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1. Kim JC, Roh SA, Cho DH, Kim TW, Yoon SN, Kim CW, Yu CS, Kim SY, Kim YS: Chemoresponsiveness associated with canonical molecular changes in colorectal adenocarcinomas. Anticancer Res; 2009 Aug;29(8):3115-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Representative molecular changes in tumor tissues, including adenomatous polyposis coli (APC) gene, wingless-type MMTV integration site family (Wnt), mismatch repair (MMR), RAF, transforming growth factor (TGF)-beta, bone morphogenetic protein, and p53, had been previously determined, with an additional 42 patients included in this analysis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / genetics. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / genetics
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Chemotherapy, Adjuvant. DNA Mismatch Repair. Disease-Free Survival. Female. Humans. Immunoenzyme Techniques. Loss of Heterozygosity. Male. Microsatellite Instability. Middle Aged. Mutation. Neoplasm Invasiveness. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Palliative Care. Survival Rate. Transforming Growth Factor beta2 / genetics. Transforming Growth Factor beta2 / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Wnt Proteins / genetics. Wnt Proteins / metabolism. raf Kinases / genetics. raf Kinases / metabolism

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  • (PMID = 19661324.001).
  • [ISSN] 1791-7530
  • [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 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor; 0 / TP53 protein, human; 0 / Transforming Growth Factor beta2; 0 / Tumor Suppressor Protein p53; 0 / Wnt Proteins; EC 2.7.11.1 / raf Kinases
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2. Lazzareschi I, Barone G, Mastrangelo S, Furfaro IF, Rando G, Riccardi R: Could APC gene screening be useful in children with hepatoblastoma? Early onset of adenocarcinoma in a child with familial adenomatous polyposis and hepatoblastoma. Tumori; 2009 Nov-Dec;95(6):819-22
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  • [Title] Could APC gene screening be useful in children with hepatoblastoma? Early onset of adenocarcinoma in a child with familial adenomatous polyposis and hepatoblastoma.
  • Familial adenomatous polyposis is an inherited disorder characterized by the development of hundreds of colorectal adenomas during adolescence, which in many cases will transform into colorectal cancer by the fourth decade of life, along with the development of various malignant tumors including hepatoblastoma.
  • We report on a female patient with a de novo interstitial deletion of 5q21.3-q23.3, encompassing the APC gene, associated with adenomatous polyposis and early colorectal cancer, hepatoblastoma, epidermoid cysts, mental retardation, several mild dysmorphic signs and lower limb venous thrombosis.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Colonic Neoplasms / genetics. Gene Deletion. Genes, APC. Genetic Testing. Hepatoblastoma / genetics. Liver Neoplasms / genetics


3. Bhatnagar N, Li X, Chen Y, Zhou X, Garrett SH, Guo B: 3,3'-diindolylmethane enhances the efficacy of butyrate in colon cancer prevention through down-regulation of survivin. Cancer Prev Res (Phila); 2009 Jun;2(6):581-9
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  • [Title] 3,3'-diindolylmethane enhances the efficacy of butyrate in colon cancer prevention through down-regulation of survivin.
  • Butyrate is an inhibitor of histone deacetylase (HDAC) and has been extensively evaluated as a chemoprevention agent for colon cancer.
  • We recently showed that mutations in the adenomatous polyposis coli (APC) gene confer resistance to HDAC inhibitor-induced apoptosis in colon cancers.
  • Here, we show that APC mutation rendered colon cancer cells resistant to butyrate-induced apoptosis due to the failure of butyrate to down-regulate survivin in these cells.
  • Another cancer-preventive agent, 3,3'-diindolylmethane (DIM), was identified to be able to down-regulate survivin in colon cancers expressing mutant APC.
  • Pretreatment with DIM enhanced butyrate-induced apoptosis in colon cancer cells expressing mutant APC.
  • Whereas overexpression of survivin blocked DIM/butyrate-induced apoptosis, knocking down of survivin by small interfering RNA increased butyrate-induced apoptosis in colon cancer cells.
  • We further showed that DIM was able to down-regulate survivin and enhance the effects of butyrate in apoptosis induction and prevention of familial adenomatous polyposis in APC(min/+) mice.
  • Thus, the combination of DIM and butyrate is potentially an effective strategy for the prevention of colon cancer.

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  • (PMID = 19470789.001).
  • [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 / R03 CA130062; United States / NCI NIH HHS / CA / 5R21CA111765; United States / NCRR NIH HHS / RR / 2P20RR015566; United States / NCI NIH HHS / CA / 1R03CA130062; United States / NCI NIH HHS / CA / R03 CA130062-02; United States / NIGMS NIH HHS / GM / P30 GM103332; United States / NCRR NIH HHS / RR / P20 RR015566; United States / NCRR NIH HHS / RR / P20 RR015566-08; United States / NCRR NIH HHS / RR / RR015566-08; United States / NCI NIH HHS / CA / R21 CA111765; United States / NCI NIH HHS / CA / CA130062-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / BIRC5 protein, human; 0 / Butyrates; 0 / DNA, Complementary; 0 / Histone Deacetylase Inhibitors; 0 / Indoles; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Fusion Proteins; SSZ9HQT61Z / 3,3'-diindolylmethane
  • [Other-IDs] NLM/ NIHMS209111; NLM/ PMC2901098
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4. Kountouras J, Zavos C, Chatzopoulos D, Katsinelos P: New aspects of Helicobacter pylori infection involvement in gastric oncogenesis. J Surg Res; 2008 May 1;146(1):149-58
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  • Gastric adenocarcinoma not located in the cardia still remains second only to lung cancer as the leading cause of cancer-related mortality worldwide, whereas adenocarcinoma of the cardia and gastroesophageal junction has been rapidly rising over the past two decades.
  • Advances have been made in genetic changes mostly of the intestinal type; its development is probably a multistep process, as has been well described in colon carcinogenesis.
  • The most common genetic abnormalities tend to be loss of heterozygosity of particularly tumor suppressor p53 gene or "adenomatous polyposis coli" gene.
  • [MeSH-major] Adenocarcinoma / microbiology. Helicobacter Infections / complications. Stomach Neoplasms / microbiology


5. Barone M, Scavo MP, Papagni S, Piscitelli D, Guido R, Di Lena M, Comelli MC, Di Leo A: ERβ expression in normal, adenomatous and carcinomatous tissues of patients with familial adenomatous polyposis. Scand J Gastroenterol; 2010 Nov;45(11):1320-8
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  • [Title] ERβ expression in normal, adenomatous and carcinomatous tissues of patients with familial adenomatous polyposis.
  • OBJECTIVES: The APC gene mutation triggers familial adenomatous polyposis (FAP) and approximately 80% of sporadic colorectal cancers.
  • FAP summarizes the natural history of colorectal cancer because low- and high-grade dysplastic lesions and adenocarcinoma are simultaneously present in the same patients free from individual and environmental variability factors.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Colon, Descending / metabolism. Colorectal Neoplasms / genetics. DNA, Neoplasm. Estrogen Receptor beta / genetics. Gene Expression Regulation, Neoplastic


6. MacLeod RJ, Hayes M, Pacheco I: Wnt5a secretion stimulated by the extracellular calcium-sensing receptor inhibits defective Wnt signaling in colon cancer cells. Am J Physiol Gastrointest Liver Physiol; 2007 Jul;293(1):G403-11
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  • [Title] Wnt5a secretion stimulated by the extracellular calcium-sensing receptor inhibits defective Wnt signaling in colon cancer cells.
  • To understand the role of the colonic extracellular calcium-sensing receptor (CaSR) in calcium chemoprotection against colon cancer, we activated the CaSR with 5 mM Ca(2+) on HT-29 cells, an adenocarcinoma cell line.
  • Inducing the expression of full-length adenomatous polyposis coli (APC) prevented CaSRmediated increases of Siah2 and Wnt5a.
  • [MeSH-minor] Adenocarcinoma. Adenomatous Polyposis Coli Protein / biosynthesis. Calcium / pharmacology. Calcium Signaling / drug effects. Cell Line, Tumor. Cells, Cultured. Humans. Nuclear Proteins / biosynthesis. Receptor Tyrosine Kinase-like Orphan Receptors. Receptors, Cell Surface / biosynthesis. Ubiquitin-Protein Ligases / biosynthesis. beta Catenin / antagonists & inhibitors

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  • (PMID = 17463182.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CASR protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / ROR2 protein, human; 0 / Receptors, Calcium-Sensing; 0 / Receptors, Cell Surface; 0 / WNT5A protein, human; 0 / Wnt Proteins; 0 / beta Catenin; EC 2.7.10.1 / Receptor Tyrosine Kinase-like Orphan Receptors; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / seven in absentia proteins; SY7Q814VUP / Calcium
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7. Shenoy S, Cassim R: Ileostomy adenocarcinoma associated with familial adenomatous polyposis (FAP): new problem in old disease. Int J Colorectal Dis; 2009 Dec;24(12):1475-6
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  • [Title] Ileostomy adenocarcinoma associated with familial adenomatous polyposis (FAP): new problem in old disease.
  • [MeSH-major] Adenocarcinoma / etiology. Adenomatous Polyposis Coli / complications. Ileostomy / adverse effects

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  • (PMID = 19488768.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
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8. Nzegwu MA, Osuagwu CC, Machembarrena JM, Ezeofor S, Picardo NG, Emegakor C, Odiakosa T: Familial adenomatous polyposis complicated with an invasive colo-rectal adenocarcinoma in a 26-year-old Nigerian male - a rare finding. Eur J Cancer Care (Engl); 2007 Mar;16(2):198-200
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  • [Title] Familial adenomatous polyposis complicated with an invasive colo-rectal adenocarcinoma in a 26-year-old Nigerian male - a rare finding.
  • Familial adenomatous polyposis is very rare in our environment.
  • He had also previously had a previous proctoscopy and rectal biopsy that showed numerous adenomatous polyps with dysplastic changes confirmed by histology.
  • Barium enema revealed multiple polyps up to the right side of the transverse colon.
  • Repeat histology after panproctocolectomy confirmed foci of invasive adenocarcinoma of the colon up to the muscle coat.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Colonic Neoplasms / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 17371432.001).
  • [ISSN] 0961-5423
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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9. Sarin S, Bernath A: Turcot syndrome (glioma polyposis): a case report. South Med J; 2008 Dec;101(12):1273-4
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  • [Title] Turcot syndrome (glioma polyposis): a case report.
  • Turcot's syndrome (glioma-polyposis) is a rare hereditary disorder characterized by association of colonic polyposis with primary tumors of the central nervous system.
  • Based on the genetic mutations, the patients with Turcot's syndrome are classified into adenomatous polyposis coli (APC) group or hereditary non-polyposis colon cancer (HNPCC) group.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Cerebellar Neoplasms / pathology. Colonic Neoplasms / pathology. Medulloblastoma / pathology. Neoplastic Syndromes, Hereditary / pathology

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  • (PMID = 19005436.001).
  • [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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10. Heath EI, Canto MI, Piantadosi S, Montgomery E, Weinstein WM, Herman JG, Dannenberg AJ, Yang VW, Shar AO, Hawk E, Forastiere AA, Chemoprevention for Barrett's Esophagus Trial Research Group: Secondary chemoprevention of Barrett's esophagus with celecoxib: results of a randomized trial. J Natl Cancer Inst; 2007 Apr 4;99(7):545-57
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  • BACKGROUND: Barrett's esophagus is a premalignant condition that is a risk factor for the development of esophageal adenocarcinoma, a disease whose incidence is rapidly increasing.
  • No statistically significant differences in total surface area of the Barrett's esophagus; in prostaglandin levels; in cyclooxygenase-1/2 mRNA levels; or in methylation of tumor suppressor genes p16, adenomatous polyposis coli, and E-cadherin were found with celecoxib compared with placebo.

