, Brown K, Steward WP, Marko D, Gescher AJ: Anthocyanin-rich red grape extract impedes adenoma development in the Apc(Min) mouse: pharmacodynamic changes and anthocyanin levels in the murine biophase. Eur J Cancer; 2010 Mar;46(4):811-7
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  • [Title] Anthocyanin-rich red grape extract impedes adenoma development in the Apc(Min) mouse: pharmacodynamic changes and anthocyanin levels in the murine biophase.
  • Here the hypothesis was tested that oenocyanin added to the diet can interfere with intestinal adenoma development in the Apc(Min) mouse, a model of intestinal carcinogenesis linked to an Apc mutation.
  • METHODS: Mice received oenocyanin (0.3%) in their diet until week 16, when adenoma number and burden were recorded.
  • RESULTS: In mice which had consumed oenocyanin, overall adenoma burden was halved and adenoma number was marginally reduced when compared with mice on control diet.
  • Expression of Akt in small intestinal adenomas from Apc(Min) mice on oenocyanin was reduced by 54% (P=0.003), when compared to controls.
  • Oenocyanin anthocyanins and glucuronide metabolites were found in the urine and intestine but not in plasma.
  • [MeSH-major] Adenoma / prevention & control. Anthocyanins / analysis. Antineoplastic Agents, Phytogenic / therapeutic use. Intestinal Neoplasms / prevention & control. Phytotherapy / methods. Vitis / chemistry
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Cell Proliferation / drug effects. Chromatography, High Pressure Liquid / methods. Disease Models, Animal. Drug Evaluation, Preclinical / methods. Intestinal Mucosa / metabolism. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. Plant Extracts / pharmacology. Plant Extracts / therapeutic use. Proto-Oncogene Proteins c-akt / metabolism. eIF-2 Kinase / metabolism

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20060287.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / C325/A6691
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthocyanins; 0 / Antineoplastic Agents, Phytogenic; 0 / Biomarkers, Tumor; 0 / Plant Extracts; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / eIF-2 Kinase
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22. Moran AE, Carothers AM, Weyant MJ, Redston M, Bertagnolli MM: Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse. Cancer Res; 2005 Feb 1;65(3):1097-104
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  • [Title] Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse.
  • Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%.
  • Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate.
  • Moreover, treatment of WT intestine with the phosphatase inhibitor, pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue.
  • Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.
  • [MeSH-major] Adenoma / prevention & control. Colonic Neoplasms / prevention & control. Cytoskeletal Proteins / metabolism. Diterpenes, Abietane / pharmacology. Phenanthrenes / pharmacology. Trans-Activators / metabolism
  • [MeSH-minor] Animals. Cadherins / metabolism. Cell Adhesion / drug effects. Cell Membrane / drug effects. Cell Membrane / metabolism. Enterocytes / drug effects. Enterocytes / metabolism. Female. Intestine, Small / cytology. Intestine, Small / drug effects. Intestine, Small / metabolism. Mice. Mice, Inbred C57BL. Phosphorylation / drug effects. Rosmarinus / chemistry. Tyrosine / metabolism. Vanadates / antagonists & inhibitors. Vanadates / pharmacology. beta Catenin

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  • (PMID = 15705912.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R29 CA 74162; United States / NCI NIH HHS / CA / T32 CA 68971
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cadherins; 0 / Cytoskeletal Proteins; 0 / Diterpenes, Abietane; 0 / Phenanthrenes; 0 / Trans-Activators; 0 / beta Catenin; 0 / pervanadate; 3WHH0066W5 / Vanadates; 42HK56048U / Tyrosine; 5957-80-2 / carnosol
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23. Musch MW, Arvans DL, Wu GD, Chang EB: Functional coupling of the downregulated in adenoma Cl-/base exchanger DRA and the apical Na+/H+ exchangers NHE2 and NHE3. Am J Physiol Gastrointest Liver Physiol; 2009 Feb;296(2):G202-10
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  • [Title] Functional coupling of the downregulated in adenoma Cl-/base exchanger DRA and the apical Na+/H+ exchangers NHE2 and NHE3.
  • Non-nutrient-dependent salt absorption across the brush-border membrane of intestinal epithelial cells is primarily mediated by coupled apical Na(+)/H(+) (aNHE) and anion exchange transport, with the latter suspected of being mediated by DRA (downregulated in adenoma; SLC26A3) that is defective in congenital chloridorrhea.

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  • (PMID = 19056765.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK-38510; United States / NIDDK NIH HHS / DK / DK-42086
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiporters; 0 / Chloride-Bicarbonate Antiporters; 0 / Chlorides; 0 / Clathrin; 0 / RNA, Messenger; 0 / SLC26A3 protein, human; 0 / SLC9A2 protein, human; 0 / Sodium Radioisotopes; 0 / Sodium-Hydrogen Antiporter; 0 / Synaptotagmin I; 0 / sodium-hydrogen exchanger 3; 1214-79-5 / 5-dimethylamiloride; 4U5MP5IUD8 / Niflumic Acid; 7DZO8EB0Z3 / Amiloride; 9NEZ333N27 / Sodium; E0399OZS9N / Cyclic AMP; Q1O6DSW23R / 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; SY7Q814VUP / Calcium; W733B0S9SD / Methazolamide
  • [Other-IDs] NLM/ PMC2643907
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24. Oikarinen SI, Pajari AM, Salminen I, Heinonen SM, Adlercreutz H, Mutanen M: Effects of a flaxseed mixture and plant oils rich in alpha-linolenic acid on the adenoma formation in multiple intestinal neoplasia (Min) mice. Br J Nutr; 2005 Oct;94(4):510-8
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  • [Title] Effects of a flaxseed mixture and plant oils rich in alpha-linolenic acid on the adenoma formation in multiple intestinal neoplasia (Min) mice.
  • To study the effects of a flaxseed mixture on adenoma formation in multiple intestinal neoplasia mice, the mice were fed a diet containing 2.7 % flaxseed, 4.5 % fibre and 3.7 % ALA.
  • The median number of adenomas in the small intestine was fifty-four for the control group, and thirty-seven (P=0.023) and forty-two (P=0.095) for flaxseed and oil groups, respectively.
  • Compared with controls (1.2 mm), the adenoma size was smaller in the flaxseed (0.9 mm; P=0.002) and oil (1.0 mm; P=0.012) groups.
  • Membrane beta-catenin and protein kinase C (PKC)-zeta levels were reduced in the adenoma v. mucosa (P<0.05), and an inverse association was found between the membrane PKC-zeta in the mucosa and the adenoma number (r -0.460, P=0.008, n 32).
  • The results suggest that the preventive effect of flaxseed on colon carcinogenesis may be due to the oil part of flaxseed, and the loss of beta-catenin and PKC-zeta from the membranes of the mucosal tissue may play a permissive role in intestinal tumour development.
  • [MeSH-major] Adenoma / prevention & control. Flax. Intestinal Neoplasms / prevention & control. Neoplasms, Multiple Primary / prevention & control. Plant Oils / administration & dosage. alpha-Linolenic Acid / administration & dosage
  • [MeSH-minor] Actins / analysis. Animals. Blotting, Western / methods. Colon / chemistry. Cyclooxygenase 2 / analysis. Fatty Acids / analysis. Intestinal Mucosa / chemistry. Lignans / metabolism. Linseed Oil / metabolism. Mice. Mice, Mutant Strains. Models, Animal. Protein Kinase C / analysis. Weight Gain. beta Catenin / analysis

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  • (PMID = 16197574.001).
  • [ISSN] 0007-1145
  • [Journal-full-title] The British journal of nutrition
  • [ISO-abbreviation] Br. J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Fatty Acids; 0 / Lignans; 0 / Plant Oils; 0 / beta Catenin; 0RBV727H71 / alpha-Linolenic Acid; 8001-26-1 / Linseed Oil; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.13 / Protein Kinase C
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25. Marsh V, Winton DJ, Williams GT, Dubois N, Trumpp A, Sansom OJ, Clarke AR: Epithelial Pten is dispensable for intestinal homeostasis but suppresses adenoma development and progression after Apc mutation. Nat Genet; 2008 Dec;40(12):1436-44
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  • [Title] Epithelial Pten is dispensable for intestinal homeostasis but suppresses adenoma development and progression after Apc mutation.
  • PTEN acts as a tumor suppressor in a range of tissue types and has been implicated in the regulation of intestinal stem cells.
  • To study Pten function in the intestine, we used various conditional transgenic strategies to specifically delete Pten from the mouse intestinal epithelium.
  • We conclude that Pten is redundant in otherwise normal intestinal epithelium and epithelial stem cells but, in the context of activated Wnt signaling, suppresses progression to adenocarcinoma through modulation of activated Akt levels.

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  • (PMID = 19011632.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 9590; United Kingdom / Medical Research Council / / G0301154; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 094ZI81Y45 / Tamoxifen; 6051-87-2 / beta-Naphthoflavone; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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26. Günther U, Bojarski C, Buhr HJ, Zeitz M, Heller F: Capsule endoscopy in small-bowel surveillance of patients with hereditary polyposis syndromes. Int J Colorectal Dis; 2010 Nov;25(11):1377-82
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  • [Title] Capsule endoscopy in small-bowel surveillance of patients with hereditary polyposis syndromes.
  • PURPOSE: Familial adenomatous polyposis (FAP) and Peutz-Jeghers syndrome (PJS) are hereditary polyposis syndromes with a high risk for benign small-bowel polyps and cancer.
  • The aim of this study was to assess the prevalence of small-bowel polyps beyond the duodenum in patients with FAP and PJS and to examine the clinical value and the optimal interval of capsule endoscopy (CE) for the surveillance of small-bowel polyps in patients with FAP.
  • RESULTS: In 13 of the 15 (87%) FAP patients, small-bowel polyps were detected by CE ranging from estimated <5 mm to >10 mm in size.
  • In three FAP patients with repeated CEs, the latest CE displayed medium- and large-sized polyps in the proximal jejunum, whereas previous CEs had detected only small-sized (<5 mm) polyps.
  • In three of the four PJS patients, large-sized small-bowel polyps were visualized by CE which could then be removed by double-balloon enteroscopy (DBE) or surgical resection.
  • CONCLUSION: CE is an effective and safe method for small-bowel surveillance in FAP and PJS.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Capsule Endoscopy. Intestine, Small / pathology. Peutz-Jeghers Syndrome / diagnosis
  • [MeSH-minor] Adenoma / classification. Adenoma / diagnosis. Humans. Syndrome

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  • (PMID = 20544205.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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27. Cardona DM, Zhang X, Liu C: Loss of carbamoyl phosphate synthetase I in small-intestinal adenocarcinoma. Am J Clin Pathol; 2009 Dec;132(6):877-82
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  • [Title] Loss of carbamoyl phosphate synthetase I in small-intestinal adenocarcinoma.
  • Carbamoyl phosphate synthetase I (CPS1), normally found in hepatocytes and small-intestine (SI) enterocytes, is the antigen of Hep Par 1 antibody.
  • Western blot analysis confirmed the immunohistochemical findings, with strong CPS1 expression within the normal mucosa and adenoma and complete loss in the invasive tumor.
  • [MeSH-minor] Adenoma / enzymology. Adenoma / pathology. Biomarkers, Tumor / metabolism. Duodenitis / enzymology. Duodenitis / pathology. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / pathology. Neoplasm Invasiveness. Retrospective Studies

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  • (PMID = 19926579.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 6.3.4.16 / Carbamoyl-Phosphate Synthase (Ammonia)
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28. Turan M, Karadayi K, Duman M, Ozer H, Arici S, Yildirir C, Koçak O, Sen M: Small bowel tumors in emergency surgery. Ulus Travma Acil Cerrahi Derg; 2010 Jul;16(4):327-33
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  • [Title] Small bowel tumors in emergency surgery.
  • BACKGROUND: The aim of the present study was to describe the clinical presentation, diagnostic work-up, surgical therapy, and prognosis of 13 patients with small bowel tumor admitted for surgical procedures in an emergency setting.
  • METHODS: From 1996 to 2008, 13 consecutive surgical cases of small bowel tumors were treated at the Cumhuriyet University Faculty of Medicine, Department of General Surgery, and Kütahya State Hospital, Department of General Surgery.
  • RESULTS: Intestinal obstruction (7 cases) and perforation (5 cases) were the most common clinical presentations, followed by intussusception (1 case).
  • Adenocarcinoma was the most frequent histologic type (4 cases), while small bowel sarcoma was seen in three cases and non-Hodgkin lymphoma in two cases.
  • The remaining cases had carcinoid tumor, small bowel angioleiomyoma, Brunner's gland adenoma, and inflammatory pseudotumor of the small intestine.
  • CONCLUSION: Small bowel tumors are rare, the symptoms often non-specific, and the accuracy of different diagnostic tests remains to be improved.
  • [MeSH-major] Adenocarcinoma / surgery. Emergencies. Intestinal Neoplasms / surgery. Surgical Procedures, Operative / methods
  • [MeSH-minor] Angiomyoma / surgery. Hemangiosarcoma / surgery. Humans. Intestinal Obstruction / etiology. Intestinal Perforation / etiology. Leiomyosarcoma / surgery. Retrospective Studies

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  • (PMID = 20849049.001).
  • [ISSN] 1306-696X
  • [Journal-full-title] Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES
  • [ISO-abbreviation] Ulus Travma Acil Cerrahi Derg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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29. Cobrin GM, Pittman RH, Lewis BS: Increased diagnostic yield of small bowel tumors with capsule endoscopy. Cancer; 2006 Jul 1;107(1):22-7
MedlinePlus Health Information. consumer health - Intestinal Cancer.