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  • (PMID = 17405999.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA084197; United States / NIDDK NIH HHS / DK / R01 DK052230; United States / NCI NIH HHS / CN / N01-CN-85185
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Cyclooxygenase Inhibitors; 0 / Placebos; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ NIHMS502090; NLM/ PMC3755596
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11. Kim MJ, Jang SJ, Yu E: Loss of E-cadherin and cytoplasmic-nuclear expression of beta-catenin are the most useful immunoprofiles in the diagnosis of solid-pseudopapillary neoplasm of the pancreas. Hum Pathol; 2008 Feb;39(2):251-8
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  • Differentiation of solid-pseudopapillary neoplasm from pancreatic endocrine neoplasm or adenocarcinoma can be difficult in the small biopsy specimen because they share common morphological features and immunoprofiles.
  • Alterations of adenomatous polyposis coli (APC)/beta-catenin pathway have been identified as a genetic event contributing to the development of solid-pseudopapillary neoplasm.
  • In the present study, to establish the diagnostic utility of beta-catenin and E-cadherin as markers for solid-pseudopapillary neoplasm, we performed immunohistochemical staining in 4 core biopsy specimens diagnosed as solid-pseudopapillary neoplasm and in tissue microarray blocks that contained histologically confirmed samples of 302 cases of adenocarcinoma, 56 cases of pancreatic endocrine neoplasm, and 50 cases of solid-pseudopapillary neoplasm.
  • Of the adenocarcinoma cases, all were positive for CK, 300 (99.3%) were positive for E-cadherin, 30 (9.9%) were positive for CD10, 2 (0.7%) were positive for synaptophysin, 1 (0.3%) was positive for CD56, and none was positive for chromogranin and nuclear expression of beta-catenin.
  • CD10 immunopositivity should be carefully interpreted in the diagnosis of solid-pseudopapillary neoplasm because pancreatic adenocarcinoma or pancreatic endocrine neoplasm can also stain for CD10.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Adenocarcinoma / surgery. Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Child. Female. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Male. Middle Aged. Tissue Array Analysis

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  • [CommentIn] Hum Pathol. 2008 Sep;39(9):1407-8 [18706351.001]
  • (PMID = 17959228.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / beta Catenin
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12. Jiménez Rodríguez RM, Suárez Artacho G, Morcillo J, Díaz Pavón JM, Morales Méndez S: [Adenocarcinoma in the fourth portion of duodenum in a patient with familial adenomatous polyposis]. Rev Esp Enferm Dig; 2007 Aug;99(8):477-8
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  • [Title] [Adenocarcinoma in the fourth portion of duodenum in a patient with familial adenomatous polyposis].
  • [Transliterated title] Adenocarcinoma de cuarta porción de duodeno en paciente con poliposis adenomatosa familiar.
  • [MeSH-major] Adenocarcinoma. Adenomatous Polyposis Coli. Duodenal Neoplasms. Neoplasms, Second Primary


13. Thompson JS, Gilroy R, Sudan D: Short bowel syndrome after continence-preserving procedures. J Gastrointest Surg; 2008 Jan;12(1):73-6
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  • Continence-preserving operations are generally performed for either ulcerative colitis (UC) or familial polyposis (FAP).
  • One UC patient developed adenocarcinoma in a continent ileostomy.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Colitis, Ulcerative / surgery. Colonic Pouches / adverse effects. Constipation / surgery. Ileostomy / adverse effects. Short Bowel Syndrome / etiology


14. Samowitz WS, Slattery ML, Sweeney C, Herrick J, Wolff RK, Albertsen H: APC mutations and other genetic and epigenetic changes in colon cancer. Mol Cancer Res; 2007 Feb;5(2):165-70
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  • [Title] APC mutations and other genetic and epigenetic changes in colon cancer.
  • Relationships between adenomatous polyposis coli (APC) mutations, BRAF V600E mutations, and the CpG island methylator phenotype (CIMP) in colon cancer have not been explored.
  • The conventional wisdom that most colon cancers contain APC, Ki-ras, and p53 mutations is incorrect.
  • The relationships of APC mutations to other genetic and epigenetic alterations add to the already impressive genetic heterogeneity of colon cancer.

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  • (PMID = 17293392.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA061757-11; United States / NCI NIH HHS / CA / CA061757-11; United States / NCI NIH HHS / CA / CA61757; United States / NCI NIH HHS / CA / CA48998; United States / NCI NIH HHS / CA / R01 CA061757
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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15. John R, El-Rouby NM, Tomasetto C, Rio MC, Karam SM: Expression of TFF3 during multistep colon carcinogenesis. Histol Histopathol; 2007 07;22(7):743-51
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  • [Title] Expression of TFF3 during multistep colon carcinogenesis.
  • The pathogenesis of colon cancer is not well understood.
  • TFF3 is a product of the colonic epithelium and has been implicated in colonic mucosal protection and also in the aggressiveness of colon cancer cells.
  • The aim of this study was to analyze the expression of TFF3 during propagation towards cancer development in the human colon.
  • Colonic tissues representing colitis, adenomatous polyposis, tubulovillous adenoma, and mucoid/adeno-carcinomas were processed for immunohistochemistry using an antibody specific for human TFF3.
  • The results were correlated with those of PCNA-labeling, quantified, and compared with those of control tissues obtained from the safe margin of macroscopically normal colonic mucosa of patients with colon cancer.
  • The data showed marked down-regulation of TFF3 expression in adenomatous polyposis, then TFF3 expression returns to about control level during adenoma and remains high during mucoid- and adeno-carcinomas.
  • The changes observed in expression of TFF3 showed an inverse correlation with cell proliferation and suggest that it might play a protective role against colon carcinogenesis.
  • [MeSH-major] Adenocarcinoma, Mucinous / chemistry. Adenoma, Villous / chemistry. Adenomatous Polyposis Coli / chemistry. Colitis / metabolism. Colonic Neoplasms / chemistry. Peptides / analysis
  • [MeSH-minor] Adult. Cell Proliferation. Cell Transformation, Neoplastic / chemistry. Colon / chemistry. Disease Progression. Humans. Immunohistochemistry. Middle Aged. Neoplasm Invasiveness. Proliferating Cell Nuclear Antigen / analysis. Trefoil Factor-3

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  • (PMID = 17455148.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Peptides; 0 / Proliferating Cell Nuclear Antigen; 0 / TFF3 protein, human; 0 / Trefoil Factor-3
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16. de Castro SM, van Eijck CH, Rutten JP, Dejong CH, van Goor H, Busch OR, Gouma DJ: Pancreas-preserving total duodenectomy versus standard pancreatoduodenectomy for patients with familial adenomatous polyposis and polyps in the duodenum. Br J Surg; 2008 Nov;95(11):1380-6
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  • [Title] Pancreas-preserving total duodenectomy versus standard pancreatoduodenectomy for patients with familial adenomatous polyposis and polyps in the duodenum.
  • BACKGROUND: Pancreas-preserving total duodenectomy (PPTD) was introduced as a replacement for pancreatoduodenectomy (PD) for familial adenomatous polyposis (FAP).
  • METHODS: All 26 patients who underwent PPTD for FAP in four centres in the Netherlands between January 2000 and January 2007 were compared with a group of 77 patients who had PD for ampulla of Vater adenocarcinoma at one centre during the same interval.
  • RESULTS: Morbidity rates were similar after PPTD for FAP (16 patients, 62 per cent) and PD for ampulla of Vater adenocarcinoma (44 patients, 57 per cent) (P = 0.694).
  • [MeSH-major] Adenocarcinoma / surgery. Adenomatous Polyposis Coli / surgery. Ampulla of Vater / surgery. Common Bile Duct Neoplasms / surgery. Pancreas / surgery. Pancreaticoduodenectomy / methods

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  • [Copyright] Copyright (c) 2008 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
  • (PMID = 18844249.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Number-of-references] 43
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17. Castells A, Balaguer F, Gonzalo V, Castellví-Bel S: [Cyclooxygenase 2 and colorectal cancer: therapeutic implications]. Gastroenterol Hepatol; 2007 May;30(5):280-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adenocarcinoma / enzymology. Colorectal Neoplasms / enzymology. Cyclooxygenase 2 / physiology. Cyclooxygenase 2 Inhibitors / therapeutic use. Neoplasm Proteins / physiology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / enzymology. Adenoma / prevention & control. Adenomatous Polyposis Coli / drug therapy. Adenomatous Polyposis Coli / enzymology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / surgery. Adult. Clinical Trials as Topic. Combined Modality Therapy. Humans. Multicenter Studies as Topic. Precancerous Conditions / drug therapy. Precancerous Conditions / enzymology. Prognosis. Risk

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  • (PMID = 17493439.001).
  • [ISSN] 0210-5705
  • [Journal-full-title] Gastroenterología y hepatología
  • [ISO-abbreviation] Gastroenterol Hepatol
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Neoplasm Proteins; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 53
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18. Jerkic S, Rosewich H, Scharf JG, Perske C, Füzesi L, Wilichowski E, Gärtner J: Colorectal cancer in two pre-teenage siblings with familial adenomatous polyposis. Eur J Pediatr; 2005 May;164(5):306-10
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  • [Title] Colorectal cancer in two pre-teenage siblings with familial adenomatous polyposis.
  • Familial adenomatous polyposis (FAP) is an autosomal dominant disorder that characteristically presents with colon cancer in early adult life.
  • Colonoscopy showed that the colon was carpeted with a myriad of polyps.
  • The diagnosis of an adenocarcinoma of the colon and further adenomatous polyps with low-grade and high-grade dysplasia was confirmed by histology.
  • CONCLUSION: Children with familial adenomatous polyposis are at risk for colon cancer and emphasise the need for early tumour recognition.
  • Gastrointestinal symptoms in children should be thoroughly evaluated and standard screening for colonic polyposis should be performed in all individuals with a positive family history and/or known mutations in cancer-associated genes, particularly in children who are under 10 years of age.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenomatous Polyposis Coli / diagnosis. Carcinoma / diagnosis. Colorectal Neoplasms / diagnosis. Siblings


19. Schneider AR, Seifert H, Trojan J, Stein J, Hoepffner NM: Frequency of colorectal polyps in patients with sporadic adenomas or adenocarcinomas of the papilla of vater--an age-matched, controlled study. Z Gastroenterol; 2005 Oct;43(10):1123-7
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  • Patients with familial adenomatous polyposis bear a particularly increased risk for periampullary tumors.
  • 50% of the colonic polyps in patients with ampullary neoplasms were located in the ascending colon.
  • [MeSH-major] Adenocarcinoma / complications. Adenoma / complications. Ampulla of Vater. Common Bile Duct Neoplasms / complications. Intestinal Polyps / epidemiology
  • [MeSH-minor] Adenoma, Villous / complications. Adenoma, Villous / surgery. Adenomatous Polyposis Coli / epidemiology. Adult. Aged. Aged, 80 and over. Colonic Polyps / diagnosis. Colonic Polyps / epidemiology. Colonoscopy. Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / epidemiology. Data Interpretation, Statistical. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prevalence. Retrospective Studies. Risk Factors. Time Factors

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  • (PMID = 16220451.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
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20. Garrean S, Hering J, Saied A, Jani J, Espat NJ: Gastric adenocarcinoma arising from fundic gland polyps in a patient with familial adenomatous polyposis syndrome. Am Surg; 2008 Jan;74(1):79-83
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  • [Title] Gastric adenocarcinoma arising from fundic gland polyps in a patient with familial adenomatous polyposis syndrome.
  • Familial adenomatous polyposis (FAP) is a rare hereditary syndrome characterized by multiple colorectal polyps and early development of colorectal cancer.
  • Herein, we present a case of gastric adenocarcinoma arising from fundic gland polyps in an FAP patient.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Stomach Neoplasms / genetics. Stomach Neoplasms / pathology