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  • [Title] Increased diagnostic yield of small bowel tumors with capsule endoscopy.
  • BACKGROUND: It is believed that cancers of the small intestine represent <2% of all malignant tumors of the gastrointestinal tract, although the accuracy of this estimate is unknown, because the current methodologies for examining the small bowel have proved inadequate.
  • Capsule endoscopy allows a more detailed inspection of the small intestine and may improve the ability to diagnose small bowel tumors.
  • The objective of this study was to evaluate the effectiveness of capsule endoscopy in diagnosing small bowel tumors and to help establish the true incidence of tumors in obscure gastrointestinal bleeding.
  • RESULTS: A diagnosis was made by capsule endoscopy in 277 patients (49.3%).
  • Of 562 patients who were included in the study, 50 patients (8.9%) were diagnosed with small bowel tumors.
  • The types of tumor diagnosed by capsule endoscopy included 8 adenocarcinomas (1.4%), 10 carcinoids (1.8%), 4 gastrointestinal stromal tumors (0.7%), 5 lymphomas (0.9%), 3 inflammatory polyps, 1 lymphangioma, 1 lymphangioectasia,1 hemangioma, 1 hamartoma, and 1 tubular adenoma.
  • It was observed that 9 of 67 patients (13%) younger than age 50 years who underwent capsule endoscopy for obscure bleeding had small bowel tumors.
  • CONCLUSIONS: Capsule endoscopy diagnosed small bowel tumors in 8.9% of patients who underwent the procedure for a variety of reasons, establishing it as an effective diagnostic modality.
  • This incidence of small bowel tumors suggests an important role for capsule endoscopy in the algorithm for the diagnostic work-up of patients with suspected small bowel lesions.
  • Capsule endoscopy may lead to earlier detection and treatment of small bowel tumors and an improved prognosis for patients with these neoplasms.
  • [MeSH-major] Capsules. Endoscopy, Gastrointestinal. Ileal Neoplasms / diagnosis. Intestine, Small / pathology. Jejunal Neoplasms / diagnosis. Video Recording

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  • [Copyright] Copyright 2006 American Cancer Society.
  • (PMID = 16736516.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsules
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30. Masselli G, Polettini E, Casciani E, Bertini L, Vecchioli A, Gualdi G: Small-bowel neoplasms: prospective evaluation of MR enteroclysis. Radiology; 2009 Jun;251(3):743-50
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  • [Title] Small-bowel neoplasms: prospective evaluation of MR enteroclysis.
  • PURPOSE: To prospectively evaluate the accuracy of magnetic resonance (MR) enteroclysis in the detection of small-bowel neoplasms in symptomatic patients, with conventional endoscopy, tissue specimen, capsule endoscopy, conventional enteroclysis, and follow-up findings as reference standards.
  • One hundred fifty patients (83 male, 67 female; mean age, 42.6 years; age range, 17-84 years) who were clinically suspected of having small-bowel neoplasm and whose previous upper and lower gastrointestinal endoscopy findings were normal underwent MR enteroclysis.
  • The MR enteroclysis findings were prospectively evaluated for the presence of focal bowel wall thickening, small-bowel masses, and small-bowel stenosis.
  • RESULTS: MR enteroclysis was successfully completed in all 150 patients and enabled correct detection of 19 small-bowel neoplasms, which were confirmed at histopathologic examination: three carcinoid neoplasms, two adenocarcinomas, two stromal tumors, five lymphomas, one angiomatous mass, three small-bowel metastases, one leiomyoma, one adenoma, and one lipoma.
  • Overall sensitivity, specificity, and accuracy in identifying patients with small-bowel lesions were 86% (19 of 22), 98% (126 of 128), and 97% (145 of 150), respectively.
  • CONCLUSION: MR enteroclysis is an accurate modality for detecting small-bowel neoplasms in symptomatic patients.
  • [MeSH-major] Intestinal Neoplasms / diagnosis. Intestine, Small. Magnetic Resonance Imaging / methods

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  • (PMID = 19304922.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Organometallic Compounds; 0 / gadoterate meglumine; 6HG8UB2MUY / Meglumine
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31. Rossmann H, Jacob P, Baisch S, Hassoun R, Meier J, Natour D, Yahya K, Yun C, Biber J, Lackner KJ, Fiehn W, Gregor M, Seidler U, Lamprecht G: The CFTR associated protein CAP70 interacts with the apical Cl-/HCO3- exchanger DRA in rabbit small intestinal mucosa. Biochemistry; 2005 Mar 22;44(11):4477-87

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The CFTR associated protein CAP70 interacts with the apical Cl-/HCO3- exchanger DRA in rabbit small intestinal mucosa.
  • DRA (down regulated in adenoma) is an intestinal anion exchanger, acting in parallel with NHE3 to facilitate ileal and colonic NaCl absorption.
  • Furthermore it is involved in small intestinal bicarbonate secretion.
  • Because DRA has a PDZ interaction motif, which may influence its properties, we searched for DRA-interacting PDZ adapter proteins in the small intestine.
  • The composition of macromolecular complexes assembled by CAP70 in the distal small bowel is unknown.
  • We suggest that CAP70 mediates regulatory functions specific to the small intestine.
  • [MeSH-major] Antiporters / metabolism. Carrier Proteins / metabolism. Chloride-Bicarbonate Antiporters / metabolism. Cystic Fibrosis Transmembrane Conductance Regulator / metabolism. Intestinal Mucosa / metabolism. Intestine, Small / metabolism

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  • (PMID = 15766278.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF314819/ AY204473
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiporters; 0 / CFTR protein, human; 0 / Carrier Proteins; 0 / Chloride-Bicarbonate Antiporters; 0 / Membrane Proteins; 0 / PDZK1 protein, human; 0 / Peptide Fragments; 0 / RNA, Messenger; 0 / SLC26A3 protein, human; 126880-72-6 / Cystic Fibrosis Transmembrane Conductance Regulator
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32. Giroux V, Lemay F, Bernatchez G, Robitaille Y, Carrier JC: Estrogen receptor beta deficiency enhances small intestinal tumorigenesis in ApcMin/+ mice. Int J Cancer; 2008 Jul 15;123(2):303-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estrogen receptor beta deficiency enhances small intestinal tumorigenesis in ApcMin/+ mice.
  • The first aim of this study was to investigate the consequence of ERbeta deficiency on intestinal tumorigenesis in the Apc(Min/+) mouse model.
  • Specifically in female, ERbeta deficiency was found to be associated with higher adenoma multiplicity in the small intestine, but not in the colon.
  • Therefore, our results demonstrate that ERbeta deficiency enhances small intestinal tumorigenesis and suggest that modulation of the TGFbeta signaling pathway could contribute to the protective role of estrogens on intestinal tumorigenesis.
  • [MeSH-major] Adenoma / metabolism. Estrogen Receptor beta / deficiency. Intestinal Neoplasms / metabolism. Intestine, Small. Transforming Growth Factor beta / metabolism

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18464259.001).
  • [ISSN] 1097-0215
  • [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 / Estrogen Receptor beta; 0 / Transforming Growth Factor beta; G34N38R2N1 / Bromodeoxyuridine
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33. Sansom OJ, Reed KR, van de Wetering M, Muncan V, Winton DJ, Clevers H, Clarke AR: Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine. J Biol Chem; 2005 Aug 5;280(31):28463-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine.
  • Cyclin D1 is postulated to be a target of the canonical Wnt pathway and critical for intestinal adenoma development.
  • Cyclin D1 levels do, however, increase in a delayed manner in a small subset of cells, suggesting such up-regulation occurs as a secondary event.
  • Finally in a smaller study, we analyzed whether cyclin D1 deficiency affected adenoma formation 20 days following induced loss of Apc.
  • Unlike AhCre(+) Apc(fl/fl) mice (which all developed adenomas), doubly mutant AhCre(+) Apc(fl/fl) cyclin D1(-/-) mice only developed small lesions.
  • Taken together, this argues that cyclin D1 up-regulation in intestinal neoplasia is important for tumor progression rather than initiation.
  • [MeSH-minor] Adenoma. Animals. Cell Line, Tumor. Colorectal Neoplasms. Gene Deletion. Gene Expression Regulation, Neoplastic. Integrases / metabolism. Intestinal Neoplasms. Mice. Mice, Inbred C57BL. Phenotype. beta Catenin

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  • (PMID = 15946945.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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34. Saurin JC, Pilleul F, Soussan EB, Manière T, D'Halluin PN, Gaudric M, Cellier C, Heresbach D, Gaudin JL, Capsule Commission of the French Society of Digestive Endoscopy (SFED): Small-bowel capsule endoscopy diagnoses early and advanced neoplasms in asymptomatic patients with Lynch syndrome. Endoscopy; 2010 Dec;42(12):1057-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small-bowel capsule endoscopy diagnoses early and advanced neoplasms in asymptomatic patients with Lynch syndrome.
  • BACKGROUND AND STUDY AIMS: Patients with Lynch syndrome are at increased risk of developing small-bowel adenocarcinoma, which usually has a bad prognosis and needs to be diagnosed early.
  • RESULTS: Histologically confirmed small-bowel neoplasms were diagnosed in three patients (8.6 %): one adenocarcinoma (T3N0M0) and two adenomas with low-grade dysplasia.
  • The clinical usefulness of systematic small-bowel screening in these patients should be confirmed through large prospective studies.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Capsule Endoscopy. Colorectal Neoplasms, Hereditary Nonpolyposis / complications. Intestinal Neoplasms / diagnosis. Intestine, Small

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  • [Copyright] © Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 20821360.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Contrast Media
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35. Pilleul F, Penigaud M, Milot L, Saurin JC, Chayvialle JA, Valette PJ: Possible small-bowel neoplasms: contrast-enhanced and water-enhanced multidetector CT enteroclysis. Radiology; 2006 Dec;241(3):796-801
MedlinePlus Health Information. consumer health - CT Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possible small-bowel neoplasms: contrast-enhanced and water-enhanced multidetector CT enteroclysis.
  • PURPOSE: To prospectively evaluate the sensitivity and specificity of contrast material-enhanced and water-enhanced multidetector computed tomographic (CT) enteroclysis in depicting small-bowel neoplasms in symptomatic patients, with endoscopic, tissue, and follow-up findings as reference standards.
  • Two hundred nineteen patients (108 male, 111 female; age range, 17-98 years; mean, 53.1 years) with clinical suspicion of small-bowel neoplasm underwent contrast- and water-enhanced multidetector CT enteroclysis after normal findings of upper and lower gastrointestinal endoscopy.
  • The prospective interpretations of CT enteroclysis results include evaluation of focal bowel wall thickening, small-bowel masses, small-bowel stenosis, mesenteric stranding, enlarged mesenteric lymph nodes, and visceral metastasis.
  • The overall sensitivity and specificity in identifying patients with small-bowel lesions were 84.7% and 96.9%, respectively.
  • Findings of pathologic examination confirmed small-bowel tumor in 50 patients with carcinoid tumor (n = 19), adenocarcinoma (n = 7), lymphoma (n = 5), jejunal adenoma (n = 9), stromal tumor (n = 5), ectopic pancreas (n = 2), angiomatous mass (n = 2), or metastasis (n = 1).
  • CONCLUSION: Contrast- and water-enhanced multidetector CT enteroclysis had an overall accuracy of 84.7% for depiction of small-bowel neoplasms.
  • [MeSH-major] Intestinal Neoplasms / radiography. Intestine, Small. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Contrast Media. Diagnosis, Differential. Endoscopy, Gastrointestinal. Female. Humans. Iopamidol / analogs & derivatives. Male. Middle Aged. Predictive Value of Tests. Prospective Studies. Reference Standards. Sensitivity and Specificity

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  • [Copyright] (c) RSNA, 2006.
  • (PMID = 17053201.001).
  • [ISSN] 0033-8419
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 17E17JBP8L / iomeprol; JR13W81H44 / Iopamidol
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36. Elahi E, Suraweera N, Volikos E, Haines J, Brown N, Davidson G, Churchman M, Ilyas M, Tomlinson I, Silver A: Five quantitative trait loci control radiation-induced adenoma multiplicity in Mom1R Apc Min/+ mice. PLoS One; 2009;4(2):e4388
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  • [Title] Five quantitative trait loci control radiation-induced adenoma multiplicity in Mom1R Apc Min/+ mice.
  • By backcrossing a recombinant line of Apc(Min/+) mice to the inbred BALB/c mouse strain, which is unusually sensitive to radiation-induced tumour development, we obtained panels of 2Gy-irradiated and sham-irradiated N2 Apc(Min/+) mice for genotyping with a genome-wide panel of microsatellites at approximately 15 cM density and phenotyping by counting adenomas in the small intestine.
  • Interval and composite interval mapping along with permutation testing identified five significant susceptibility quantitative trait loci (QTLs) responsible for radiation induced tumour multiplicity in the small intestine.
  • Our study locates the QTL regions responsible for increased radiation-induced intestinal tumorigenesis in Apc(Min/+) mice and identifies candidate genes with predicted functional polymorphisms that are involved in spindle checkpoint and chromosomal stability (Bub1b, Casc5, and Bub1), DNA repair (Recc1 and Prkdc) or inflammation (Duox2, Itgb2l and Cxcl5).