21. Dixon E, Vollmer CM Jr, Sahajpal A, Cattral MS, Grant DR, Taylor BR, Langer B, Gallinger S, Greig PD: Transduodenal resection of peri-ampullary lesions. World J Surg; 2005 May;29(5):649-52
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  • Pathology of the lesions was as follows: 11 with benign ampullary adenomas, including 4 with familial adenomatous polyposis (FAP); 7 with peri-ampullary adenocarcinomas; and 1 with a benign stricture.
  • Three of the 4 patients with FAP have recurrent adenomatous change; 2 of the 7 with carcinoma have metastatic adenocarcinoma.
  • Intraoperative frozen section assessment is recommended in cases of potential adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / surgery. Ampulla of Vater. Common Bile Duct Neoplasms / surgery. Digestive System Surgical Procedures
  • [MeSH-minor] Adenomatous Polyposis Coli / surgery. Adult. Aged. Aged, 80 and over. Female. Frozen Sections. Humans. Middle Aged. Retrospective Studies. Sensitivity and Specificity

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  • [Cites] Arch Surg. 1996 Apr;131(4):366-71 [8615720.001]
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  • (PMID = 15827855.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Chetty R, Serra S, Salahshor S, Alsaad K, Shih W, Blaszyk H, Woodgett JR, Tsao MS: Expression of Wnt-signaling pathway proteins in intraductal papillary mucinous neoplasms of the pancreas: a tissue microarray analysis. Hum Pathol; 2006 Feb;37(2):212-7
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  • It is less frequently involved in conventional ductal pancreatic adenocarcinoma.
  • A tissue microarray of 18 cases of IPMN was stained for proteins involved in the Wnt pathway: adenomatous polyposis coli (APC), pan-beta-catenin, axin 2, glycogen synthase 3alphabeta and 3beta, c-myc, E-cadherin, and cyclin D1.


23. Uragami N, Koizumi K, Chino A, Fujisaki J, Hoshino E, Takahashi H, Fujita R, Ueno M: Cancer in familial adenomatous polyposis. Gastrointest Endosc; 2005 Jan;61(1):104
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  • [Title] Cancer in familial adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Rectal Neoplasms / pathology

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  • (PMID = 15672067.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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24. Ulaş M, Neşşar G, Bostanoğlu A, Aydoğ G, Kayaalp C, Ozoğul Y, Seven C: Development of two cancers in the same patient after ileorectal and ileal pouch anal anastomosis for familial adenomatous polyposis. Med Princ Pract; 2006;15(1):83-6
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  • [Title] Development of two cancers in the same patient after ileorectal and ileal pouch anal anastomosis for familial adenomatous polyposis.
  • OBJECTIVE: To report a case of a patient with familial adenomatous polyposis.
  • CLINICAL PRESENTATION AND INTERVENTION: A 36-year-old male patient who suffered from rectal bleeding was treated with colectomy and ileorectal anastomosis for familial adenomatous polyposis (FAP) in 1974.
  • After 19 years, in situ adenocarcinoma was detected in the rectal stump.
  • [MeSH-major] Adenocarcinoma, Mucinous / diagnosis. Adenomatous Polyposis Coli / surgery. Anal Canal / surgery. Carcinoma, Squamous Cell / diagnosis. Colonic Neoplasms / complications. Ileostomy

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  • (PMID = 16340235.001).
  • [ISSN] 1011-7571
  • [Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre
  • [ISO-abbreviation] Med Princ Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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25. Berkhout M, Nagtegaal ID, Cornelissen SJ, Dekkers MM, van de Molengraft FJ, Peters WH, Nagengast FM, van Krieken JH, Jeuken JW: Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas. Mod Pathol; 2007 Dec;20(12):1253-62
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  • [Title] Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas.
  • Patients with familial adenomatous polyposis (FAP) have a high risk of developing duodenal carcinomas.
  • Hypermethylation was observed in the immunoglobulin superfamily genes member 4 (IGSF4), TIMP metallopeptidase inhibitor 3 (TIMP3), Estrogen receptor 1 (ESR1), adenomatous polyposis coli (APC), H-cadherin (CDH13) and paired box gene 6 (PAX6) genes.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Chromosome Aberrations. DNA Methylation. Duodenal Neoplasms / genetics


26. Kemp Z, Rowan A, Chambers W, Wortham N, Halford S, Sieber O, Mortensen N, von Herbay A, Gunther T, Ilyas M, Tomlinson I: CDC4 mutations occur in a subset of colorectal cancers but are not predicted to cause loss of function and are not associated with chromosomal instability. Cancer Res; 2005 Dec 15;65(24):11361-6
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  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / secondary. Adenoma / genetics. Adenoma / pathology. Adenomatous Polyposis Coli Protein / genetics. DNA Mutational Analysis. DNA, Neoplasm. Genes, ras / genetics. Humans. Microsatellite Repeats. Ploidies. Polymorphism, Single-Stranded Conformational. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16357143.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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27. Leal RF, Ayrizono Mde L, Coy CS, Callejas-Neto F, Fagundes JJ, Góes JR: [Gastroduodenal polyposis in patients with familiar adenomatous polyposis after rectocolectomy]. Arq Gastroenterol; 2007 Apr-Jun;44(2):133-6
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  • [Title] [Gastroduodenal polyposis in patients with familiar adenomatous polyposis after rectocolectomy].
  • [Transliterated title] Polipose gastroduodenal em doentes com polipose adenomatosa familiar Pós-Retocolectomia.
  • BACKGROUND: The extra colonic manifestations, like upper gastrointestinal tract polyps and duodenal cancer are disorders that affect long-term morbidity and mortality of patients with familial adenomatous polyposis, after rectocolectomy.
  • AIM: To describe the frequency of those disorders in patients with familial adenomatous polyposis and to review efficacy of upper gastrointestinal endoscopic surveillance.
  • METHODS: Between 1984 and 2005, 62 patients with familial adenomatous polyposis after rectocolectomy, were studied retrospectively, by Coloproctology Group, Medical Sciences Faculty, State University of Campinas, SP, Brazil.
  • Eight (15,4%) had gastric adenomatous polyps, 14 (27%), duodenal polyps and 5 (9,6%) duodenal and gastric polyps.
  • Two patients (3,8%) had adenomatous duodenal polyps with severe dysplasia, and one (1,9%) had adenocarcinoma of the duodenal papilla.
  • CONCLUSION: The upper gastrointestinal endoscopic surveillance has importance and the aim is to detect as early as possible the occurrence of duodenal adenocarcinoma and upper gastrointestinal polyps with severe dysplasia.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Duodenal Neoplasms / diagnosis. Endoscopy, Digestive System. Polyps / diagnosis. Stomach Neoplasms / diagnosis

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  • (PMID = 17962858.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
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28. Roh SA, Choi EY, Cho DH, Jang SJ, Kim SY, Kim YS, Kim JC: Growth and invasion of sporadic colorectal adenocarcinomas in terms of genetic change. J Korean Med Sci; 2010 Mar;25(3):353-60
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  • Adenomatous polyposis coli (APC) and/or Wnt-activated alterations occurred in 66% patients, whereas mismatch repair (MMR) defects and/or RAF-mediated alterations were identified in 47% patients.
  • [MeSH-major] Adenocarcinoma. Colorectal Neoplasms. Gene Expression Regulation, Neoplastic

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  • (PMID = 20191032.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen; 0 / Repressor Proteins; 0 / S100 Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 142662-27-9 / S100A4 protein, human; EC 2.7.- / Protein Kinases; EC 2.7.1.- / NUAK1 protein, human; EC 3.4.24.24 / MMP2 protein, human; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC2826746
  • [Keywords] NOTNLM ; Colorectal Neoplasms / Growth / Invasion / Molecular / Sporadic / Tumorigenesis
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29. Giles RH, Lolkema MP, Snijckers CM, Belderbos M, van der Groep P, Mans DA, van Beest M, van Noort M, Goldschmeding R, van Diest PJ, Clevers H, Voest EE: Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis. Oncogene; 2006 May 18;25(21):3065-70
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  • Although we observed upregulated levels of VHL in very early CRC lesions from sporadic and familial adenomatous polyposis patients - presumably due to activated Wnt signaling - a clear reduction of VHL expression is observed in later stages of CRC progression, coinciding with stabilization of HIF1alpha.
  • [MeSH-major] Adenocarcinoma / etiology. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / etiology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Nerve Tissue Proteins / physiology. TCF Transcription Factors / physiology. Von Hippel-Lindau Tumor Suppressor Protein / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli / pathology. Animals. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Line. Colon / cytology. Colon / metabolism. Colon / pathology. Colonic Polyps / genetics. Colonic Polyps / metabolism. Colonic Polyps / pathology. Disease Progression. Epithelial Cells / metabolism. Erythropoietin / genetics. Gene Expression Regulation, Neoplastic. Genes, Reporter. Humans. Intestinal Mucosa / cytology. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Kidney. L Cells (Cell Line). Mice. Mice, Knockout. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Promoter Regions, Genetic. Recombinant Fusion Proteins / biosynthesis. Recombinant Fusion Proteins / genetics. Signal Transduction / physiology. Transcription Factor 7-Like 2 Protein. Wnt3 Protein

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  • (PMID = 16407833.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / CTNNB1 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf4 protein, mouse; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / beta Catenin; 11096-26-7 / Erythropoietin; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Vhlh protein, mouse; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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30. Geddert H, Zur Hausen A, Gabbert HE, Sarbia M: EBV-infection in cardiac and non-cardiac gastric adenocarcinomas is associated with promoter methylation of p16, p14 and APC, but not hMLH1. Anal Cell Pathol (Amst); 2010;33(3):143-9
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  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Adenomatous Polyposis Coli Protein / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA Methylation / genetics. Nuclear Proteins / genetics. Promoter Regions, Genetic / genetics. Stomach Neoplasms / genetics. Tumor Suppressor Protein p14ARF / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / virology. Adult. Aged. Aged, 80 and over. Epstein-Barr Virus Infections / genetics. Epstein-Barr Virus Infections / physiopathology. Female. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 20978327.001).
  • [ISSN] 2210-7185
  • [Journal-full-title] Analytical cellular pathology (Amsterdam)
  • [ISO-abbreviation] Anal Cell Pathol (Amst)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / APC protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / Tumor Suppressor Protein p14ARF
  • [Other-IDs] NLM/ PMC4605817
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31. Ho CM, Lai HC, Huang SH, Chien TY, Lin MC, Chang SF: Promoter methylation of sFRP5 in patients with ovarian clear cell adenocarcinoma. Eur J Clin Invest; 2010 Apr;40(4):310-8
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  • [Title] Promoter methylation of sFRP5 in patients with ovarian clear cell adenocarcinoma.
  • BACKGROUND: Specific tumour suppressor genes with promoter methylation in ovarian clear cell adenocarcinoma (OCCA) can be one important epigenetic mark distinguishing OCCA from ovarian serous adenocarcinoma (OSA), benign endometriotic cysts and normal ovarian epitheliums.
  • MATERIALS AND METHODS: Five OCCA cell lines, 63 cancer tissues (48 OCCA and 15 OSA), 10 benign endometriotic cysts and five normal ovarian epitheliums were analysed by methylation-specific PCR using pooled DNAs to determine the methylation status of the promoter of the target genes, including genes for secreted frizzled-related proteins (sFRP1 to 5), adenomatous polyposis coli (APC), retinoblastoma protein 1 (Rb1), breast cancer 1 gene (BRCA1), p14(ARF), p15(INK4b), p16(INK4a) and survivin.
  • [MeSH-major] Adenocarcinoma, Clear Cell / pathology. DNA Methylation. Eye Proteins. Membrane Proteins. Ovarian Neoplasms / pathology