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  • (PMID = 19194513.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Amino Acids; 0 / Genetic Markers; 0 / Proteins; EC 3.1.1.4 / Group II Phospholipases A2; EC 3.1.1.4 / Pla2g2a protein, mouse
  • [Other-IDs] NLM/ PMC2633613
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37. Luo F, Brooks DG, Ye H, Hamoudi R, Poulogiannis G, Patek CE, Winton DJ, Arends MJ: Mutated K-ras(Asp12) promotes tumourigenesis in Apc(Min) mice more in the large than the small intestines, with synergistic effects between K-ras and Wnt pathways. Int J Exp Pathol; 2009 Oct;90(5):558-74
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  • [Title] Mutated K-ras(Asp12) promotes tumourigenesis in Apc(Min) mice more in the large than the small intestines, with synergistic effects between K-ras and Wnt pathways.
  • Here, we show that a conditional mutant K-ras mouse model (K-ras(Asp12)/Cre), with transient intestinal Cre activation by beta-Naphthoflavone (beta-NF) treatment, displayed transgene recombination and K-ras(Asp12) expression in the murine intestines, but developed few intestinal adenomas over 2 years.
  • However, when crossed with Apc(Min/+) mice, the K-ras(Asp12)/Cre/Apc(Min/+) offspring showed acceleration of intestinal tumourigenesis with significantly changed average lifespan (P < 0.05) decreased to 18.4 +/- 5.4 weeks from 20.9 +/- 4.7 weeks (control Apc(Min/+) mice).
  • The numbers of adenomas in the small intestine and large intestine were significantly (P < 0.01) increased by 1.5-fold and 5.7-fold, respectively, in K-ras(Asp12)/Cre/Apc(Min/+) mice compared with Apc(Min/+) mice, with the more marked increase in adenoma prevalence in the large intestine.
  • To explore possible mechanisms for K-ras(Asp12) and Apc(Min) co-operation, the Mitogen-activated protein kinase (Mapk), Akt and Wnt signalling pathways, including selected target gene expression levels, were evaluated in normal large intestine and large intestinal tumours.
  • In conclusion, intestinal expression of K-ras(Asp12) promotes mutant Apc-initiated intestinal adenoma formation in vivo more in the large intestine than the small intestine, with evidence of synergistic co-operation between mutant K-ras and Apc involving increased expression of some Wnt-pathway target genes.

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  • (PMID = 19765110.001).
  • [ISSN] 1365-2613
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Wnt Proteins; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Oncogene Protein p21(ras); EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2768154
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38. Uchiyama S, Itoh H, Naganuma S, Nagaike K, Fukushima T, Tanaka H, Hamasuna R, Chijiiwa K, Kataoka H: Enhanced expression of hepatocyte growth factor activator inhibitor type 2-related small peptide at the invasive front of colon cancers. Gut; 2007 Feb;56(2):215-26

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhanced expression of hepatocyte growth factor activator inhibitor type 2-related small peptide at the invasive front of colon cancers.
  • BACKGROUND: Hepatocyte growth factor activator inhibitor type 2-related small peptide (H2RSP) is a small nuclear protein abundantly expressed in the gastrointestinal epithelium.
  • AIMS: To investigate the expression and localisation of H2RSP in normal, injured and neoplastic human intestinal tissue.
  • METHODS: Immunohistochemical examination and in situ hybridisation for H2RSP were performed using normal and diseased intestinal specimens.
  • RESULTS: In the normal intestine, H2RSP was observed in the nuclei of surface epithelial cells and this nuclear localisation was impaired in regenerating epithelium.
  • CONCLUSION: In the normal intestine, the nuclear accumulation of H2RSP is a marker of differentiated epithelial cells.
  • [MeSH-minor] Adenoma / chemistry. Adenoma / immunology. Adenoma / pathology. Animals. CHO Cells. Cell Count. Cell Differentiation / physiology. Cell Division / physiology. Cell Line, Tumor. Colitis, Ulcerative / immunology. Colitis, Ulcerative / pathology. Colorectal Neoplasms / chemistry. Colorectal Neoplasms / immunology. Colorectal Neoplasms / pathology. Cricetinae. Cricetulus. Epithelial Cells / chemistry. Epithelial Cells / immunology. Epithelial Cells / pathology. Humans. Hyperplasia. Immunohistochemistry / methods. In Situ Hybridization / methods. Intestinal Polyps / chemistry. Intestinal Polyps / immunology. Intestinal Polyps / pathology. Intestines / chemistry. Intestines / immunology. Intestines / pathology. Lymphatic Metastasis. Neoplasm Invasiveness. beta Catenin / analysis

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  • (PMID = 16809422.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / C19orf33 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC1856747
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39. Holmberg J, Genander M, Halford MM, Annerén C, Sondell M, Chumley MJ, Silvany RE, Henkemeyer M, Frisén J: EphB receptors coordinate migration and proliferation in the intestinal stem cell niche. Cell; 2006 Jun 16;125(6):1151-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EphB receptors coordinate migration and proliferation in the intestinal stem cell niche.
  • More than 10(10) cells are generated every day in the human intestine.
  • Wnt proteins are key regulators of proliferation and are known endogenous mitogens for intestinal progenitor cells.
  • The positioning of cells within the stem cell niche in the intestinal epithelium is controlled by B subclass ephrins through their interaction with EphB receptors.
  • We report that EphB receptors, in addition to directing cell migration, regulate proliferation in the intestine.
  • EphB signaling promotes cell-cycle reentry of progenitor cells and accounts for approximately 50% of the mitogenic activity in the adult mouse small intestine and colon.
  • These data establish EphB receptors as key coordinators of migration and proliferation in the intestinal stem cell niche.

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  • (PMID = 16777604.001).
  • [ISSN] 0092-8674
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH066332; United States / NIDCD NIH HHS / DC / R01 DC006225; United States / NIDDK NIH HHS / DK / R01 DK059164; United States / NIMH NIH HHS / MH / R01 MH66332
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins; EC 2.7.10.1 / Receptor, EphB2; EC 2.7.10.1 / Receptor, EphB3
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40. Dong K, Li B, Li BH, Guan QL, Huo YZ: [Clinical analysis of Peutz-Jeghers syndrome:a report of 6 cases]. Zhonghua Wei Chang Wai Ke Za Zhi; 2005 Jul;8(4):336-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Repeated abdominal pain, intussusception and intestinal polyp with bleeding were main manifestations.
  • Case 1 and case 4 had polyps synchronous with adenoma, and case 2 had polyp with gastric cancer.
  • Main treatment included polyp resection and partial small intestinal and colon resection.
  • CONCLUSIONS: Patients with PJS have family history of cancer and a high incidence of polyp recurrence of small intestine.
  • [MeSH-major] Peutz-Jeghers Syndrome / diagnosis. Peutz-Jeghers Syndrome / surgery
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Intestine, Small / surgery. Male. Pedigree

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  • (PMID = 16167257.001).
  • [ISSN] 1671-0274
  • [Journal-full-title] Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery
  • [ISO-abbreviation] Zhonghua Wei Chang Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
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41. Preston SL, Leedham SJ, Oukrif D, Deheregoda M, Goodlad RA, Poulsom R, Alison MR, Wright NA, Novelli M: The development of duodenal microadenomas in FAP patients: the human correlate of the Min mouse. J Pathol; 2008 Feb;214(3):294-301
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  • The morphological changes associated with the adenoma-carcinoma sequence are well documented in the colorectum.
  • Small intestinal carcinogenesis is thought to progress through a similar adenoma-to-carcinoma pathway, but there is a relative dearth of studies examining the associated morphological changes.
  • The best-known mouse model of intestinal neoplasia, the multiple intestinal neoplasia (Min) mouse, has been criticized as a genetic model of intestinal neoplasia, as the majority of its tumours occur in the small intestine.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyposis Coli / pathology. Duodenal Neoplasms / pathology


42. National Toxicology Program: Toxicology and carcinogenesis studies of sodium dichromate dihydrate (Cas No. 7789-12-0) in F344/N rats and B6C3F1 mice (drinking water studies). Natl Toxicol Program Tech Rep Ser; 2008 Jul;(546):1-192
Hazardous Substances Data Bank. SODIUM DICHROMATE .

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  • Increased incidences of histiocytic cellular infiltration also occurred in the small intestine (duodenum), mesenteric lymph node, and pancreatic lymph node of males and/or females exposed to 57.3 mg/L or greater.
  • The incidences of neoplasms of the small intestine (duodenum, jejunum, or ileum) were increased in exposed groups of male and female mice.
  • The incidences of adenoma of the duodenum in 257.4 mg/L males and 172 and 516 mg/L females were significantly greater than those in the controls.
  • The incidence of adenoma of the jejunum in 516 mg/L females was significantly increased compared to that in the controls.
  • When the incidences of adenoma and carcinoma were combined for all sites of the small intestine, the incidences were significantly increased in 85.7 and 257.4 mg/L males and 172 and 516 mg/L females compared to those in the controls.
  • There was clear evidence of carcinogenic activity of sodium dichromate dihydrate in male and female B6C3F1 mice based on increased incidences of neoplasms of the small intestine (duodenum, jejunum, or ileum).
  • Exposure to sodium dichromate dihydrate resulted in histiocytic cellular infiltration in the liver, small intestine, and pancreatic and mesenteric lymph nodes of rats and mice and diffuse epithelial hyperplasia in the small intestine of male and female mice.
  • [MeSH-minor] Administration, Oral. Animals. Female. Intestinal Neoplasms / chemically induced. Intestinal Neoplasms / pathology. Intestine, Small / drug effects. Intestine, Small / pathology. Liver / drug effects. Liver / pathology. Lymph Nodes / drug effects. Lymph Nodes / pathology. Male. Mice. Mice, Inbred Strains. Mouth Neoplasms / chemically induced. Mouth Neoplasms / pathology. Rats. Rats, Inbred F344. Water Supply

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  • (PMID = 18716633.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromates; 0 / Water Pollutants, Chemical; C9G6VY6ZZ4 / sodium bichromate
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43. Mutanen M, Pajari AM, Paivarinta E, Misikangas M, Rajakangas J, Marttinen M, Oikarinen S: Berries as chemopreventive dietary constituents--a mechanistic approach with the ApcMin/+ mouse. Asia Pac J Clin Nutr; 2008;17 Suppl 1:123-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We wanted to see if pure ellagic acid, natural ellagitannins and three wild berries have any effect on the adenoma formation in Apc- mutated Min/+ mice.
  • Ellagic acid had no effect on the number or size of adenomas in the distal or total small intestine but it increased adenoma size in the duodenum when compared with the control diet (p < 0.05).
  • Neither cloudberry seed nor pulp had any effect on the adenoma formation.
  • [MeSH-major] Adenoma / prevention & control. Cell Transformation, Neoplastic / drug effects. Ellagic Acid / pharmacology. Fruit / chemistry. Hydrolyzable Tannins / pharmacology. Intestinal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / pharmacology. Cyclin D1 / metabolism. Genes, APC. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Mice. Mice, Mutant Strains. Random Allocation. beta Catenin / metabolism

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  • (PMID = 18296318.001).
  • [ISSN] 0964-7058
  • [Journal-full-title] Asia Pacific journal of clinical nutrition
  • [ISO-abbreviation] Asia Pac J Clin Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Hydrolyzable Tannins; 0 / beta Catenin; 0 / ellagitannin; 136601-57-5 / Cyclin D1; 19YRN3ZS9P / Ellagic Acid
  • [Number-of-references] 10
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44. Alferez D, Wilkinson RW, Watkins J, Poulsom R, Mandir N, Wedge SR, Pyrah IT, Smith NR, Jackson L, Ryan AJ, Goodlad RA: Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) mice. Mol Cancer Ther; 2008 Mar;7(3):590-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) mice.
  • Both the epidermal growth factor (EGF) and the vascular endothelial growth factor (VEGF) pathways are associated with intestinal cancer, and therapeutic approaches targeting either EGF receptor (EGFR) or VEGF receptor (VEGFR) signaling have recently been approved for patients with advanced colorectal cancer.
  • The Apc(Min/+) mouse is a well-characterized in vivo model of intestinal tumorigenesis, and animals with this genetic mutation develop macroscopically detectable adenomas from approximately 6 weeks of age.
  • This reduction in both adenoma number and size resulted in a total reduction in tumor burden in the small intestine of nearly 75% in both studies (P < 0.01).
  • Therefore, targeting both VEGFR- and EGFR-dependent signaling may be a beneficial strategy in early intestinal cancer.
  • [MeSH-major] Adenoma / pathology. Genes, APC. Intestinal Neoplasms / pathology. Receptor, Epidermal Growth Factor / metabolism. Receptors, Vascular Endothelial Growth Factor / metabolism. Signal Transduction

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  • (PMID = 18347145.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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45. Korsisaari N, Kasman IM, Forrest WF, Pal N, Bai W, Fuh G, Peale FV, Smits R, Ferrara N: Inhibition of VEGF-A prevents the angiogenic switch and results in increased survival of Apc+/min mice. Proc Natl Acad Sci U S A; 2007 Jun 19;104(25):10625-30
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  • Anti-VEGF-A monoclonal antibodies, in combination with chemotherapy, result in a survival benefit in patients with metastatic colorectal and non-small cell lung cancer, but little is known regarding the impact of anti-VEGF-A therapy on benign or premalignant tumors.
  • The Apc+/min mice have been widely used as a model recapitulating early intestinal adenoma formation.
  • To investigate whether tumor growth in Apc+/min mice is mediated by VEGF-A-dependent angiogenesis, we used two independent approaches to inhibit VEGF-A: monotherapy with a monoclonal antibody (Mab) targeting VEGF-A and genetic deletion of VEGF-A selectively in intestinal epithelial cells.
  • Short-term (3 or 6 weeks) treatment with anti-VEGF-A Mab G6-31 resulted in a nearly complete suppression of adenoma growth throughout the small intestine.
  • Deletion of VEGF-A in intestinal epithelial cells of Apc+/min mice yielded a significant inhibition of tumor growth, albeit of lesser magnitude than that resulting from Mab G6-31 administration.
  • These results establish that inhibition of VEGF-A signaling is sufficient for tumor growth cessation and confers a long-term survival benefit in an intestinal adenoma model.
  • Therefore, VEGF-A inhibition may be a previously uncharacterized strategy for the prevention of the angiogenic switch and growth in intestinal adenomas.
  • [MeSH-minor] Adenoma / blood supply. Adenoma / genetics. Adenoma / immunology. Adenoma / therapy. Animals. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Gene Deletion. In Situ Hybridization. Intestinal Neoplasms / blood supply. Intestinal Neoplasms / genetics. Intestinal Neoplasms / immunology. Intestinal Neoplasms / therapy. Mice. Mice, Inbred C57BL. Signal Transduction / immunology. Survival Analysis. Time Factors

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  • (PMID = 17553957.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC1888576
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46. Phesse TJ, Parry L, Reed KR, Ewan KB, Dale TC, Sansom OJ, Clarke AR: Deficiency of Mbd2 attenuates Wnt signaling. Mol Cell Biol; 2008 Oct;28(19):6094-103
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  • We have previously shown that deficiency of the methyl binding domain protein Mbd2 dramatically reduces adenoma burden on an Apc(Min/+) background.
  • To investigate the mechanism underlying this phenomenon, we have determined the effect of Mbd2 deficiency upon the phenotypes imposed by the conditional deletion of Apc in the small intestine.
  • These results therefore provide a mechanistic basis for the epigenetic control of adenoma formation mediated through Mbd2.

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 18644872.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / G0301154; United Kingdom / Biotechnology and Biological Sciences Research Council / / ; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lect2 protein, mouse; 0 / Mbd2 protein, mouse; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC2547016
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47. Ignatenko NA, Besselsen DG, Roy UK, Stringer DE, Blohm-Mangone KA, Padilla-Torres JL, Guillen-R JM, Gerner EW: Dietary putrescine reduces the intestinal anticarcinogenic activity of sulindac in a murine model of familial adenomatous polyposis. Nutr Cancer; 2006;56(2):172-81
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  • [Title] Dietary putrescine reduces the intestinal anticarcinogenic activity of sulindac in a murine model of familial adenomatous polyposis.
  • Sulindac increased steady-state RNA levels and enzymatic activity of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase and intestinal levels of monoacetylspermidine, spermidine, and spermine in the small intestine of mice.
  • Dietary putrescine increased intestinal putrescine contents, whereas the combination of dietary putrescine and sulindac yielded the highest levels of intestinal putrescine and correlated with a statistically significant reduction in AMD enzyme activity.
  • Dietary putrescine did not statistically significantly increase tumorigenesis, although it significantly increased the grade of adenoma dysplasia (P < 0.05).
  • The effectiveness of sulindac to suppress intestinal carcinogenesis was partially abrogated by dietary putrescine.

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  • (PMID = 17474863.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA072008; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / R01 CA123065; United States / NCI NIH HHS / CA / CA 72008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclooxygenase Inhibitors; 0 / Ornithine Decarboxylase Inhibitors; 0 / Polyamines; 0 / RNA, Messenger; 184SNS8VUH / Sulindac; 2FZ7Y3VOQX / Spermine; EC 4.1.1.17 / Ornithine Decarboxylase; EC 4.1.1.50 / Adenosylmethionine Decarboxylase; U87FK77H25 / Spermidine; V10TVZ52E4 / Putrescine
  • [Other-IDs] NLM/ NIHMS440120; NLM/ PMC4132951
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48. Morton D, Bailey KL, Stout CL, Weaver RJ, White KA, Lorenzen MJ, Ball DJ: N-Methyl-N-Nitrosourea (MNU): A positive control chemical for p53+/- mouse carcinogenicity studies. Toxicol Pathol; 2008 Dec;36(7):926-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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  • Nine males and five females treated with MNU had adenomas or adenocarcinomas of the small intestine, whereas no intestinal neoplasms were observed in control mice.
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / pathology. Adenoma / chemically induced. Adenoma / pathology. Animals. Antigens, CD3 / metabolism. Duodenal Neoplasms / chemically induced. Duodenal Neoplasms / pathology. Female. Genes, p53. Heterozygote. Injections, Intraperitoneal. Intestine, Small / pathology. Jejunal Neoplasms / chemically induced. Jejunal Neoplasms / pathology. Lymphoma / chemically induced. Lymphoma / pathology. Male. Mice. Mice, Knockout. Thymus Gland / pathology. Thymus Neoplasms / chemically induced. Thymus Neoplasms / pathology

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  • (PMID = 18827072.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Carcinogens; 684-93-5 / Methylnitrosourea
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49. van Es JH, van Gijn ME, Riccio O, van den Born M, Vooijs M, Begthel H, Cozijnsen M, Robine S, Winton DJ, Radtke F, Clevers H: Notch/gamma-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells. Nature; 2005 Jun 16;435(7044):959-63
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  • [Title] Notch/gamma-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells.
  • The self-renewing epithelium of the small intestine is ordered into stem/progenitor crypt compartments and differentiated villus compartments.
  • [MeSH-major] Adenoma / pathology. Cell Proliferation / drug effects. Endopeptidases / metabolism. Goblet Cells / cytology. Intestine, Small / cytology. Membrane Proteins / antagonists & inhibitors. Protease Inhibitors / pharmacology


50. Oue N, Mitani Y, Aung PP, Sakakura C, Takeshima Y, Kaneko M, Noguchi T, Nakayama H, Yasui W: Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma. J Pathol; 2005 Oct;207(2):185-98
The Lens. Cited by Patents in .

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  • [Title] Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma.
  • Regenerating islet-derived family, member 4 (Reg IV) is a candidate marker for cancer and inflammatory bowel disease.
  • In the stomach, foveolar epithelium was negative for Reg IV, whereas goblet cells of intestinal metaplasia and neuroendocrine cells at the base of intestinal metaplasia expressed Reg IV.
  • Neuroendocrine cells of the small intestine and colon showed strong expression of Reg IV, whereas goblet cells of the small intestine and colon showed weak or no expression of Reg IV.
  • Among 143 gastric adenocarcinomas, Reg IV expression was detected in 42 (29.4%) and was associated with both the intestinal mucin phenotype and neuroendocrine differentiation.
  • These data suggest that Reg IV is expressed by gastrointestinal and pancreatic tumours, including adenocarcinomas and carcinoid tumours, and that Reg IV is associated with intestinal and neuroendocrine differentiation of the stomach and gastric carcinoma.
  • [MeSH-minor] Adenoma / chemistry. Biomarkers, Tumor / analysis. Blotting, Western / methods. Breast Neoplasms / chemistry. Carcinoid Tumor / chemistry. Cell Differentiation / physiology. Cell Line, Tumor. Colon / metabolism. Colorectal Neoplasms / chemistry. Female. Humans. Immunohistochemistry / methods. Intestine, Small / metabolism. Lung Neoplasms / chemistry. Pancreas / metabolism. Pancreatic Neoplasms / chemistry. Phenotype. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Stomach / metabolism

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16086444.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Neoplasm Proteins; 0 / REG4 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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51. Päivärinta E, Pajari AM, Törrönen R, Mutanen M: Ellagic acid and natural sources of ellagitannins as possible chemopreventive agents against intestinal tumorigenesis in the Min mouse. Nutr Cancer; 2006;54(1):79-83
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ellagic acid and natural sources of ellagitannins as possible chemopreventive agents against intestinal tumorigenesis in the Min mouse.
  • We wanted to see whether pure ellagic acid and natural ellagitannins from cloudberry (Rubus chamaemorus) seed and pulp have any effect on adenoma formation in Apc-mutated Min mice.
  • After the 10-wk feeding period, ellagic acid had no effect on the number or size of adenomas in the distal or total small intestine, but it increased adenoma size in the duodenum when compared with the control diet (1.50+/-0.29 vs. 1.16+/-0.31 mm; P=0.029).
  • Neither cloudberry seed nor pulp diets had any effect on the adenoma formation.
  • [MeSH-major] Adenoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Ellagic Acid / therapeutic use. Hydrolyzable Tannins / therapeutic use. Intestinal Neoplasms / prevention & control

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  • (PMID = 16800775.001).
  • [ISSN] 0163-5581
  • [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 / Anticarcinogenic Agents; 0 / Hydrolyzable Tannins; 19YRN3ZS9P / Ellagic Acid
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52. Selbaková M, Svoboda J, Kutil J, Musilová S, Cízková I, Michal M: [An unusual cause of duodenal obstruction--a case report]. Rozhl Chir; 2007 Jul;86(7):376-8
MedlinePlus Health Information. consumer health - Intestinal Cancer.

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  • A summary of related literature to Brunner's gland adenoma follows.
  • This very rare benign pathology of the small intestine presents itself with no specific clinical symptomatology, often as dyspepsia or ulcerous disease.
  • Diagnosis is based on endoscopy and radiographic methods.
  • [MeSH-major] Adenoma / complications. Brunner Glands. Duodenal Neoplasms / complications. Duodenal Obstruction / etiology

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  • (PMID = 17879716.001).
  • [ISSN] 0035-9351
  • [Journal-full-title] Rozhledy v chirurgii : měsíčník Československé chirurgické společnosti
  • [ISO-abbreviation] Rozhl Chir
  • [Language] cze
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
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53. Shi L, Itoh F, Itoh S, Takahashi S, Yamamoto M, Kato M: Ephrin-A1 promotes the malignant progression of intestinal tumors in Apc(min/+) mice. Oncogene; 2008 May 22;27(23):3265-73
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  • [Title] Ephrin-A1 promotes the malignant progression of intestinal tumors in Apc(min/+) mice.
  • We generated transgenic mice carrying Fabpl(4xat-132) ephrin-A1, which express ephrin-A1 in the intestinal epithelial cells.
  • Those mice were then mated with Apc(min/+) mice to produce the compound mice, which overexpress ephrin-A1 in the intestinal tumors of Apc(min/+) mice.
  • We compared the number, size and histopathological features of the intestinal tumors in the Fabpl(4xat-132) ephrin-A1/Apc(min/+) compound mice with those of the Apc(min/+) mice.
  • The compound mice showed an increased number of intestinal tumors, significantly in the large intestine, and developed more invasive tumors.
  • Among the 20 mice of each type examined, 5 Apc(min/+) mice developed 5 invasive tumors, 1 invasive tumor in each mouse, in the proximal or middle portions of the small intestine.
  • On the other hand, 14 out of 20 compound mice developed 29 invasive tumors and 16 of them were in the distal small intestine and the large intestine, where transgenic ephrin-A1 was highly expressed.
  • These results suggested that the increased expression of ephrin-A1 accelerated the malignant progression of the intestinal adenoma to invasive tumors.
  • [MeSH-major] Adenoma / genetics. Ephrin-A1 / physiology. Genes, APC. Intestinal Neoplasms / genetics
  • [MeSH-minor] Animals. Disease Progression. Fatty Acid-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic / physiology. Humans. Intestinal Mucosa / metabolism. Mice. Mice, Transgenic. Neoplasm Invasiveness. Neoplasms, Multiple Primary / genetics. Recombinant Fusion Proteins / genetics. Tumor Burden / genetics