32. Yamachika T, Nakanishi H, Yasui K, Ikehara Y, Niwa T, Wanibuchi H, Tatematsu M, Fukushima S: Establishment and characterization of a human colonic mucinous carcinoma cell line with predominant goblet-cell differentiation from liver metastasis. Pathol Int; 2005 Sep;55(9):550-7
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  • Many human colorectal adenocarcinoma cell lines have been developed.
  • In the present study a novel colorectal adenocarcinoma cell line (designated as COLM-6) with predominant goblet-cell differentiation was established from the rectal mucinous adenocarcinoma of a Japanese woman.
  • They were also positive for adenomatous polyposis coli (APC) cytoplasmically and expressed beta-catenin in their cytoplasm and cell membrane without nuclear accumulation.
  • These results indicate that COLM-6 cell line has unique characteristics and may provide a useful tool to study the mechanism of growth and differentiation of colonic epithelium as well as the biological behavior of colorectal mucinous adenocarcinoma.
  • [MeSH-major] Adenocarcinoma, Mucinous / secondary. Cell Line, Tumor / pathology. Colorectal Neoplasms / pathology. Goblet Cells / pathology. Liver Neoplasms / secondary


33. Bafandeh Y, Daghestani D, Esmaili H, Aharizad S: Distribution of cancer and adenomatous polyps in the colorectum: study in an Iranian population. Asian Pac J Cancer Prev; 2006 Jan-Mar;7(1):65-8
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  • [Title] Distribution of cancer and adenomatous polyps in the colorectum: study in an Iranian population.
  • OBJECTIVE: There is consensus that the majority of colorectal carcinomas (CRCs) arise from adenomatous polyps.
  • MATERIALS AND METHODS: We reviewed, retrospectively , endoscopically reported anatomic sites of all adenomatous polyps and CRCs which were histologically confirmed from Jan 1992 to Dec 2005 in Tabriz, the North-west of Iran.
  • One hundred and forty-three CRC's and 180 adenomatous polyps (in 145 patients) were found.
  • Patients with polyposis syndromes were excluded the analysis.
  • The propensity for polyps to be found in the descending colon was of borderline significance (p=0.07).
  • However, because of the occurrence of the neoplasms in the right colon total colonoscopy should still be considered for screening purposes.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / pathology. Adenomatous Polyposis Coli / epidemiology. Adenomatous Polyposis Coli / pathology. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / pathology

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  • (PMID = 16629518.001).
  • [ISSN] 1513-7368
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Thailand
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34. Zhang LX, Pan SY, Chen D, Xie EF, Gao L, Shu YQ, Lu ZH, Cheng L, Yang D, Zhang JN: [Effect of adenomatous polyposis coli(APC) promoter methylation on gene transcription in lung cancer cell lines]. Ai Zheng; 2007 Jun;26(6):576-80
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  • [Title] [Effect of adenomatous polyposis coli(APC) promoter methylation on gene transcription in lung cancer cell lines].
  • BACKGROUND & OBJECTIVE: Hypermethylation of CpG islands in adenomatous polyposis coli (APC) gene has been detected in a variety of human tumors, which is involved in the pathogenesis of these tumors.
  • METHODS: The methylation status of APC promoter 1A in lung adenocarcinoma cell line SPCA1, small cell lung cancer cell line NCI-H446, and big cell lung cancer cell line NCI-H460 was detected by methylation-specific polymerase chain reaction (MSP) and microarray methylated cord blood DNA served as positive control, and unmethylated cord blood DNA served as negative control.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. DNA Methylation. Genes, APC. Lung Neoplasms / metabolism. Transcription, Genetic
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Cell Line, Tumor. CpG Islands / genetics. Humans. Promoter Regions, Genetic. Small Cell Lung Carcinoma / metabolism. Small Cell Lung Carcinoma / pathology

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  • (PMID = 17562260.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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35. 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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  • 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.
  • 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.

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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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36. Subramaniam MM, Putti TC, Anuar D, Chong PY, Shah N, Salto-Tellez M, Soong R: Clonal characterization of sporadic cribriform-morular variant of papillary thyroid carcinoma by laser microdissection-based APC mutation analysis. Am J Clin Pathol; 2007 Dec;128(6):994-1001
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  • Analyses of gross C-MV of PTC lesions has linked adenomatous polyposis coli (APC) mutations to its pathogenesis; however, the extent of involvement of mutations in the development of individual components is unclear.
  • [MeSH-major] Adenocarcinoma, Papillary / genetics. Genes, APC. Microdissection / methods. Thyroid Neoplasms / genetics

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  • (PMID = 18024325.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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37. Breuhahn K, Singh S, Schirmacher P, Bläker H: Large-scale N-terminal deletions but not point mutations stabilize beta-catenin in small bowel carcinomas, suggesting divergent molecular pathways of small and large intestinal carcinogenesis. J Pathol; 2008 Jul;215(3):300-7
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  • Small intestinal adenocarcinoma is rare and its molecular pathogenesis is incompletely understood.
  • Stabilization of beta-catenin, a mediator of wnt/wingless signalling, can be detected in 50% of sporadic carcinomas but, in contrast to colorectal cancer, this finding can not be explained by the inactivation of adenomatous polyposis coli (APC).
  • In order to elucidate the molecular background of beta-catenin stabilization in small intestinal adenocarcinoma, we investigated 20 non-familial adenomatous polyposis coli (FAP)-associated tumours, including five microsatellite-unstable carcinomas for beta-catenin alterations, by immunohistochemistry, western blot analysis and sequence analysis on the RNA and DNA levels.
  • In contrast to colon carcinomas, neither APC nor CTNNB1 point mutations seem to play a significant role in carcinogenesis, indicating divergent mechanisms of wnt/wingless control in the small and the large intestine.
  • [MeSH-major] Adenocarcinoma / genetics. Intestinal Neoplasms / genetics. Sequence Deletion. beta Catenin / genetics
  • [MeSH-minor] Adenomatous Polyposis Coli. Adult. Aged. Aged, 80 and over. Cell Nucleus / metabolism. Cell Transformation, Neoplastic. Colorectal Neoplasms / genetics. Cytoplasm / metabolism. DNA Mutational Analysis. Duodenal Neoplasms / genetics. Exons. Female. Genes, APC. Humans. Ileal Neoplasms / genetics. Immunoblotting. Immunohistochemistry. Jejunal Neoplasms / genetics. Male. Middle Aged. Point Mutation. Sequence Analysis, RNA. Wnt Proteins / genetics

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  • [Copyright] Copyright (c) 2008 Pathological Society of Great Britain and Ireland.
  • (PMID = 18491352.001).
  • [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 / CTNNB1 protein, human; 0 / Wnt Proteins; 0 / beta Catenin
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38. Prall F, Weirich V, Ostwald C: Phenotypes of invasion in sporadic colorectal carcinomas related to aberrations of the adenomatous polyposis coli (APC ) gene. Histopathology; 2007 Feb;50(3):318-30
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  • [Title] Phenotypes of invasion in sporadic colorectal carcinomas related to aberrations of the adenomatous polyposis coli (APC ) gene.
  • AIMS: To determine whether the dissociation of tumour cells from neoplastic glands in colorectal carcinomas is caused by disruption of the wnt-signalling pathway and whether the adenomatous polyposis coli (APC) protein is implicated in this.
  • [MeSH-major] Adenocarcinoma, Mucinous / genetics. Colorectal Neoplasms / genetics. Genes, APC. Loss of Heterozygosity / genetics. Mutation


39. Raoof M, Canter RJ, Paty PB: Variable phenotypic expression of identical MYH germline mutations in siblings with attenuated familial adenomatous polyposis. Am Surg; 2007 Dec;73(12):1250-3
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  • [Title] Variable phenotypic expression of identical MYH germline mutations in siblings with attenuated familial adenomatous polyposis.
  • Germline mutations in the Mutant-Y-homologue (MYH) gene have been linked to an attenuated form of familial adenomatous polyposis in patients who express a wild-type adenomatous polyposis coli gene.
  • We report a case of siblings with identical germline mutations in the MYH gene, one of whom developed a locally advanced colon adenocarcinoma with few other adenomatous lesions, whereas the other had numerous benign colonic polyps.
  • The variable genotype-phenotype manifestations of MYH mutations and the attenuated familial adenomatous polyposis syndrome are discussed.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. DNA Glycosylases / genetics. Germ-Line Mutation / genetics

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  • (PMID = 18186383.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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40. 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
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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.
  • Surprisingly, BCAC were noted in the colon of even Apc(Min/+) mice of both ages, and mainly located in the distal and middle segments of the colon.
  • [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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41. Gasser M, Gerstlauer C, Grimm M, Bueter M, Lebedeva T, Lutz J, Maeder U, Ribas C, Ribas C, Nichiporuk E, Thalheimer A, Heemann U, Thiede A, Meyer D, Waaga-Gasser AM: Comparative analysis of predictive biomarkers for therapeutical strategies in colorectal cancer. Ann Surg Oncol; 2007 Apr;14(4):1272-84
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  • In addition, protein and gene expression of p53, CEA, and adenomatous polyposis coli (APC) was assessed in the tumors of those patients.
  • [MeSH-major] Adenocarcinoma / blood. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Colorectal Neoplasms / blood. Tumor Suppressor Protein p53 / blood

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  • (PMID = 17211733.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 0 / Tumor Suppressor Protein p53
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42. Okkels H, Sunde L, Lindorff-Larsen K, Thorlacius-Ussing O, Gandrup P, Lindebjerg J, Stubbeteglbjaerg P, Oestergaard JR, Nielsen FC, Krarup HB: Polyposis and early cancer in a patient with low penetrant mutations in MSH6 and APC: hereditary colorectal cancer as a polygenic trait. Int J Colorectal Dis; 2006 Dec;21(8):847-50
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  • [Title] Polyposis and early cancer in a patient with low penetrant mutations in MSH6 and APC: hereditary colorectal cancer as a polygenic trait.
  • Hereditary non-polyposis colorectal cancer and familial adenomatus polyposis are autosomal dominant diseases accounting for 5-7% of all colorectal cancer cases.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Colonic Neoplasms / genetics. DNA-Binding Proteins / genetics. Mutation. Rectal Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenoma / genetics. Adenomatous Polyposis Coli / genetics. Adolescent. Codon, Nonsense. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Humans. Male. Multifactorial Inheritance. Mutation, Missense. Pedigree. Phenotype