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  • (PMID = 18246128.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ephrin-A1; 0 / Fabp1 protein, mouse; 0 / Fatty Acid-Binding Proteins; 0 / Recombinant Fusion Proteins
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54. Sakamoto K, Tominaga Y, Yamauchi K, Nakatsu Y, Sakumi K, Yoshiyama K, Egashira A, Kura S, Yao T, Tsuneyoshi M, Maki H, Nakabeppu Y, Tsuzuki T: MUTYH-null mice are susceptible to spontaneous and oxidative stress induced intestinal tumorigenesis. Cancer Res; 2007 Jul 15;67(14):6599-604
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] MUTYH-null mice are susceptible to spontaneous and oxidative stress induced intestinal tumorigenesis.
  • Recently, biallelic germ-line mutations of MUTYH have been found in patients predisposed to a recessive form of hereditary multiple colorectal adenoma and carcinoma with an increased incidence of G:C to T:A somatic mutations in the APC gene.
  • The increased incidence of intestinal tumors in MUTYH-null mice (11 tumors in 10 of 121 mice) was statistically significant compared with the wild type (no intestinal tumors in 109 mice).
  • Two adenomas and seven adenocarcinomas were observed in the small intestines, and two adenomas but no carcinomas were found in the colons.
  • In MUTYH-null mice treated with KBrO(3), the occurrence of small intestinal tumors dramatically increased.
  • The mean number of polyps induced in the small intestines of these mice was 61.88 (males, 72.75; females, 51.00), whereas it was 0.85 (males, 0.50; females, 1.00) in wild-type mice.
  • The tumors developed predominantly in the duodenum and in the upper region of the (jejunum) small intestines.
  • We conclude that MUTYH suppresses spontaneous tumorigenesis in mammals, thus providing experimental evidence for the association between biallelic germ-line MUTYH mutations and a recessive form of human hereditary colorectal adenoma and carcinoma.
  • [MeSH-major] DNA Glycosylases / genetics. DNA Glycosylases / physiology. Genetic Predisposition to Disease. Intestinal Neoplasms / genetics
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Animals. Carcinoma / genetics. Carcinoma / metabolism. Female. Humans. Intestine, Small / metabolism. Male. Mice. Mice, Transgenic. Mutation. Oxidative Stress

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  • (PMID = 17638869.001).
  • [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] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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55. Milicic A, Harrison LA, Goodlad RA, Hardy RG, Nicholson AM, Presz M, Sieber O, Santander S, Pringle JH, Mandir N, East P, Obszynska J, Sanders S, Piazuelo E, Shaw J, Harrison R, Tomlinson IP, McDonald SA, Wright NA, Jankowski JA: Ectopic expression of P-cadherin correlates with promoter hypomethylation early in colorectal carcinogenesis and enhanced intestinal crypt fission in vivo. Cancer Res; 2008 Oct 1;68(19):7760-8
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] Ectopic expression of P-cadherin correlates with promoter hypomethylation early in colorectal carcinogenesis and enhanced intestinal crypt fission in vivo.
  • P-cadherin is normally expressed in the basal layer of squamous epithelia and absent from the healthy intestine and colon.
  • We have previously shown it to be expressed in all inflamed, hyperplastic, and dysplastic intestinal and colonic mucosa.
  • This study aimed to better understand the mechanisms controlling the expression of P-cadherin and the biological effects of its ectopic presence in the intestine and colon.
  • We then created transgenic mice that overexpressed P-cadherin specifically in the intestinal and colonic epithelium under the liver fatty acid binding protein promoter.
  • Forced ectopic expression of P-cadherin accompanied by indomethacin-induced inflammation resulted in a 3-fold higher crypt fission rate within the small and large intestines in the homozygous mice compared with the wild-type animals (P < 0.02).
  • We conclude that epigenetic demethylation of the P-cadherin promoter in the human intestine permits its ectopic expression very early in the colorectal adenoma-carcinoma sequence and persists during invasive cancer.

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  • (PMID = 18829530.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / A4584; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins
  • [Other-IDs] NLM/ PMC2561210; NLM/ UKMS2285
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56. Markova M, Koratkar RA, Silverman KA, Sollars VE, MacPhee-Pellini M, Walters R, Palazzo JP, Buchberg AM, Siracusa LD, Farber SA: Diversity in secreted PLA2-IIA activity among inbred mouse strains that are resistant or susceptible to Apc Min/+ tumorigenesis. Oncogene; 2005 Sep 22;24(42):6450-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The secreted phospholipase A2 type IIA (Pla2g2a) gene was previously identified as a modifier of intestinal adenoma multiplicity in Apc Min/+ mice.
  • To determine if intestinal secreted phospholipase A2 (sPLA2) activity was also attenuated in susceptible strains, we developed a sensitive assay to directly quantitate sPLA2 activity in the murine intestinal tract utilizing a fluorescent BODIPY-labeled phospholipid substrate.
  • Here, we report assay conditions that distinguish between secreted and cytosolic PLA2 enzyme activities in extracts of intestinal tissue.
  • The small intestine exhibited higher activity levels than the large intestine.
  • Consistent with predictions from the sPLA2-IIA gene sequence in inbred strains, we detected low levels of enzyme activity in inbred strains containing sPLA2-IIA mutations; these strains were also associated with greater numbers of intestinal polyps.
  • Immunohistochemical analyses of intestinal tissues were consistent with sPLA2-IIA activity levels.
  • This approach enables further studies of the mechanisms of sPLA2 action influencing the development and tumorigenesis of the small intestine and colon in both mice and humans.
  • [MeSH-minor] Amino Acid Sequence. Animals. Boron Compounds. Group II Phospholipases A2. Immunohistochemistry. Intestinal Neoplasms / enzymology. Intestine, Large / enzymology. Intestine, Small / enzymology. Mice. Mice, Inbred Strains. Molecular Sequence Data. Molecular Weight. Phospholipases A2. Sequence Homology, Amino Acid. Species Specificity

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  • (PMID = 16007193.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA72027; United States / NCI NIH HHS / CA / R01 CA89560; United States / NIDDK NIH HHS / DK / R01 DK060369
  • [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] England
  • [Chemical-registry-number] 0 / 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene; 0 / Boron Compounds; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Group II Phospholipases A2; EC 3.1.1.4 / Phospholipases A2; EC 3.1.1.4 / Pla2g2a protein, mouse
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57. Hata K, Tanaka T, Kohno H, Suzuki R, Qiang SH, Yamada Y, Oyama T, Kuno T, Hirose Y, Hara A, Mori H: beta-Catenin-accumulated crypts in the colonic mucosa of juvenile ApcMin/+ mice. Cancer Lett; 2006 Jul 28;239(1):123-8
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • Although Apc(Min/+) mice are widely used for an animal model of human familial adenomatous polyposis (FAP), a majority of intestinal polyps locate in the small intestine.
  • We recently reported that numerous beta-catenin-accumulated crypts (BCAC), which are reliable precursor lesions for colonic adenocarcinoma, develop in the large bowel of aged Apc(Min/+) mice.
  • In this study, we determined the presence and location of BCAC in the large intestine of juvenile Apc(Min/+) mice (3 and 5 weeks of age).
  • [MeSH-major] Adenoma / metabolism. Adenomatous Polyposis Coli / metabolism. Colon / metabolism. Colonic Neoplasms / metabolism. Intestinal Mucosa / metabolism. beta Catenin / metabolism

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  • (PMID = 16168560.001).
  • [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 / beta Catenin
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58. Sadakata H, Okazawa H, Sato T, Supriatna Y, Ohnishi H, Kusakari S, Murata Y, Ito T, Nishiyama U, Minegishi T, Harada A, Matozaki T: SAP-1 is a microvillus-specific protein tyrosine phosphatase that modulates intestinal tumorigenesis. Genes Cells; 2009 Mar;14(3):295-308
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

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  • [Title] SAP-1 is a microvillus-specific protein tyrosine phosphatase that modulates intestinal tumorigenesis.
  • The expression of SAP-1 in mouse intestine is minimal during embryonic development but increases markedly after birth.
  • SAP-1-deficient mice manifested no marked changes in morphology of the intestinal epithelium.
  • These results thus suggest that SAP-1 is a microvillus-specific RPTP that regulates intestinal tumorigenesis.
  • [MeSH-major] Adenoma / metabolism. Intestinal Neoplasms / metabolism. Intestine, Small / metabolism. Microvilli / metabolism. Receptor-Like Protein Tyrosine Phosphatases, Class 3 / metabolism


59. National Toxicology Program: Toxicology and carcinogenesis studies of methylene blue trihydrate (Cas No. 7220-79-3) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2008 May;(540):1-224
Hazardous Substances Data Bank. METHYLENE BLUE .

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  • The incidences of pancreatic islet cell adenoma and adenoma or carcinoma (combined) were increased in all dosed groups of males, were significantly increased in 25 mg/kg males, and exceeded the historical range in controls (all routes).
  • The incidences of carcinoma and of adenoma or carcinoma (combined) of the small intestine occurred with a positive trend in males.
  • [MeSH-minor] Administration, Oral. Anemia / chemically induced. Anemia / pathology. Animals. Body Weight / drug effects. CHO Cells. Chromosome Aberrations / chemically induced. Cricetinae. Cricetulus. DNA Damage. Female. Intestinal Neoplasms / chemically induced. Intestinal Neoplasms / pathology. Intestine, Small / drug effects. Intestine, Small / pathology. Islets of Langerhans / drug effects. Islets of Langerhans / pathology. Lymphoma / chemically induced. Lymphoma / pathology. Male. Methemoglobinemia / chemically induced. Methemoglobinemia / pathology. Mice. Mice, Inbred Strains. Pancreatic Neoplasms / chemically induced. Pancreatic Neoplasms / pathology. Rats. Rats, Inbred F344. Sister Chromatid Exchange / drug effects

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  • (PMID = 18685714.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Mutagens; T42P99266K / Methylene Blue
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60. Hu R, Khor TO, Shen G, Jeong WS, Hebbar V, Chen C, Xu C, Reddy B, Chada K, Kong AN: Cancer chemoprevention of intestinal polyposis in ApcMin/+ mice by sulforaphane, a natural product derived from cruciferous vegetable. Carcinogenesis; 2006 Oct;27(10):2038-46
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer chemoprevention of intestinal polyposis in ApcMin/+ mice by sulforaphane, a natural product derived from cruciferous vegetable.
  • Our results clearly demonstrated that ApcMin/+ mice fed with SFN-supplemented diet developed significantly less and smaller polyps with higher apoptotic and lower proliferative indices in their small intestine, in a SFN dose-dependent manner.
  • Measurement of SFN and its metabolite SFN-GSH in the small intestine using LC-MS indicates that the concentrations between 3 and 30 nmol/g are required to prevent, or retard adenoma formation in the gastrointestinal tract of ApcMin/+ mice.
  • [MeSH-major] Anticarcinogenic Agents / administration & dosage. Colorectal Neoplasms / prevention & control. Genes, APC. Intestinal Polyps / drug therapy. Thiocyanates / administration & dosage
  • [MeSH-minor] Adenoma / prevention & control. Animals. Cell Proliferation / drug effects. Codon, Nonsense. Extracellular Signal-Regulated MAP Kinases / metabolism. Isothiocyanates. MAP Kinase Signaling System / drug effects. Mice


61. Greenspan EJ, Nichols FC, Rosenberg DW: Molecular alterations associated with sulindac-resistant colon tumors in ApcMin/+ mice. Cancer Prev Res (Phila); 2010 Sep;3(9):1187-97
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • As expected, in the small intestine, sulindac significantly reduced tumor size and multiplicity relative to untreated controls (average of 2.3 versus 42.0 tumors per mouse, respectively; P < 0.0001).
  • Generation of a panel of prostanoids was comparably suppressed in the small intestine and colon by sulindac treatment.

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  • (PMID = 20716632.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA114635-01A2; United States / NCI NIH HHS / CA / 5R01CA114635; United States / NCI NIH HHS / CA / R01 CA114635-01A2; United States / NCI NIH HHS / CA / R01 CA125691; United States / NCI NIH HHS / CA / R01 CA114635; United States / NCI NIH HHS / CA / R01 CA125691-01A2; United States / NCI NIH HHS / CA / CA125691-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 184SNS8VUH / Sulindac
  • [Other-IDs] NLM/ NIHMS202345; NLM/ PMC2933289
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62. Zhu L, Gibson P, Currle DS, Tong Y, Richardson RJ, Bayazitov IT, Poppleton H, Zakharenko S, Ellison DW, Gilbertson RJ: Prominin 1 marks intestinal stem cells that are susceptible to neoplastic transformation. Nature; 2009 Jan 29;457(7229):603-7
The Lens. Cited by Patents in .

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  • [Title] Prominin 1 marks intestinal stem cells that are susceptible to neoplastic transformation.
  • Lineage-tracing studies of adult Prom1(+/C-L) mice containing the Rosa26-YFP reporter allele showed that Prom1(+) cells are located at the base of crypts in the small intestine, co-express Lgr5 (ref.
  • 2), generate the entire intestinal epithelium, and are therefore the small intestinal stem cell.
  • Prom1 was reported recently to mark cancer stem cells of human intestinal tumours that arise frequently as a consequence of aberrant wingless (Wnt) signalling.
  • Lineage tracing demonstrated that the progeny of these cells replaced the mucosa of the entire small intestine with neoplastic tissue that was characterized by focal high-grade intraepithelial neoplasia and crypt adenoma formation.
  • Our data indicate that Prom1 marks stem cells in the adult small intestine that are susceptible to transformation into tumours retaining a fraction of mutant Prom1(+) tumour cells.

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  • (PMID = 19092805.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA129541; United States / NIMH NIH HHS / MH / R01 MH079079-03; United States / NCI NIH HHS / CA / R01CA129541; United States / NCI NIH HHS / CA / P01 CA096832-01A10003; United States / NCI NIH HHS / CA / P01CA96832; United States / NCI NIH HHS / CA / R01 CA129541-02; United States / NCI NIH HHS / CA / P30CA021765; United States / NIMH NIH HHS / MH / R01 MH079079-05; United States / NCI NIH HHS / CA / R01 CA129541-01; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIMH NIH HHS / MH / R01 MH079079; United States / NIMH NIH HHS / MH / R01 MH079079-02; United States / NIMH NIH HHS / MH / R01 MH079079-01A2; United States / NCI NIH HHS / CA / P01 CA096832; United States / NCI NIH HHS / CA / CA096832-01A10003; United States / NIMH NIH HHS / MH / R01 MH079079-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers; 0 / CTNNB1 protein, mouse; 0 / Glycoproteins; 0 / Lgr5 protein, mouse; 0 / Peptides; 0 / Receptors, G-Protein-Coupled; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ NIHMS75275; NLM/ PMC2633030
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63. Hu Y, Lu X, Luo G: Effect of Recql5 deficiency on the intestinal tumor susceptibility of Apc(min) mice. World J Gastroenterol; 2010 Mar 28;16(12):1482-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of Recql5 deficiency on the intestinal tumor susceptibility of Apc(min) mice.
  • RESULTS: Recql5 deficiency in Apc(min/+) mice resulted in a significant increase in the tumor incidence in both the colon (P = 0.0162) and the small intestine (P < 0.01).

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  • (PMID = 20333788.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA103736; United States / NCI NIH HHS / CA / R01 CA88939
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 3.6.4.12 / RecQ Helicases; EC 5.99.- / Recql5 protein, mouse
  • [Other-IDs] NLM/ PMC2846253
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64. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • At present, it is unknown at which stage FDG accumulation occurs during the adenoma carcinoma sequence.
  • 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.
  • The [(18)F]FDG accumulation in small intestine carcinomas was well beyond background accumulation (P<.0001).
  • On PET scanning, two rats showed focal accumulation of the abdominal area, corresponding to small intestine carcinomas.
  • CONCLUSION: Adenocarcinomas had a significantly higher [(18)F]FDG uptake than background bowel uptake.

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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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65. Caldwell GM, Jones CE, Taniere P, Warrack R, Soon Y, Matthews GM, Morton DG: The Wnt antagonist sFRP1 is downregulated in premalignant large bowel adenomas. Br J Cancer; 2006 Mar 27;94(6):922-7
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Wnt antagonist sFRP1 is downregulated in premalignant large bowel adenomas.
  • In this study, we set out to investigate the relationship between sFRP1 expression and large bowel adenomas, a precursor of colorectal cancer.
  • Lithium treatment of a small bowel mucosal cell line (FHs 74 int) induced sFRP1 within 8 h, indicating that this gene is positively regulated by beta-catenin, contrasting with the suppression of sFRP1 expression, we saw previously in advanced colorectal cancers.
  • We therefore investigated a series of 12 adenomas and matched large bowel mucosa samples.
  • Immunohistochemical analysis using a polyclonal antibody supported these findings, with sFRP1 expression reduced in many of the adenoma samples examined. sFRP1 staining in normal mucosa adjacent to the dysplastic tissue was also reduced compared with the normal controls, suggesting that sFRP1 expression may be suppressed in a field of mucosa rather than in individual cells.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Intercellular Signaling Peptides and Proteins / biosynthesis. Membrane Proteins / biosynthesis
  • [MeSH-minor] Cell Transformation, Neoplastic. Chemoprevention. DNA Methylation. Down-Regulation. Humans. Immunohistochemistry. Intestinal Mucosa. Intestine, Large / physiology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured. Wnt Proteins / physiology

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  • (PMID = 16523202.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / SFRP1 protein, human; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC2361362
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66. Andreu P, Peignon G, Slomianny C, Taketo MM, Colnot S, Robine S, Lamarque D, Laurent-Puig P, Perret C, Romagnolo B: A genetic study of the role of the Wnt/beta-catenin signalling in Paneth cell differentiation. Dev Biol; 2008 Dec 15;324(2):288-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Wnt/beta-catenin signalling plays a key role in the homeostasis of the intestinal epithelium.
  • We demonstrated that acute activation of Wnt/beta-catenin signalling induces de novo specification of Paneth cells in both the small intestine and colon and that colon cancers resulting from Apc mutations expressed many genes involved in Paneth cell differentiation.
  • [MeSH-minor] Adenoma / genetics. Animals. Cell Lineage. Cell Proliferation. Colorectal Neoplasms / genetics. Gene Deletion. Gene Dosage. Gene Expression Profiling. Gene Expression Regulation. Genes, APC. Humans. Mice. Mutation

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  • (PMID = 18948094.001).
  • [ISSN] 1095-564X
  • [Journal-full-title] Developmental biology
  • [ISO-abbreviation] Dev. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
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67. Goodlad RA, Ryan AJ, Wedge SR, Pyrah IT, Alferez D, Poulsom R, Smith NR, Mandir N, Watkins AJ, Wilkinson RW: Inhibiting vascular endothelial growth factor receptor-2 signaling reduces tumor burden in the ApcMin/+ mouse model of early intestinal cancer. Carcinogenesis; 2006 Oct;27(10):2133-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibiting vascular endothelial growth factor receptor-2 signaling reduces tumor burden in the ApcMin/+ mouse model of early intestinal cancer.
  • The Apc(Min/+) mouse model is a clinically relevant model of early intestinal cancer.
  • We used AZD2171, an oral, highly potent and selective vascular endothelial growth factor (VEGF) signaling inhibitor, to investigate the role of VEGF receptor-2 (VEGFR-2) signaling in adenoma development and growth in Apc(Min/+) mice.
  • In the early-intervention study, AZD2171 reduced the number of macroscopic polyps in the small bowel and colon.
  • Macropolyp diameter was lower in the small bowel, but remained unchanged in the colon.
  • In animals receiving AZD2171, microscopic evaluation of the small intestine showed a significant reduction in the number of larger lesions.
  • In the late-intervention study, AZD2171 treatment reduced macropolyp diameter (but not number) in the small intestine.
  • Microscopic analysis revealed that AZD2171 significantly reduced the number of larger micropolyps in the small bowel, with no large micropolyps present in the colon.
  • AZD2171 treatment had no effect on microvessel density or localization of beta-catenin staining in adenomas or non-tumor intestinal tissue, but significantly reduced the number of cells expressing VEGFR-2 mRNA.
  • In conclusion, the effects of AZD2171 in the small intestine of Apc(Min/+) mice are consistent with an antiangiogenic mechanism of action, limiting growth of adenomas to < or =1 mm.
  • These data also suggest that an early step in adenoma development may depend on VEGFR-2 signaling.
  • Together, these results indicate that VEGFR-2 signaling may play key roles in the development and progression of intestinal adenomas.
  • [MeSH-major] Adenoma / prevention & control. Genes, APC / physiology. Intestinal Neoplasms / prevention & control. Intestinal Polyps / drug therapy. Quinazolines / therapeutic use. Signal Transduction / drug effects. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors

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  • (PMID = 16782971.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Quinazolines; 0 / RNA, Messenger; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; NQU9IPY4K9 / cediranib
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68. Nakanishi M, Montrose DC, Clark P, Nambiar PR, Belinsky GS, Claffey KP, Xu D, Rosenberg DW: Genetic deletion of mPGES-1 suppresses intestinal tumorigenesis. Cancer Res; 2008 May 1;68(9):3251-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic deletion of mPGES-1 suppresses intestinal tumorigenesis.
  • In the present study, we evaluated the chemopreventive efficacy of targeting the terminal synthase microsomal PGE(2) synthase 1 (mPGES-1), which is responsible for generating PGE(2), in two murine models of intestinal cancer.
  • We report for the first time that genetic deletion of mPGES-1 in Apc-mutant mice results in marked and persistent suppression of intestinal cancer growth by 66%, whereas suppression of large adenomas (>3 mm) was almost 95%.
  • [MeSH-major] Adenoma / genetics. Gene Deletion. Intestinal Neoplasms / genetics. Intramolecular Oxidoreductases / genetics
  • [MeSH-minor] Animals. Cell Proliferation. Dinoprostone / metabolism. Disease Progression. Female. Homozygote. Intestinal Polyps / genetics. Intestinal Polyps / metabolism. Intestinal Polyps / pathology. Intestine, Small / blood supply. Intestine, Small / metabolism. Isoenzymes / genetics. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Protein Transport. beta Catenin / metabolism

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  • (PMID = 18451151.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-114635
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / beta Catenin; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.3 / prostaglandin-E synthase; K7Q1JQR04M / Dinoprostone
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69. Roy HK, Kim YL, Wali RK, Liu Y, Koetsier J, Kunte DP, Goldberg MJ, Backman V: Spectral markers in preneoplastic intestinal mucosa: an accurate predictor of tumor risk in the MIN mouse. Cancer Epidemiol Biomarkers Prev; 2005 Jul;14(7):1639-45
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  • [Title] Spectral markers in preneoplastic intestinal mucosa: an accurate predictor of tumor risk in the MIN mouse.
  • METHODS: We used the MIN mouse, a model whose germ line adenomatous polyposis coli truncation leads to spontaneous intestinal tumorigenesis, thus replicating the human syndrome, familial adenomatous polyposis.
  • Additionally, these markers spatially correlated with future adenoma development (small intestine > colon).
  • CONCLUSIONS: We report, for the first time, that spectral markers, assayed by four-dimensional ELF, were able to sensitively identify a genetic predisposition for intestinal tumorigenesis before the occurrence of phenotypic manifestations.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Intestinal Mucosa / metabolism

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  • (PMID = 16030095.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R21CA102750-01; United States / NCI NIH HHS / CA / 1RO3CA10549-01; United States / NCI NIH HHS / CA / 1U01CA11125-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib
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70. Camargo FD, Gokhale S, Johnnidis JB, Fu D, Bell GW, Jaenisch R, Brummelkamp TR: YAP1 increases organ size and expands undifferentiated progenitor cells. Curr Biol; 2007 Dec 4;17(23):2054-60
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 the intestine, expression of endogenous YAP1 is restricted to the progenitor/stem cell compartment, and activation of YAP1 expands multipotent undifferentiated progenitor cells, which differentiate upon cessation of YAP1 expression.
  • YAP1 stimulates Notch signaling, and administration of gamma-secretase inhibitors suppressed the intestinal dysplasia caused by YAP1.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Cell Proliferation. Intestine, Small / cytology. Liver / anatomy & histology. Phosphoproteins / metabolism. Stem Cells / cytology
  • [MeSH-minor] Adenoma / metabolism. Animals. Cell Differentiation. Colorectal Neoplasms / metabolism. Humans. Mice. Mice, Transgenic. Oligonucleotide Array Sequence Analysis. Organ Size. Signal Transduction


71. Rajakangas J, Misikangas M, Päivärinta E, Mutanen M: Chemoprevention by white currant is mediated by the reduction of nuclear beta-catenin and NF-kappaB levels in Min mice adenomas. Eur J Nutr; 2008 Apr;47(3):115-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIMS OF THE STUDY: To study if white currant is chemopreventive in an experimental model for intestinal tumorigenesis and further study the effects on beta-catenin and NF-kappaB signaling pathways.
  • METHODS: Multiple intestinal neoplasia (Min) mice were fed an AIN-93G based control diet or a diet containing 10% freeze dried white currant (Ribes x pallidum) for 10 weeks.
  • Cell signaling parameters were analysed from intestinal adenomas and surrounding mucosa by Western blotting and immunohistochemistry.
  • RESULTS: The white currant diet reduced the number of adenomas from 81 (min-max 47-114) to 51 (36-84) in the total small intestine of Min mice (P<0.02).
  • Most of the adenomas develop in the distal part of the small intestine, and in this area white currant reduced the number from 49 to 29.5 (P<0.01) and also the size of the adenomas from 0.88 mm to 0.70 mm (P<0.02).
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents, Phytogenic / pharmacology. Fruit / chemistry. Intestinal Mucosa / pathology. Intestinal Neoplasms / prevention & control. NF-kappa B / metabolism. beta Catenin / metabolism

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  • (PMID = 18389329.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / beta Catenin
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72. Hariri LP, Tumlinson AR, Wade NH, Besselsen DG, Utzinger U, Gerner EW, Barton JK: Ex vivo optical coherence tomography and laser-induced fluorescence spectroscopy imaging of murine gastrointestinal tract. Comp Med; 2007 Apr;57(2):175-85
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  • In this study, we combined the 2 modalities to survey the GI tract of a variety of mouse strains and ages and to sample dysplasias and inflammatory bowel disease (IBD) of the intestines.
  • Histology was used to classify tissue regions as normal, Peyer patch, dysplasia, adenoma, or IBD.