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  • (PMID = 16525781.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Codon, Nonsense; 0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein
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43. Kohno H, Takahashi M, Yasui Y, Suzuki R, Miyamoto S, Kamanaka Y, Naka M, Maruyama T, Wakabayashi K, Tanaka T: A specific inducible nitric oxide synthase inhibitor, ONO-1714 attenuates inflammation-related large bowel carcinogenesis in male Apc(Min/+) mice. Int J Cancer; 2007 Aug 1;121(3):506-13
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  • We previously reported that dextran sodium sulfate (DSS) strongly enhances colon carcinogenesis in the Apc(Min/+) mice and the over-expression of inducible nitric oxide synthase (iNOS) contributes to this enhancement.
  • In the current study, we investigated the effect of a selective iNOS inhibitor, ONO-1714 on colitis-related colon carcinogenesis in the Apc(Min/+) mouse treated with DSS.
  • Feeding with ONO-1714 significantly inhibited the occurrence of colonic adenocarcinoma in a dose-dependent manner in the Apc(Min/+) mice.
  • Our findings may suggest that ONO-1714 could therefore serve as an effective agent for suppression of colitis-related colon cancer development in the Apc(Min/+) mice.
  • [MeSH-major] Adenocarcinoma / prevention & control. Amidines / pharmacology. Colitis / complications. Colonic Neoplasms / prevention & control. Nitric Oxide Synthase Type II / antagonists & inhibitors
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Animals. Cyclooxygenase 2 / metabolism. Dextran Sulfate. Dose-Response Relationship, Drug. Heterocyclic Compounds, 2-Ring / administration & dosage. Heterocyclic Compounds, 2-Ring / pharmacology. Interleukin-1beta / metabolism. Intestinal Mucosa / metabolism. Male. Mice. Mice, Inbred C57BL. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Triglycerides / blood. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17417780.001).
  • [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 / 7-chloro-3-imino-5-methyl-2-azabicyclo(4.1.0)heptane; 0 / Amidines; 0 / Heterocyclic Compounds, 2-Ring; 0 / Interleukin-1beta; 0 / RNA, Messenger; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 9042-14-2 / Dextran Sulfate; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2
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44. Femia AP, Giannini A, Fazi M, Tarquini E, Salvadori M, Roncucci L, Tonelli F, Dolara P, Caderni G: Identification of mucin depleted foci in the human colon. Cancer Prev Res (Phila); 2008 Dec;1(7):562-7
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  • [Title] Identification of mucin depleted foci in the human colon.
  • Aberrant crypt foci (ACF) originally described in rodents treated with colon-specific carcinogens have been identified also in humans at high risk of colon cancer (CRC) and are extensively used as cancer biomarkers.
  • Recently, we described dysplastic foci depleted of mucins (MDF) in the colon of rats treated with colon-specific carcinogens.
  • Like colon tumors, MDFs show activation of Wnt signaling driven by mutations in the beta-catenin gene and Apc, a key gene in colorectal carcinogenesis.
  • Familial adenomatous polyposis (FAP) subjects, carrying germ-line mutations in the APC gene, are at high risk of CRC.
  • Therefore, we first searched for MDF-like lesions in unsectioned colon samples from FAP patients and then in patients with sporadic CRC.
  • MDFs were present in the colon of FAP patients (average of 0.0577 lesions/cm(2)) and at a much lower density in CRC patients (average of 0.0006 lesions/cm(2)).
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Colonic Neoplasms / pathology. Mucins / metabolism. Precancerous Conditions / pathology

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  • (PMID = 19139006.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mucins
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45. Pervaiz MA, Eppolito A, Schmidt K: Papillary thyroid cancer in a patient with MUTYH-associated polyposis (MAP). Fam Cancer; 2010 Dec;9(4):595-7
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  • [Title] Papillary thyroid cancer in a patient with MUTYH-associated polyposis (MAP).
  • We describe a patient with MUTYH-associated polyposis diagnosed with colon cancer at 33 years of age, as well as gastric polyps at a later age.
  • MUTYH-associated polyposis is an autosomal recessively inherited disease which has clinical overlap with Familial adenomatous polyposis and its attenuated form, in that it is associated with risk of colon cancer at a young age.
  • Extra-intestinal cancers have also been reported in patients with MUTYH-associated polyposis; however the tumor spectrum is still evolving.
  • National Comprehensive Cancer Network guidelines recommend screening for colon, duodenal and gastric polyps in individuals with MUTYH-associated polyposis.
  • These will likely continue to evolve as the MUTYH-associated polyposis tumor spectrum is better understood as a result of future case reports and research.
  • [MeSH-major] Adenocarcinoma, Papillary / genetics. Adenomatous Polyposis Coli / genetics. DNA Glycosylases / genetics. Germ-Line Mutation / genetics. Thyroid Neoplasms / genetics

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  • (PMID = 20625837.001).
  • [ISSN] 1573-7292
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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46. Hlubek F, Pfeiffer S, Budczies J, Spaderna S, Jung A, Kirchner T, Brabletz T: Securin (hPTTG1) expression is regulated by beta-catenin/TCF in human colorectal carcinoma. Br J Cancer; 2006 Jun 5;94(11):1672-7
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  • Overexpression of the transcriptional activator beta-catenin, mostly owing to loss-of-function mutations of the adenomatous polyposis coli (APC) tumour suppressor gene, is crucial for the initiation and progression of human colorectal carcinogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Colorectal Neoplasms / genetics. Gene Expression Regulation, Neoplastic / physiology. Neoplasm Proteins / blood. Neoplasm Proteins / genetics. TCF Transcription Factors / metabolism. beta Catenin / metabolism

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  • [ISO-abbreviation] Br. J. Cancer
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47. Gatalica Z, Torlakovic E: Pathology of the hereditary colorectal carcinoma. Fam Cancer; 2008;7(1):15-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pathologic examination of the biopsy or resection specimen can help in identification of unsuspected cases of certain forms of hereditary CRC due to the characteristic morphologic findings.
  • The most common form of hereditary CRC is Lynch syndrome (hereditary non-polyposis colorectal cancer, HNPCC) which is characterized by proximally located tumors frequently showing mucinous and medullary type histologic features.
  • The presence of intra-epithelial lymphocytes is single most helpful morphologic feature in identification of CRC caused by deficiency in MMR proteins, for which MSI-H status is a good marker but morphologic features and MSI-H do not differentiate tumors caused by germline mutations in one of the MMR genes (Lynch syndrome) from sporadic CRC due to inactivation of MLH-1 through promoter methylation.
  • Hereditary CRC may also arise in various familial polyposis syndromes which include familial adenomatous polyposis (FAP), attenuated FAP and other multiple adenomas syndromes as well as various hamartomatous polyposis syndromes.
  • All of these rare conditions have characteristic clinical presentation and histopathologic features of polyps and most of them have defined genetic abnormality.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. Lymphocytes, Tumor-Infiltrating / pathology. Peutz-Jeghers Syndrome / pathology
  • [MeSH-minor] Adenocarcinoma, Mucinous / pathology. Biomarkers, Tumor. Carcinoma, Medullary / pathology. DNA Mismatch Repair. Diagnosis, Differential. Genetic Predisposition to Disease. Genomic Instability. Germ-Line Mutation. Humans

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  • (PMID = 17564815.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 96
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48. Iarŭmov N, Toshev S, Petrova D, Angelov K, Gribnev P, Sokolov M: [Genetic counseling, surgical prophylaxis and treatment for familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer]. Khirurgiia (Sofiia); 2007;(3):46-53
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  • [Title] [Genetic counseling, surgical prophylaxis and treatment for familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer].
  • FAP is an autosomal dominant disorder characterized by the appearance of thousands of adenomatous polyps.
  • If an adenoma or adenocarcinoma of the colon is identified, total abdominal colectomy with an ileorectal anastomosis is recommended.
  • [MeSH-major] Adenomatous Polyposis Coli. Colorectal Neoplasms, Hereditary Nonpolyposis. Genetic Counseling. Intestine, Large / surgery


49. Kim DH, Kim JW, Cho JH, Baek SH, Kakar S, Kim GE, Sleisenger MH, Kim YS: Expression of mucin core proteins, trefoil factors, APC and p21 in subsets of colorectal polyps and cancers suggests a distinct pathway of pathogenesis of mucinous carcinoma of the colorectum. Int J Oncol; 2005 Oct;27(4):957-64
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  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma, Mucinous / metabolism. Adenomatous Polyposis Coli Protein / biosynthesis. Colorectal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Mucins / chemistry. Peptides / metabolism. Proto-Oncogene Proteins p21(ras) / biosynthesis. Tumor Suppressor Proteins / metabolism

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  • (PMID = 16142311.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucins; 0 / Peptides; 0 / TFF1 protein, human; 0 / TFF3 protein, human; 0 / Tumor Suppressor Proteins; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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50. Zhang MQ, Chen ZM, Wang HL: Immunohistochemical investigation of tumorigenic pathways in small intestinal adenocarcinoma: a comparison with colorectal adenocarcinoma. Mod Pathol; 2006 Apr;19(4):573-80
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  • [Title] Immunohistochemical investigation of tumorigenic pathways in small intestinal adenocarcinoma: a comparison with colorectal adenocarcinoma.
  • Small intestinal adenocarcinoma is an uncommon neoplasm morphologically similar to or indistinguishable from colorectal adenocarcinoma.
  • Although much has been learned about genetic pathways critical to colorectal tumorigenesis, little is known about molecular alterations involved in the development of small intestinal adenocarcinoma.
  • These included adenomatous polyposis coli and beta-catenin involved in the Wnt signaling pathway, and DNA mismatch repair enzymes hMLH1, hMSH2 and hMSH6 involved in the microsatellite instability pathway.
  • The results show that complete loss of adenomatous polyposis coli immunoreactivity, presumably resulting from its gene mutations, was observed in eight of 26 (31%) small intestinal adenocarcinomas and 36 of 51 (71%) colorectal adenocarcinomas (P = 0.0008).
  • Small intestinal tumorigenesis appears to follow a distinct, yet unidentified, molecular pathway(s) from its colorectal counterpart despite their morphologic similarity.
  • [MeSH-major] Adenocarcinoma / pathology. Colorectal Neoplasms / pathology. Intestinal Neoplasms / pathology. Intestine, Small / pathology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / analysis. Carrier Proteins / analysis. Cell Transformation, Neoplastic. DNA-Binding Proteins / analysis. Humans. Immunohistochemistry. Neoplasm Proteins / analysis. Nuclear Proteins / analysis. Retinoblastoma Protein / analysis. Signal Transduction. Tumor Suppressor Protein p53 / analysis. beta Catenin / analysis

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  • (PMID = 16501564.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein; 0 / MLH1 protein, human; 0 / MLH2 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Retinoblastoma Protein; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin
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51. Kim B, Byun SJ, Kim YA, Kim JE, Lee BL, Kim WH, Chang MS: Cell cycle regulators, APC/beta-catenin, NF-kappaB and Epstein-Barr virus in gastric carcinomas. Pathology; 2010 Jan;42(1):58-65
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  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / virology. Adenomatous Polyposis Coli Protein / metabolism. Adult. Aged. Aged, 80 and over. Cell Cycle Proteins / metabolism. Comorbidity. Female. Humans. In Situ Hybridization. Kaplan-Meier Estimate. Korea / epidemiology. Male. Middle Aged. NF-kappa B / metabolism. Neoplasm Staging. Survival Rate. beta Catenin / metabolism

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  • (PMID = 20025482.001).
  • [ISSN] 1465-3931
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / NF-kappa B; 0 / beta Catenin
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52. Prudhomme M, Dehni N, Dozois RR, Tiret E, Parc R: Causes and outcomes of pouch excision after restorative proctocolectomy. Br J Surg; 2006 Jan;93(1):82-6
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  • Five patients had familial adenomatous polyposis, in three of whom desmoid tumours were the cause of failure.
  • Finally, two patients with multiple colorectal adenocarcinoma developed recurrent cancer (one) or sepsis (one).
  • [MeSH-minor] Adenomatous Polyposis Coli / surgery. Adolescent. Adult. Aged. Child. Colitis, Ulcerative / surgery. Colonic Neoplasms / surgery. Crohn Disease / surgery. Humans. Middle Aged. Recurrence. Treatment Outcome. Wound Healing

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  • [Copyright] Copyright 2005 British Journal of Surgery Society Ltd.
  • (PMID = 16288450.001).
  • [ISSN] 0007-1323
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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53. Clément G, Jablons DM, Benhattar J: Targeting the Wnt signaling pathway to treat Barrett's esophagus. Expert Opin Ther Targets; 2007 Mar;11(3):375-89
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  • The clinical significance of this disease is its associated predisposition to esophageal adenocarcinoma (EAC).
  • Although mutations in adenomatous polyposis coli (APC) or beta-catenin are rare in EAC, alterations of upstream components, such as overexpression of Wnt2 ligand or downregulation of Wnt antagonists may play dominant roles in the activation of the Wnt pathway.