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  • (PMID = 17536618.001).
  • [ISSN] 1532-0820
  • [Journal-full-title] Comparative medicine
  • [ISO-abbreviation] Comp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109385; United States / NIAID NIH HHS / AI / SWAIR-CA83148
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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73. Genander M, Halford MM, Xu NJ, Eriksson M, Yu Z, Qiu Z, Martling A, Greicius G, Thakar S, Catchpole T, Chumley MJ, Zdunek S, Wang C, Holm T, Goff SP, Pettersson S, Pestell RG, Henkemeyer M, Frisén J: Dissociation of EphB2 signaling pathways mediating progenitor cell proliferation and tumor suppression. Cell; 2009 Nov 13;139(4):679-92
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

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  • EphB receptors represent a rare exception; they promote cell proliferation in the intestinal epithelium and function as tumor suppressors by controlling cell migration and inhibiting invasive growth.
  • Cyclin D1 regulation becomes uncoupled from EphB signaling during the progression from adenoma to colon carcinoma in humans, allowing continued proliferation with invasive growth.
  • The dissociation of EphB2 signaling pathways enables the selective inhibition of the mitogenic effect without affecting the tumor suppressor function and identifies a pharmacological strategy to suppress adenoma growth.

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  • (PMID = 19914164.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075503; United States / NCI NIH HHS / CA / P30CA56036; United States / NCI NIH HHS / CA / R01CA75503; United States / NIMH NIH HHS / MH / MH066332-07; United States / NCI NIH HHS / CA / R01 CA070896; United States / NIMH NIH HHS / MH / 2R01 MH66332; United States / NIMH NIH HHS / MH / R01 MH066332-07; United States / NCI NIH HHS / CA / R01CA70896; United States / NIMH NIH HHS / MH / R01 MH066332; United States / NCI NIH HHS / CA / R01CA86072; United States / NCI NIH HHS / CA / R01 CA086072; United States / NCI NIH HHS / CA / P30 CA056036
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / Ccnd1 protein, mouse; 136601-57-5 / Cyclin D1; EC 2.7.10.1 / Receptor, EphB2
  • [Other-IDs] NLM/ NIHMS160201; NLM/ PMC2786256
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74. Schmelz EM, Xu H, Sengupta R, Du J, Banerjee S, Sarkar FH, Rishi AK, Majumdar AP: Regression of early and intermediate stages of colon cancer by targeting multiple members of the EGFR family with EGFR-related protein. Cancer Res; 2007 Jun 1;67(11):5389-96
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • In the present study, we evaluated the therapeutic effectiveness of ERRP on early and intermediate stages of colon cancer by examining regression of chemically induced aberrant crypt foci (ACF) in the colon of CF1 mice and intestinal adenomas in APC(Min+/-) (Min) mice.
  • In Min mice, ERRP caused the regression of adenomas throughout the small intestine (P < 0.05) and reduced their size (P < 0.001).
  • This could partly be attributed to inhibition of proliferation and stimulation of apoptosis in the intestinal mucosa and was associated with decreased activation of several EGFR family members, suppression of downstream effector nuclear factor kappaB and down-regulation of cyclooxygenase-2.
  • In conclusion, our data show that ERRP is effective in regressing both early and intermediate intestinal lesions and could be an effective therapeutic agent for colon cancer.
  • [MeSH-minor] 1,2-Dimethylhydrazine. Adenoma / chemically induced. Adenoma / drug therapy. Adenoma / metabolism. Adenoma / pathology. Animals. Apoptosis / drug effects. Carcinogens. Cell Growth Processes / drug effects. Female. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Male. Mice. Mice, Inbred C57BL. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Neoplasm Staging. Precancerous Conditions / chemically induced. Precancerous Conditions / drug therapy. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Receptors, Estrogen / genetics. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / pharmacology. Transforming Growth Factor alpha / metabolism

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  • (PMID = 17545620.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG014343
  • [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 / Carcinogens; 0 / Drosophila Proteins; 0 / ERR protein, Drosophila; 0 / NF-kappa B; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; IX068S9745 / 1,2-Dimethylhydrazine
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79. Naishiro Y, Yamada T, Idogawa M, Honda K, Takada M, Kondo T, Imai K, Hirohashi S: Morphological and transcriptional responses of untransformed intestinal epithelial cells to an oncogenic beta-catenin protein. Oncogene; 2005 Apr 28;24(19):3141-53
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morphological and transcriptional responses of untransformed intestinal epithelial cells to an oncogenic beta-catenin protein.
  • Aberrant transactivation of a certain set of target genes by the beta-catenin and T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factor complexes has been implicated in the process of intestinal epithelial cells entering early colorectal carcinogenesis.
  • A rat intestinal epithelial cell line IEC6 became elongated, extended protrusions at cell periphery, and increased stress fibers and focal contacts upon the induction of beta-catenin protein stabilized by deletion of the N-terminal glycogen synthase kinase-3beta (GSKbeta) phosphorylation sites (beta-catenin DeltaN89).
  • [MeSH-minor] Adenoma / metabolism. Animals. Cell Adhesion. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cells, Cultured. Chromatin Immunoprecipitation. Colon / metabolism. Colorectal Neoplasms / metabolism. DNA-Binding Proteins / metabolism. Extracellular Matrix / metabolism. Genes, Reporter. Glycogen Synthase Kinase 3 / metabolism. HeLa Cells. Humans. Immunohistochemistry. Intercellular Signaling Peptides and Proteins / metabolism. Intestine, Small / metabolism. Luciferases / metabolism. Lymphoid Enhancer-Binding Factor 1. Male. Mice. Mice, Inbred C57BL. Microscopy, Fluorescence. Oligonucleotide Array Sequence Analysis. Protein Structure, Tertiary. Rats. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Time Factors. Transcription Factors / metabolism. Wnt Proteins. beta Catenin

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  • (PMID = 15735679.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Ctnnb1 protein, rat; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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80. Becker L, Huang Q, Mashimo H: Immunostaining of Lgr5, an intestinal stem cell marker, in normal and premalignant human gastrointestinal tissue. ScientificWorldJournal; 2008 Nov 23;8:1168-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunostaining of Lgr5, an intestinal stem cell marker, in normal and premalignant human gastrointestinal tissue.
  • Lgr5 has recently been identified as a murine marker of intestinal stem cells.
  • Using standard immunostaining, we compared expression of Lgr5 in normal colon and small intestine vs. small intestinal and colonic adenomas and Barrett's esophagus.
  • Our findings suggest that (1) Lgr5 is a potential marker of intestinal stem cells in humans and (2) loss of restriction to the stem cell niche is an early event in the premalignant transformation of stem cells and may play a role in carcinogenesis.
  • [MeSH-minor] AC133 Antigen. Adenoma / metabolism. Antigens, CD / metabolism. Biomarkers / metabolism. Glycoproteins / metabolism. Humans. Immunohistochemistry. Peptides / metabolism

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  • (PMID = 19030762.001).
  • [ISSN] 1537-744X
  • [Journal-full-title] TheScientificWorldJournal
  • [ISO-abbreviation] ScientificWorldJournal
  • [Language] eng
  • [Grant] United States / BLRD VA / BX / I01 BX000663; United States / NIDDK NIH HHS / DK / T32 DK 07760
  • [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 / AC133 Antigen; 0 / Antigens, CD; 0 / Biomarkers; 0 / Glycoproteins; 0 / LGR5 protein, human; 0 / PROM1 protein, human; 0 / Peptides; 0 / Prom1 protein, mouse; 0 / Receptors, G-Protein-Coupled
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81. Chen X, Ehrhardt WM, Halberg RB, Aronow BJ, Dove WF: Cellular expression patterns of genes upregulated in murine and human colonic neoplasms. J Histochem Cytochem; 2008 May;56(5):433-41
The Lens. Cited by Patents in .

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  • Markers overexpressed in colonic tumors of the multiple intestinal neoplasia (Min) mouse have been recently identified by cDNA subtractive hybridization and by microarray analysis.
  • The second class of markers shows elevated expression in neoplastic cells and also in the postmitotic Paneth cells of the small intestine.
  • Finally, the third class of marker shows detectable intestinal expression only within tumors but not in the normal intestinal epithelium.
  • Deficiency for the tumor-associated glycoprotein clusterin does not affect the multiplicity or growth rate of intestinal tumors in Min mice.

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  • (PMID = 18180384.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R37 CA063677; United States / NCI NIH HHS / CA / U01 CA084227; United States / NCI NIH HHS / CA / R37-CA63677; United States / NCI NIH HHS / CA / U01-CA84227
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Clusterin
  • [Other-IDs] NLM/ PMC2324186
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82. Thomson M, Venkatesh K, Elmalik K, van der Veer W, Jaacobs M: Double balloon enteroscopy in children: diagnosis, treatment, and safety. World J Gastroenterol; 2010 Jan 7;16(1):56-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Double balloon enteroscopy in children: diagnosis, treatment, and safety.
  • AIM: To assess the feasibility and utility of double balloon enteroscopy (DBE) in the management of small bowel diseases in children.
  • RESULTS: The entire small bowel was examined in 6 patients, and a length between 200 cm and 320 cm distal to pylorus in the remaining 8.
  • Polyps were detected and successfully removed in all 5 patients with PJ syndrome, in a patient with tubulo-villous adenoma of the duodenum, in a patient with significant anemia and occult bleeding, and in a patient with Cowden's syndrome.
  • A diagnosis was made in a patient with multiple angiomata not amenable to endotherapy, and in 1 with a discrete angioma which was treated with argon plasma coagulation.
  • CONCLUSION: Double balloon enteroscopy can be a useful diagnostic and therapeutic tool for small bowel disease in children, allowing endo-therapeutic intervention beyond the reach of the conventional endoscope.
  • [MeSH-major] Endoscopy, Gastrointestinal / methods. Intestinal Diseases / diagnosis. Intestinal Diseases / therapy. Intestine, Small / pathology

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  • (PMID = 20039449.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2799917
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83. Xu L, Zhong F, Guo FF, Zhao WJ, Sun XR, Wei XF: [Expression of motilin and its precursor mRNA in normal parenchyma, benign and malignant tumors of human thyroid]. Zhonghua Bing Li Xue Za Zhi; 2008 Apr;37(4):243-9
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  • METHODS: RT-PCR, Southern blot and molecular cloning were used to detect motilin transcript expression in human thyroid and mucous membrane of small intestine.
  • Real-time PCR and immunohistochemical techniques were used to quantify motilin precursor mRNA and motilin peptide in thyroid tissue samples including adenoma, medullary carcinoma, follicular carcinoma, papillary carcinoma and nodular goiter. RESULTS:.
  • Thyroid tumors (acidophilic adenoma, medullary carcinoma, follicular carcinoma, papillary carcinoma and nodular goiter) showed intense and diffuse immunostaining for motilin peptide.
  • Moreover, the expression of motilin and its precursor mRNA in thyroid medullar carcinoma and acidophilic adenoma were significantly higher than those of normal thyroid tissue (P < 0.05).
  • The expressions of both motilin and its precursor mRNA in thyroid medullary carcinoma and acidophilic adenoma are significantly increased.
  • Motilin may be involved in the pathogenesis of medullary carcinoma and acidophilic adenoma of the thyroid.

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  • (PMID = 18844033.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA Precursors; 0 / RNA, Messenger; 52906-92-0 / Motilin
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84. National Toxicology Program: NTP Toxicology and carcinogenesis studies of bromodichloromethane (CAS No. 75-27-4) in male F344/N rats and female B6C3F1 mice (Drinking Water Studies). Natl Toxicol Program Tech Rep Ser; 2006 Feb;(532):1-248
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  • Bromodichloromethane has been shown to be carcinogenic at multiple sites in rats (large intestine and kidney) and in mice (liver and kidney) after administration by gavage in corn oil.
  • The incidences of hepatocellular adenoma or carcinoma (combined) occurred with a negative trend, and the incidence in the 700 mg/L group was significantly decreased relative to the control group.
  • In cytogenetic tests with cultured Chinese hamster ovary cells, bromodichloromethane induced a small increase in sister chromatid exchanges (SCEs) in one of four trials conducted in the presence of induced rat liver S9 enzymes; no significant increase in SCEs occurred without S9, and no induction of chromosomal aberrations occurred in bromodichloromethane-treated Chinese hamster ovary cells with or without S9.

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  • (PMID = 16741555.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Mutagens; 0 / Trihalomethanes; 7LN464CH2O / bromodichloromethane
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85. Cooper K, Squires H, Carroll C, Papaioannou D, Booth A, Logan RF, Maguire C, Hind D, Tappenden P: Chemoprevention of colorectal cancer: systematic review and economic evaluation. Health Technol Assess; 2010 Jun;14(32):1-206
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  • BACKGROUND: Colorectal cancer (CRC) is the third most common cancer in the UK: incidence increases with age, median age at diagnosis being over 70 years.
  • Most develop from adenomatous polyps arising from the intestine lining.
  • A small study of aspirin in FAP patients produced no statistically significant reduction in polyp number but a possible reduction in polyp size.
  • There was a statistically significant 21% reduction in risk of adenoma recurrence [relative risk (RR) 0.79, 95% confidence interval (CI) 0.68 to 0.92] in an analysis of aspirin versus no aspirin in individuals with a history of adenomas or CRC.
  • Non-aspirin NSAID use in FAP individuals produced a non-statistically significant reduction in adenoma incidence after 4 years of treatment and follow-up and reductions in polyp number and size.
  • In individuals with a history of adenomas there was a statistically significant 34% reduction in adenoma recurrence risk (RR 0.66, 95% CI 0.60 to 0.72) and a statistically significant 55% reduction in advanced adenoma incidence (RR 0.45, 95% CI 0.35 to 0.58).
  • There was no significant effect of folic acid versus placebo on adenoma recurrence (RR 1.16, 95% CI 0.97 to 1.39) or advanced adenoma incidence in individuals with a history of adenomas.
  • In individuals with a history of adenomas there was a statistically significant 18% reduction in risk of adenoma recurrence (RR 0.82, 95% CI 0.69 to 0.98) and a non-significant reduction in risk of advanced adenomas (RR 0.77, 95% CI 0.50 to 1.17).
  • There were no studies of antioxidant use in individuals with FAP or HNPCC, and in individuals with a history of adenomas no statistically significant differences in relative risk of adenoma recurrence were found.

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  • (PMID = 20594533.001).
  • [ISSN] 2046-4924
  • [Journal-full-title] Health technology assessment (Winchester, England)
  • [ISO-abbreviation] Health Technol Assess
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antioxidants; 0 / Cyclooxygenase 2 Inhibitors; 01YAE03M7J / beta Carotene; 935E97BOY8 / Folic Acid; H6241UJ22B / Selenium; SY7Q814VUP / Calcium
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86. Burkart AL, Sheridan T, Lewin M, Fenton H, Ali NJ, Montgomery E: Do sporadic Peutz-Jeghers polyps exist? Experience of a large teaching hospital. Am J Surg Pathol; 2007 Aug;31(8):1209-14
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  • The polyps were reviewed by 3 pathologists to confirm the diagnosis.
  • Clinical information to confirm or refute a diagnosis of Peutz-Jeghers syndrome (PJS) was collected.
  • Of the 8 potential sporadic PJP, only 3 polyps from 3 patients had unequivocal PJP histologic features, all from the small intestine.
  • One patient had a history of high-grade dysplasia in a tubulovillous adenoma in the colon at 53 years, but no family cancer history.
  • Another had a history of pituitary adenoma at age 39, and the last had ductal breast carcinoma diagnosed 4 years before the discovery of the polyp.
  • [MeSH-major] Hospitals, Teaching. Intestinal Polyps / pathology. Peutz-Jeghers Syndrome / pathology

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  • (PMID = 17667545.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Husøy T, Knutsen HK, Cruciani V, Olstørn HB, Mikalsen SO, Løberg EM, Alexander J: Connexin43 is overexpressed in Apc(Min/+)-mice adenomas and colocalises with COX-2 in myofibroblasts. Int J Cancer; 2005 Sep 1;116(3):351-8
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  • The expression of gap junction proteins, connexins, in the intestine and their role in tumorigenesis are poorly characterised.
  • Truncating mutations in the tumour suppressor gene adenomatous polyposis coli (APC) are early and important events, both in inheritable (familial adenomatous polyposis, FAP) and spontaneous forms of intestinal cancer.
  • Multiple intestinal neoplasia (Min) mice, a FAP model with inherited heterozygous mutation in Apc, spontaneously develop numerous intestinal adenomas.
  • We further examine the expression of connexin43 (Cx43) and other connexins as a function of heterozygous and homozygous Apc mutation in normal intestinal tissues and adenomas of Min-mice.
  • Qualitative analysis of connexin mRNA in intestine revealed a similar expression pattern in Min- and wild-type (wt) mice.
  • Connexin26 and connexin40 proteins were found in equal amounts in Min and wt epithelia of large and small intestine, respectively.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyposis Coli / genetics. Connexin 43 / biosynthesis. Genes, APC. Prostaglandin-Endoperoxide Synthases / physiology

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  • (PMID = 15800939.001).
  • [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 / Connexin 43; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib
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88. van der Weyden L, Arends MJ, Dovey OM, Harrison HL, Lefebvre G, Conte N, Gergely FV, Bradley A, Adams DJ: Loss of Rassf1a cooperates with Apc(Min) to accelerate intestinal tumourigenesis. Oncogene; 2008 Jul 24;27(32):4503-8
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  • [Title] Loss of Rassf1a cooperates with Apc(Min) to accelerate intestinal tumourigenesis.
  • In this study we set out to test the hypothesis that loss of Rassf1a can cooperate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate intestinal tumourigenesis using the Apc-Min (Apc(Min/+)) mouse model, as mutational or deletional inactivation of APC is a frequent early event in the genesis of intestinal cancer.
  • Further, loss of RASSF1A has also been reported to occur in premalignant adenomas of the bowel.
  • By interbreeding isoform specific Rassf1a knockout mice with Apc(+/Min) mice, we showed that loss of Rassf1a results in a significant increase in adenomas of the small intestine and accelerated intestinal tumourigenesis leading to the earlier death of adenocarcinoma-bearing mice and decreased overall survival.
  • Collectively these data demonstrate cooperation between inactivation of Rassf1a and Apc resulting in accelerated intestinal tumourigenesis, with adenomas showing increased nuclear accumulation of beta-catenin, supporting a mechanistic link via loss of the known interaction of Rassf1 with beta-TrCP that usually mediates degradation of beta-catenin.

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  • (PMID = 18391979.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / / 079643; United Kingdom / Cancer Research UK / / A8449; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 0 / RASSF1 protein, mouse; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ EMS52273; NLM/ PMC3706934
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89. Ramocki NM, Wilkins HR, Magness ST, Simmons JG, Scull BP, Lee GH, McNaughton KK, Lund PK: Insulin receptor substrate-1 deficiency promotes apoptosis in the putative intestinal crypt stem cell region, limits Apcmin/+ tumors, and regulates Sox9. Endocrinology; 2008 Jan;149(1):261-7
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  • [Title] Insulin receptor substrate-1 deficiency promotes apoptosis in the putative intestinal crypt stem cell region, limits Apcmin/+ tumors, and regulates Sox9.
  • Using IRS-1(-/-), IRS-1(+/-), and IRS-1(+/+) mice, we tested the hypothesis that reduced IRS-1 expression increases apoptosis of intestinal crypt cells and protects against Apc(min/+) (Min)/beta-catenin-driven intestinal tumors.
  • Expression of Sox9, a transcriptional target of Tcf/beta-catenin and putative biomarker of crypt stem cells, was assessed in intestine of different IRS-1 genotypes and cell lines.
  • Compared with IRS-1(+/+)/Min, IRS-1(-/-)/Min mice had fewer Sox9-positive cells in intestinal crypts and reduced Sox9 mRNA in intestine.
  • IRS-1 overexpression increased Sox9 expression in an intestinal epithelial cell line.
  • We conclude that even small reductions in endogenous IRS-1 increase apoptosis of crypt stem or progenitor cells, protect against beta-catenin-driven intestinal tumors, and reduce Sox9, a Tcf/beta-catenin target and putative stem/progenitor cell biomarker.

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  • (PMID = 17916629.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM000678; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NCI NIH HHS / CA / P30 CA016086; United States / NCI NIH HHS / CA / CA-16086; United States / NIDDK NIH HHS / DK / R01 DK040247; United States / NCI NIH HHS / CA / T32 CA072319; United States / NIGMS NIH HHS / GM / K12 GM000678; United States / NIDDK NIH HHS / DK / DK-40247; United States / NCI NIH HHS / CA / CA-72319; United States / NIDDK NIH HHS / DK / P30-DK-34987
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / High Mobility Group Proteins; 0 / Insulin Receptor Substrate Proteins; 0 / Irs1 protein, mouse; 0 / SOX9 Transcription Factor; 0 / Sox9 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2194604
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90. Howells LM, Britton RG, Mazzoletti M, Greaves P, Broggini M, Brown K, Steward WP, Gescher AJ, Sale S: Preclinical colorectal cancer chemopreventive efficacy and p53-modulating activity of 3',4',5'-trimethoxyflavonol, a quercetin analogue. Cancer Prev Res (Phila); 2010 Aug;3(8):929-39
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  • Consumption of TMFol reduced small intestinal adenoma burden in Apc(Min) mice by 47%, compared with control mice (P < 0.002).

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  • [Copyright] 2010 AACR.
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  • (PMID = 20628003.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / A6894; United Kingdom / Cancer Research UK / / C325-A6894; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3',4',5'-trimethoxyflavone; 0 / Antineoplastic Agents, Phytogenic; 0 / Flavonoids; 9IKM0I5T1E / Quercetin
  • [Other-IDs] NLM/ PMC2917785; NLM/ UKMS28639
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91. Wang Y, Giel-Moloney M, Rindi G, Leiter AB: Enteroendocrine precursors differentiate independently of Wnt and form serotonin expressing adenomas in response to active beta-catenin. Proc Natl Acad Sci U S A; 2007 Jul 3;104(27):11328-33
SciCrunch. The Antibody Registry: Reagent: Antibodies .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Wnt signaling is required for the maintenance of intestinal stem cells and self-renewal of the intestinal epithelium.
  • Intestinal cancers are frequently associated with mutations that activate the Wnt pathway.
  • The role of Wnt signaling on differentiation of lineage-specific precursors in the intestine is not well characterized.
  • Activation of the Wnt pathway by conditionally deleting exon 3 of the beta-catenin gene at an early stage of enteroendocrine cell differentiation induced small-intestinal adenomas expressing serotonin, a feature not previously described in other tumors induced by Wnt in mice.
  • These results provide direct evidence that some intestinal lineages are specified independently of the Wnt pathway and may lead to a better understanding of the spectrum of neuroendocrine differentiation frequently seen in human gastrointestinal cancer.

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  • (PMID = 17592150.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32-DK007542; United States / NIDDK NIH HHS / DK / P30 DK034928; United States / NIDDK NIH HHS / DK / DK67166; United States / NIDDK NIH HHS / DK / DK52870; United States / NIDDK NIH HHS / DK / P30-DK34928; United States / NIDDK NIH HHS / DK / DK43673; United States / NIDDK NIH HHS / DK / T32 DK007542; United States / NIDDK NIH HHS / DK / R01 DK067166; United States / NIDDK NIH HHS / DK / R01 DK043673
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CTNNB1 protein, human; 0 / NEUROG3 protein, human; 0 / Nerve Tissue Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 333DO1RDJY / Serotonin
  • [Other-IDs] NLM/ PMC2040898
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92. Laurent E, McCoy JW 3rd, Macina RA, Liu W, Cheng G, Robine S, Papkoff J, Lambeth JD: Nox1 is over-expressed in human colon cancers and correlates with activating mutations in K-Ras. Int J Cancer; 2008 Jul 1;123(1):100-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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  • Nox1 was overexpressed compared with paired normal tissue in 57% of tumors as early as the adenoma stage, with no correlation of expression level with tumor stage.
  • Transgenic mice expressing K-Ras(G12V) in the intestinal epithelium also expressed markedly elevated Nox1 in both small and large intestine.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18398843.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / K12 GM000680; United States / NCI NIH HHS / CA / R01 CA084138; United States / NCI NIH HHS / CA / CA 84138; United States / NIGMS NIH HHS / GM / K12-GM 00680
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; EC 1.6.3.- / NOX1 protein, human; EC 1.6.3.1 / NADPH Oxidase
  • [Other-IDs] NLM/ NIHMS505983; NLM/ PMC3774003
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93. Hung KE, Maricevich MA, Richard LG, Chen WY, Richardson MP, Kunin A, Bronson RT, Mahmood U, Kucherlapati R: Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment. Proc Natl Acad Sci U S A; 2010 Jan 26;107(4):1565-70
The Lens. Cited by Patents in .

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  • Most genetically engineered mouse (GEM) models for colon cancer are based on tissuewide or germline gene modification, resulting in tumors predominantly of the small intestine.
  • We have developed a stochastic somatic mutation model for sporadic colon cancer that presents with isolated primary tumors in the distal colon and recapitulates the entire adenoma-carcinoma-metastasis axis seen in human colon cancer.

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  • (PMID = 20080688.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK078033; United States / NCI NIH HHS / CA / 5U01CA084301; United States / NCI NIH HHS / CA / U01 CA084301; United States / NCI NIH HHS / CA / 5P50CA127003; United States / NIDDK NIH HHS / DK / P30 DK043351; United States / NIBIB NIH HHS / EB / 5R01EB001872; United States / NIDDK NIH HHS / DK / 5K08DK078033; United States / NIBIB NIH HHS / EB / R01 EB001872; United States / NCI NIH HHS / CA / P50 CA127003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2824379
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94. Niwa Y, Nakamura M, Omiya N, Itoh A, Hirooka Y, Goto H: Ileal cancer and erosions in the small intestine revealed by capsule endoscopy. Endoscopy; 2007 Feb;39 Suppl 1:E7-8
Hazardous Substances Data Bank. (L)-ALANINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ileal cancer and erosions in the small intestine revealed by capsule endoscopy.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Capsule Endoscopy. Colonic Neoplasms / diagnosis. Endoscopy, Gastrointestinal. Enteritis / diagnosis. Gastrointestinal Hemorrhage / diagnosis. Ileal Neoplasms / diagnosis. Intestinal Polyps / diagnosis. Neoplasms, Multiple Primary / diagnosis

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  • (PMID = 17285495.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Quinolones; 111911-87-6 / rebamipide; OF5P57N2ZX / Alanine
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