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  • (PMID = 17298295.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA093708-03; United States / NCI NIH HHS / CA / R01 CA093708; United States / NCI NIH HHS / CA / R01 CA093708-03
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Wnt Proteins
  • [Number-of-references] 125
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54. Yang Y, Fruehauf J, Xiang S, Li CJ: Genomic instability in precancerous lesions before inactivation of tumor suppressors p53 and APC in patients. Cell Cycle; 2006 Jul;5(13):1443-7
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  • The paradigm that inactivation of tumor suppressors [e.g. p53 or adenomatous polyposis coli (APC) genes] leads to GIN is largely based on experiments in vitro and in animal models.
  • We analyzed specimens from endoscopic biopsies or esophagectomies in patients with BE (ten cases, including five cases with multilayered epithelium (ME)), BE-associated esophageal adenocarcinoma (ten cases), or with normal gastro-esophageal junction (five cases).
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Genomic Instability. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16855398.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Tumor Suppressor Protein p53
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55. Adibelli ZH, Yildirim M, Ozan E, Oztekin O, Kucukzeybek B: Fibroadenoma of the breast in a man associated with adenocarcinoma of the rectum and polyposis coli. JBR-BTR; 2010 Jan-Feb;93(1):12-4
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  • [Title] Fibroadenoma of the breast in a man associated with adenocarcinoma of the rectum and polyposis coli.
  • We present herein the first case of a fibroadenoma of the breast in a 68-year-old man with adenocarcinoma of the rectum and polyposis coli.
  • [MeSH-major] Adenocarcinoma / complications. Adenomatous Polyposis Coli / complications. Breast Neoplasms, Male / complications. Fibroadenoma / complications. Rectal Neoplasms / complications

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  • (PMID = 20397428.001).
  • [ISSN] 0302-7430
  • [Journal-full-title] JBR-BTR : organe de la Société royale belge de radiologie (SRBR) = orgaan van de Koninklijke Belgische Vereniging voor Radiologie (KBVR)
  • [ISO-abbreviation] JBR-BTR
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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56. Mackey R, Walsh RM, Chung R, Brown N, Smith A, Church J, Burke C: Pancreas-sparing duodenectomy is effective management for familial adenomatous polyposis. J Gastrointest Surg; 2005 Nov;9(8):1088-93; discussion 1093
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  • [Title] Pancreas-sparing duodenectomy is effective management for familial adenomatous polyposis.
  • Duodenal adenocarcinoma remains the leading cause of cancer death in familial adenomatous polyposis patients following colectomy.
  • Pancreas-sparing duodenectomy represents a definitive treatment for advanced duodenal polyposis and can obviate the need for pancreaticoduodenectomy.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Duodenal Neoplasms / surgery. Duodenum / surgery. Pancreaticoduodenectomy / methods

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  • (PMID = 16269379.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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57. de Ferro SM, Suspiro A, Fidalgo P, Lage P, Rodrigues P, Fragoso S, Vitoriano I, Baltazar C, Albuquerque C, Bettencourt A, Leitão CN: Aggressive phenotype of MYH-associated polyposis with jejunal cancer and intra-abdominal desmoid tumor: report of a case. Dis Colon Rectum; 2009 Apr;52(4):742-5
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  • [Title] Aggressive phenotype of MYH-associated polyposis with jejunal cancer and intra-abdominal desmoid tumor: report of a case.
  • MYH-associated polyposis is an inherited autosomal recessive disease, linked to biallelic germline MYH mutations, which predisposes to the development of multiple colorectal adenomas and cancer.
  • We report the case of a young male patient with an aggressive MYH-associated polyposis phenotype.
  • Based on this report, we believe that screening of the entire small bowel should be recommended in MYH-associated polyposis patients, especially in those with duodenal adenomas.
  • Similar to patients with familial adenomatous polyposis, desmoid tumors also may be part of the clinical spectrum of MYH-associated polyposis and may prove to be a significant clinical problem in patients submitted to prophylactic colectomy.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms / genetics. Fibromatosis, Aggressive / genetics. Jejunal Neoplasms / genetics. Neoplasms, Multiple Primary / genetics. Peritoneal Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenoma / genetics. Adult. DNA Glycosylases / genetics. Duodenal Neoplasms / genetics. Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Intestinal Neoplasms / genetics. Intestinal Obstruction / etiology. Liver Neoplasms / secondary. Male. Mesentery. Mutation. Phenotype. Syndrome


58. Roa JC, Anabalón L, Roa I, Melo A, Araya JC, Tapia O, de Aretxabala X, Muñoz S, Schneider B: Promoter methylation profile in gallbladder cancer. J Gastroenterol; 2006 Mar;41(3):269-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Gallbladder Neoplasms / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Acid Anhydride Hydrolases / genetics. Acid Anhydride Hydrolases / metabolism. Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Adult. Aged. Aged, 80 and over. Cadherins / genetics. Cadherins / metabolism. Carrier Proteins / genetics. Carrier Proteins / metabolism. Chile. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Humans. Immunohistochemistry. Male. Middle Aged. MutL Protein Homolog 1. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Survival Analysis

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  • (PMID = 16699861.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / CDH1 protein, human; 0 / Cadherins; 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Neoplasm; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / fragile histidine triad protein; EC 3.6.- / Acid Anhydride Hydrolases; EC 3.6.1.3 / MutL Protein Homolog 1
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59. Ferrari A, Rognone A, Casanova M, Zaffignani E, Piva L, Collini P, Bertario L, Sala P, Leo E, Belli F, Gallino G: Colorectal carcinoma in children and adolescents: the experience of the Istituto Nazionale Tumori of Milan, Italy. Pediatr Blood Cancer; 2008 Mar;50(3):588-93
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  • PATIENTS AND METHODS: Among the children/adolescents (age 9-18, median 12 years), 5/7 had unfavorable CRC histotypes (poorly differentiated or mucinous adenocarcinoma) and all but one had advanced disease at onset.
  • [MeSH-major] Adenocarcinoma / epidemiology. Colorectal Neoplasms / epidemiology
  • [MeSH-minor] Adenocarcinoma, Mucinous / drug therapy. Adenocarcinoma, Mucinous / epidemiology. Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / surgery. Adenomatous Polyposis Coli / epidemiology. Adolescent. Adult. Age of Onset. Antineoplastic Agents / therapeutic use. Chemotherapy, Adjuvant. Child. Colorectal Neoplasms, Hereditary Nonpolyposis / epidemiology. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Italy / epidemiology. Male. Neoplasms, Second Primary / epidemiology. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17405155.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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60. Zippi M, De Felici I, Febbraro I, Mattei E, Traversa G, Occhigrossi G: [Distal hyperplastic polyps as a marker for advanced neoplasm of the proximal colon. Our experience]. Clin Ter; 2007 Sep-Oct;158(5):421-4
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  • [Title] [Distal hyperplastic polyps as a marker for advanced neoplasm of the proximal colon. Our experience].
  • Five hyperplastic polyps of the rectum were associated with 5 adenomas located 1 in the rectum, 2 in the sigmoid colon, and 1 in the descendens colon and 1 in the ascendens colon.
  • While, 5 adenomas were associated with 5 adenocarcinoma.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / etiology. Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / diagnosis. Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Colonoscopy. Female. Humans. Hyperplasia. Intestinal Polyps / complications. Intestinal Polyps / diagnosis. Male. Middle Aged. Predictive Value of Tests. Rectal Neoplasms / complications. Rectal Neoplasms / diagnosis. Retrospective Studies

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  • (PMID = 18062348.001).
  • [ISSN] 0009-9074
  • [Journal-full-title] La Clinica terapeutica
  • [ISO-abbreviation] Clin Ter
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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61. Chambers WM, McC Mortensen NJ: Should ileal pouch-anal anastomosis include mucosectomy? Colorectal Dis; 2007 Jun;9(5):384-92
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  • OBJECTIVE: Debate exists as to the benefits of performing mucosectomy as part of pouch surgery for ulcerative colitis (UC) and familial adenomatous polyposis (FAP).
  • Potential reasons for functional problems were investigated, as were rates of 'cuffitis', dysplasia, polyposis and cancer in the ileal pouch and anal canal.
  • Performing mucosectomy results in some clinical benefits in terms of lower rates of inflammation and dysplasia in the retained mucosa in UC patients and lower rates of cuff polyposis in FAP patients.
  • [MeSH-minor] Adenocarcinoma / prevention & control. Adenomatous Polyposis Coli / surgery. Anastomosis, Surgical / adverse effects. Anastomosis, Surgical / methods. Anus Neoplasms / prevention & control. Arsenates. Colitis, Ulcerative / surgery. Humans. Ileal Neoplasms / prevention & control. Randomized Controlled Trials as Topic

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  • (PMID = 17504334.001).
  • [ISSN] 1462-8910
  • [Journal-full-title] Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
  • [ISO-abbreviation] Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenates; N7CIZ75ZPN / arsenic acid
  • [Number-of-references] 70
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62. Canter RJ, Kesmodel SB, Heitjan DF, Veeramachaneni NK, Mokadam NA, Drebin JA, Fraker DL: Suppression of beta-catenin by antisense oligomers augments tumor response to isolated limb perfusion in a rodent model of adenomatous polyposis coli-mutant colon cancer. Ann Surg Oncol; 2005 Sep;12(9):733-42
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  • [Title] Suppression of beta-catenin by antisense oligomers augments tumor response to isolated limb perfusion in a rodent model of adenomatous polyposis coli-mutant colon cancer.
  • METHODS: Adenomatous polyposis coli-mutant human CRC xenografts were implanted into athymic rats.
  • [MeSH-major] Adenocarcinoma / drug therapy. Colonic Neoplasms / drug therapy. Oligodeoxyribonucleotides, Antisense / administration & dosage. beta Catenin / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / genetics. Animals. Antineoplastic Agents, Alkylating / administration & dosage. Cell Line, Tumor. Chemotherapy, Cancer, Regional Perfusion / methods. Extremities. Female. Genetic Therapy. Melphalan / administration & dosage. Models, Animal. Rats. Remission Induction

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  • (PMID = 16132380.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Oligodeoxyribonucleotides, Antisense; 0 / beta Catenin; Q41OR9510P / Melphalan
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63. Qian B, Ke PQ, Wang L, Liu WJ, Li MX: [Expression and methylation of adenomatous polyposis coli gene in endometrioid adenocarcinoma]. Ai Zheng; 2008 Jun;27(6):585-9
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  • [Title] [Expression and methylation of adenomatous polyposis coli gene in endometrioid adenocarcinoma].
  • Adenomatous polyposis coli (APC) gene, a tumor suppressor gene, is expressed in many tissues, and has a certain relationship with ovarian cancer.
  • This study was to observe the expression and DNA methylation of APC gene in endometrioid adenocarcinoma, and explore its correlations to the occurrence and development of this disease.
  • METHODS: The methylation, mRNA and protein expression of APC gene were detected by methylation-specific polymerase chain reaction (PCR), reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry in 30 specimens of normal proliferative endometrium, 30 specimens of atypical hyperplastic endometrium and 60 specimens of endometrioid adenocarcinoma.
  • RESULTS: The methylation rate of APC gene was significantly higher, the positive rates of APC mRNA and protein were significantly lower in endometrioid adenocarcinoma than in atypical hyperplastic endometrium and normal proliferative endometrium (65.0% vs. 33.3% and 23.3%, 33.3% vs. 63.3% and 73.3%, 30.0% vs. 50.0% and 66.7%,P<0.05).
  • CONCLUSION: The expression and DNA methylation of APC gene are certainly related with the occurrence and development of endometrioid adenocarcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Carcinoma, Endometrioid / genetics. DNA Methylation. Endometrial Neoplasms / genetics

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  • (PMID = 18570730.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / RNA, Messenger
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64. Dai WB, Ren ZP, Chen WL, DU J, Shi Z, Tang DY: [Expression and significance of APC, beta-catenin, C-myc, and Cyclin D1 proteins in colorectal carcinoma]. Ai Zheng; 2007 Sep;26(9):963-6
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  • This study was to examine the expression of adenomatous polyposis coli (APC), beta-catenin, C-myc, and Cyclin D1 in different colorectal tissues, and investigate their possible roles in the carcinogenesis of colorectal carcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Colorectal Neoplasms / metabolism. Cyclin D1 / metabolism. Proto-Oncogene Proteins c-myc / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenoma / metabolism. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Precancerous Conditions / metabolism

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  • (PMID = 17927853.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CCND1 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1
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65. Roy UK, Henkhaus RS, Ignatenko NA, Mora J, Fultz KE, Gerner EW: Wild-type APC regulates caveolin-1 expression in human colon adenocarcinoma cell lines via FOXO1a and C-myc. Mol Carcinog; 2008 Dec;47(12):947-55
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  • [Title] Wild-type APC regulates caveolin-1 expression in human colon adenocarcinoma cell lines via FOXO1a and C-myc.
  • The role of caveolin-1 in colon carcinogenesis is controversial.
  • We report here, for the first time, that caveolin-1 is transcriptionally induced in colon cancer cells in response to conditional expression of a full length adenomatous polyposis coli (APC) gene.
  • Our results would be consistent with the interpretation that caveolin-1 may have tumor suppressing functions during early stages of colon carcinogenesis.

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  • (PMID = 18444242.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA72008; United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / CA95060; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / P50 CA095060-05; United States / NCI NIH HHS / CA / R01 CA123065; United States / NCI NIH HHS / CA / P01 CA072008; United States / NCI NIH HHS / CA / P30 CA023074-209010; United States / NCI NIH HHS / CA / R01 CA123065-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caveolin 1; 0 / FOXO1 protein, human; 0 / Forkhead Transcription Factors; 0 / Proto-Oncogene Proteins c-myc
  • [Other-IDs] NLM/ NIHMS766917; NLM/ PMC4847746
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66. Conlin A, Smith G, Carey FA, Wolf CR, Steele RJ: The prognostic significance of K-ras, p53, and APC mutations in colorectal carcinoma. Gut; 2005 Sep;54(9):1283-6
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  • BACKGROUND: Accumulation of molecular alterations, including mutations in Kirsten-ras (K-ras), p53, and adenomatous polyposis coli (APC), contribute to colorectal carcinogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Colorectal Neoplasms / genetics. Genes, ras. Mutation

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  • (PMID = 15843421.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1774675
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67. Achneck HE, Wong IY, Kim PJ, Fernandes MA, Walther Z, Seymour NE, Jain D: Ileostomy adenocarcinomas in the setting of ulcerative colitis. J Clin Gastroenterol; 2005 May-Jun;39(5):396-400
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  • Adenocarcinomas arising at ileostomy sites in patients after colon resection for various diseases, such as ulcerative colitis (UC), familial adenomatous polyposis coli, and Crohn's disease, are rare occurrences but have been reported increasingly in the last 20 years.
  • We report a case of adenocarcinoma arising in an ileostomy site in an 85-year-old woman with longstanding UC.
  • A subsequent biopsy revealed adenocarcinoma with signet-ring cells and abundant extracellular mucin.
  • The literature on adenocarcinoma arising in the 23 patients with ulcerative colitis who received a Brooke or Kock ileostomy and had no prior history of neoplasm is reviewed.
  • [MeSH-major] Adenocarcinoma, Mucinous / etiology. Colitis, Ulcerative / surgery. Ileal Neoplasms / etiology. Ileostomy

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  • (PMID = 15815208.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 37
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68. Halberg RB, Waggoner J, Rasmussen K, White A, Clipson L, Prunuske AJ, Bacher JW, Sullivan R, Washington MK, Pitot HC, Petrini JH, Albertson DG, Dove WF: Long-lived Min mice develop advanced intestinal cancers through a genetically conservative pathway. Cancer Res; 2009 Jul 15;69(14):5768-75
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  • C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenomas along the entire length of the intestine and consequently die at an early age.

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  • (PMID = 19584276.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA084227-05; United States / NIGMS NIH HHS / GM / R01 GM056888-12; United States / NIGMS NIH HHS / GM / GM056888-12; United States / NCI NIH HHS / CA / U01 CA084118; United States / NCI NIH HHS / CA / R01 CA063677-15A2; United States / NCI NIH HHS / CA / P30 CA014520; United States / NIGMS NIH HHS / GM / GM059413-12; United States / NCI NIH HHS / CA / U01 CA84227; United States / NCI NIH HHS / CA / R01 CA063677; United States / NCI NIH HHS / CA / U01 CA084227; United States / NCI NIH HHS / CA / R37 CA063677; United States / NCI NIH HHS / CA / U01 CA84118; United States / NIGMS NIH HHS / GM / R01 GM059413; United States / NCI NIH HHS / CA / CA063677-15A2; United States / NIGMS NIH HHS / GM / R01 GM056888; United States / NCI NIH HHS / CA / R37 CA63677; United States / NIGMS NIH HHS / GM / R01 GM059413-12; United States / NCI NIH HHS / CA / U01 CA084227-05
  • [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 / Adenomatous Polyposis Coli Protein; 0 / Alkylating Agents; 0 / Cell Cycle Proteins; 0 / Nijmegen breakage syndrome 1 protein, mouse; 0 / Nuclear Proteins; P8M1T4190R / Ethylnitrosourea
  • [Other-IDs] NLM/ NIHMS119622; NLM/ PMC2775466
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69. Sudo T, Murakami Y, Uemura K, Hayashidani Y, Takesue Y, Sueda T: Development of an intraductal papillary-mucinous neoplasm of the pancreas in a patient with familial adenomatous polyposis. Pancreas; 2005 Nov;31(4):428-9
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  • [Title] Development of an intraductal papillary-mucinous neoplasm of the pancreas in a patient with familial adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma, Mucinous / etiology. Adenomatous Polyposis Coli / complications. Carcinoma, Pancreatic Ductal / etiology. Carcinoma, Papillary / etiology. Pancreatic Neoplasms / etiology


70. Hoffmann AC, Vallböhmer D, Prenzel K, Metzger R, Heitmann M, Neiss S, Ling F, Hölscher AH, Schneider PM, Brabender J: Methylated DAPK and APC promoter DNA detection in peripheral blood is significantly associated with apparent residual tumor and outcome. J Cancer Res Clin Oncol; 2009 Sep;135(9):1231-7
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  • BACKGROUND: Death-associated protein kinase (DAPK) and adenomatous polyposis coli gene (APC) have been recently shown to be associated with outcome in patients with esophageal carcinoma, especially adenocarcinoma.
  • CONCLUSIONS: Preoperative measurement of methylated DAPK and APC promoter DNA in peripheral blood may contribute to better estimate postoperative survival chances of patients with esophageal carcinoma, especially adenocarcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Apoptosis Regulatory Proteins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. DNA Methylation / genetics. DNA, Neoplasm / blood. Esophageal Neoplasms / genetics. Neoplasm, Residual / genetics. Promoter Regions, Genetic / genetics

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  • (PMID = 19259700.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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71. Bougatef K, Krichene A, Marrakchi R, Kourda N, Blondeau Lahely Y, Moussa A, Troudi W, Jileni SB, Najjar T, Soubrier F, Ammar Elgaaied AB: Do we know all there is to know about Familial Adenomatous Polyposis? Gastroenterol Clin Biol; 2007 Dec;31(12):1062-6
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  • [Title] Do we know all there is to know about Familial Adenomatous Polyposis?
  • Familial Adenomatous Polyposis (FAP) and Attenuated FAP (AFAP) are caused by a germline mutation in the Adenomatous polyposis coli (APC) gene.
  • This report describes a Tunisian patient with an attenuated FAP phenotype, presenting seven colon polyps and an adenocarcinoma but no detectable germline mutations in the FAP target genes.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics

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  • (PMID = 18176357.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Codon; 0 / Codon, Terminator; JAC85A2161 / Adenine
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72. Das P, Jain D, Vaiphei K, Wig JD: Abberant crypt foci -- importance in colorectal carcinogenesis and expression of p53 and mdm2: a changing concept. Dig Dis Sci; 2008 Aug;53(8):2183-8
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  • Till date, in human ACF, K-ras, beta-catenin, carcinoembryonic antigen (CEA) and adenomatous polyposis coli (APC) protein expression have been investigated, but the expression of late markers of colon carcinogenesis have not been studied in great detail.
  • [MeSH-major] Adenocarcinoma / chemistry. Cell Transformation, Neoplastic / chemistry. Colorectal Neoplasms / chemistry. Precancerous Conditions / chemistry. Proto-Oncogene Proteins c-mdm2 / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 18080767.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2
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73. Murphy HR, Taylor W, Ellis A, Sturgess R: An unusual case of Turcot's syndrome associated with ileal adenocarcinoma, intestinal non-Hodgkin's lymphoma, and duodenal adenocarcinoma. Review of the classification and genetic basis of Turcot's syndrome. Fam Cancer; 2005;4(2):139-43
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  • [Title] An unusual case of Turcot's syndrome associated with ileal adenocarcinoma, intestinal non-Hodgkin's lymphoma, and duodenal adenocarcinoma. Review of the classification and genetic basis of Turcot's syndrome.
  • A 38-year-old man with a history of colonic and small bowel polyposis and glioblastoma was investigated for dyspepsia.
  • Although cases of Turcot's syndrome (TS) (colonic polyposis and primary brain tumour occurring in the same patient) have been previously described, association with haematological malignancy is rare.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Brain Neoplasms / pathology. Duodenal Neoplasms / pathology. Glioblastoma / pathology. Ileal Neoplasms / pathology. Intestinal Neoplasms / pathology. Lymphoma, B-Cell, Marginal Zone / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 15951965.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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74. Constantin V, Socea B, Moculescu C, Sireţeanu G, Popa F: [Enteral non-Hodgkin lymphoma in young age--difficult diagnosis]. Chirurgia (Bucur); 2009 Sep-Oct;104(5):607-10
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  • We present the case of a 22-years-old patient, having colonic polyposis and multicentric non-Hodgkin lymphoma of the terminal ileum and ascending colon.
  • The rest of malignant colonic tumors developed on patients with rectocolonic polyposis were adenocarcinoma.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenomatous Polyposis Coli / diagnosis. Adult. Colectomy / methods. Colon, Ascending / pathology. Diagnosis, Differential. Humans. Male. Prognosis. Treatment Outcome


75. Kets CM, Hoogerbrugge N, Bodmer D, Willems R, Brunner HG, van Krieken JH, Ligtenberg MJ: Unfavorable pathological characteristics in familial colorectal cancer with low-level microsatellite instability. Mod Pathol; 2006 Dec;19(12):1624-30
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  • A high degree of microsatellite instability (MSI) in colorectal cancer (CRC) is a hallmark of hereditary non-polyposis colorectal cancer (HNPCC), caused by germline defects in the mismatch repair (MMR) genes.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Microsatellite Instability

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  • (PMID = 16980941.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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76. Herbst A, Bommer GT, Kriegl L, Jung A, Behrens A, Csanadi E, Gerhard M, Bolz C, Riesenberg R, Zimmermann W, Dietmaier W, Wolf I, Brabletz T, Göke B, Kolligs FT: ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition. Gastroenterology; 2009 Aug;137(2):639-48, 648.e1-9
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  • RESULTS: ITF-2B is strongly expressed in colon adenomas but frequently down-regulated in carcinomas because of LOH at 18q21.
  • Loss of ITF-2B expression correlates with loss of p21(Cip1) expression in primary colon carcinomas.
  • ITF-2B, which is up-regulated during early colorectal carcinogenesis because of loss of adenomatous polyposis coli, is a target for LOH on chromosome 18q, along with deleted in colorectal carcinoma and Smad4.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 19394332.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors
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77. Trna J, Husová L, Oliverius M, Dastych M Jr, Senkyrík M, Príbramská V: [The case of familial adenomatous polyposis and a proposal for the system of dispensarisation]. Vnitr Lek; 2009 Jun;55(6):587-92
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  • [Title] [The case of familial adenomatous polyposis and a proposal for the system of dispensarisation].
  • We present a case of a 46 years old female with familial adenomatous polyposis of the colon.
  • The adenocarcinoma had been treated using all available oncology therapeutic modalities.
  • [MeSH-major] Adenomatous Polyposis Coli / therapy
  • [MeSH-minor] Adenocarcinoma / surgery. Colonic Neoplasms / surgery. Digestive System Surgical Procedures / adverse effects. Female. Humans. Middle Aged. Short Bowel Syndrome / etiology. Short Bowel Syndrome / therapy

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  • (PMID = 19662891.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
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78. 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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  • However, loss of Pten in the context of Apc deficiency accelerates tumorigenesis through increased activation of Akt, leading to rapid development of adenocarcinoma.
  • 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.
  • [MeSH-major] Adenoma / genetics. Adenomatous Polyposis Coli Protein / genetics. Intestinal Neoplasms / genetics. Intestine, Small / pathology. PTEN Phosphohydrolase / genetics

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  • (PMID = 19011632.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Grant] 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 3.1.3.67 / PTEN Phosphohydrolase; EC 3.1.3.67 / Pten protein, mouse
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79. Guo L, Zhong D, Lau S, Liu X, Dong XY, Sun X, Yang VW, Vertino PM, Moreno CS, Varma V, Dong JT, Zhou W: Sox7 Is an independent checkpoint for beta-catenin function in prostate and colon epithelial cells. Mol Cancer Res; 2008 Sep;6(9):1421-30
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  • [Title] Sox7 Is an independent checkpoint for beta-catenin function in prostate and colon epithelial cells.
  • Although nearly all colorectal cancers contain mutations in beta-catenin or adenomatous polyposis coli/axin, epigenetic silencing of Sox7 was still observed.

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  • (PMID = 18819930.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106826-01A1; United States / NCI NIH HHS / CA / CA106826-04; United States / NCI NIH HHS / CA / R01 CA106826-02; United States / NCI NIH HHS / CA / CA077337; United States / NCI NIH HHS / CA / R01 CA106826-04; United States / NCI NIH HHS / CA / R01 CA077337; United States / NCI NIH HHS / CA / CA106826-02; United States / NCI NIH HHS / CA / CA106826-01A1; United States / NCI NIH HHS / CA / CA106826-03; United States / NCI NIH HHS / CA / R01 CA077337-05; United States / NCI NIH HHS / CA / CA077337-05; United States / NCI NIH HHS / CA / R01 CA106826-03; United States / NCI NIH HHS / CA / R01 CA106826
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / High Mobility Group Proteins; 0 / RNA, Messenger; 0 / SOX7 protein, human; 0 / SOXF Transcription Factors; 0 / TCF Transcription Factors; 0 / Transcription Factors; 0 / beta Catenin; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ NIHMS72222; NLM/ PMC2652859
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80. Akatsu T, Aiura K, Takahashi S, Kameyama K, Kitajima M, Kitagawa Y: Recurrent pancreatitis caused by ampullary carcinoma and minor papilla adenoma in familial polyposis: report of a case. Surg Today; 2008;38(5):440-4
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  • [Title] Recurrent pancreatitis caused by ampullary carcinoma and minor papilla adenoma in familial polyposis: report of a case.
  • We report a case of relapsing pancreatitis in familial adenomatous polyposis (FAP) with severe duodenal adenomatosis (Spigelman's stage IV).
  • [MeSH-major] Adenocarcinoma / etiology. Adenoma / etiology. Adenomatous Polyposis Coli / complications. Ampulla of Vater. Common Bile Duct Neoplasms / etiology. Pancreatic Neoplasms / etiology. Pancreatitis / etiology


81. Soravia C, DeLozier CD, Dobbie Z, Berthod CR, Arrigoni E, Bründler MA, Blouin JL, Foulkes WD, Hutter P: Double frameshift mutations in APC and MSH2 in the same individual. Int J Colorectal Dis; 2005 Sep;20(5):466-470
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  • Here we report the case of a proband whose father was known for familial adenomatous polyposis.
  • The number of polyps (less than ten) was not typical of polyposis; therefore, the diagnosis of HNPCC was entertained.
  • Prophylactic colectomy was performed, and an adenocarcinoma developing within the adenoma was diagnosed (pT1N0).
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Frameshift Mutation. Genes, APC. MutS Homolog 2 Protein / genetics

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  • (PMID = 15834612.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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82. Brosens LA, van Hattem A, Hylind LM, Iacobuzio-Donahue C, Romans KE, Axilbund J, Cruz-Correa M, Tersmette AC, Offerhaus GJ, Giardiello FM: Risk of colorectal cancer in juvenile polyposis. Gut; 2007 Jul;56(7):965-7
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  • [Title] Risk of colorectal cancer in juvenile polyposis.
  • BACKGROUND: Juvenile polyposis (JP) is an autosomal-dominant syndrome characterised by the development of hamartomatous gastrointestinal polyps and is associated with colorectal cancer.

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  • (PMID = 17303595.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 51085; United States / NCI NIH HHS / CA / CA 53801; United States / NCI NIH HHS / CA / CA 63721; United States / NCI NIH HHS / CA / P50 CA 93-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1994351
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83. Frattini M, Perrone F, Suardi S, Balestra D, Caramuta S, Colombo F, Licitra L, Cantù G, Pierotti MA, Pilotti S: Phenotype-genotype correlation: challenge of intestinal-type adenocarcinoma of the nasal cavity and paranasal sinuses. Head Neck; 2006 Oct;28(10):909-15
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  • [Title] Phenotype-genotype correlation: challenge of intestinal-type adenocarcinoma of the nasal cavity and paranasal sinuses.
  • BACKGROUND: Intestinal-type adenocarcinoma (ITAC) of the nasal cavity and paranasal sinuses shows microscopic features indistinguishable from colorectal cancer.
  • Our aim was to verify whether the morphologic resemblances mirror genetic profile similarities.
  • METHODS: Twenty consecutive surgically treated ITAC cases, previously investigated for p16(INK4a) and TP53, were investigated for hMLH1, hMSH2, and beta-catenin immunoreactivity, and for adenomatous polyposis coli (APC), K-ras, and BRAF gene mutations.
  • [MeSH-major] Adenocarcinoma / genetics. Nasal Cavity. Nose Neoplasms / genetics. Paranasal Sinus Neoplasms / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / genetics. Carrier Proteins / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA Mismatch Repair. Gene Expression Regulation, Neoplastic. Genes, ras / genetics. Genotype. Humans. Loss of Heterozygosity. MutS Homolog 2 Protein / genetics. Mutation. Nuclear Proteins / genetics. Phenotype. Proto-Oncogene Proteins B-raf / genetics. beta Catenin / genetics

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  • [Copyright] (c) 2006 Wiley Periodicals, Inc.
  • (PMID = 16906516.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / beta Catenin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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84. Jasperson KW, Blazer KR, Lowstuter K, Weitzel JN: Working through a diagnostic challenge: colonic polyposis, Amsterdam criteria, and a mismatch repair mutation. Fam Cancer; 2008;7(4):281-5
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  • [Title] Working through a diagnostic challenge: colonic polyposis, Amsterdam criteria, and a mismatch repair mutation.
  • The two most common causes of hereditary colorectal cancer are Lynch syndrome and familial adenomatous polyposis (FAP).
  • The phenotype of Lynch syndrome, also known as hereditary nonpolyposis colorectal cancer (HNPCC), is differentiated in part from FAP by the lack of profuse colonic polyposis.
  • Here we describe a proband who presented with greater than 50 adenomatous colonic polyps prior to developing cancer of the colon and urinary bladder, and a family history that fulfills the Amsterdam criteria.
  • We outline evidence supporting the pathogenicity of the identified hMSH6 mutation (arg772trp) and suggest possible etiologies for the unexplained colonic adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenomatous Polyposis Coli / complications. Colonic Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. DNA-Binding Proteins

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  • (PMID = 18176851.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000043; United States / NCI NIH HHS / CA / R25 CA085771; United States / NCRR NIH HHS / RR / M01 RR00043; United States / NCI NIH HHS / CA / R25 CA85771
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein
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85. Brücher BL, Geddert H, Langner C, Höfler H, Fink U, Siewert JR, Sarbia M: Hypermethylation of hMLH1, HPP1, p14(ARF), p16(INK4A) and APC in primary adenocarcinomas of the small bowel. Int J Cancer; 2006 Sep 15;119(6):1298-302
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  • Small bowel adenocarcinoma (SB-AC) is a very rare tumor entity.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Intestinal Neoplasms / genetics. Intestine, Small / pathology. Neoplasm Proteins / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / genetics. Adult. Aged. Aged, 80 and over. Carrier Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA, Neoplasm / genetics. Female. Humans. Male. Membrane Proteins / genetics. Middle Aged. Nuclear Proteins / genetics. Tumor Suppressor Protein p14ARF / genetics

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  • (PMID = 16619216.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Neoplasm; 0 / MLH1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / TMEFF2 protein, human; 0 / Tumor Suppressor Protein p14ARF
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86. Lolis ED, Likoudis P, Voiniadis P, Hassiakos D, Samanides L: Synchronous rectal and colon cancer caused by familial polyposis coli during pregnancy. J Obstet Gynaecol Res; 2007 Apr;33(2):199-202
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  • [Title] Synchronous rectal and colon cancer caused by familial polyposis coli during pregnancy.
  • The management of colon and rectal cancer during pregnancy is controversial and challenging.
  • Rectal or colon cancer during pregnancy is a very rare event.
  • A 29-year-old woman, pregnant with her second child, was diagnosed with rectal cancer causing bowel obstruction and synchronous colon cancer during the 27th week of gestation.
  • Both cancers occurred as a result of familial polyposis.
  • This is the first case of synchronous rectal and colon cancer caused by familial polyposis during pregnancy reported in the published literature.
  • [MeSH-major] Adenocarcinoma / etiology. Adenomatous Polyposis Coli / complications. Neoplasms, Multiple Primary / etiology. Pregnancy Complications, Neoplastic / etiology. Rectal Neoplasms / etiology


87. Kim JC, Ka IH, Lee YM, Koo KH, Kim HC, Yu CS, Jang SJ, Kim YS, Lee HI, Lee KH: MYH, OGG1, MTH1, and APC alterations involved in the colorectal tumorigenesis of Korean patients with multiple adenomas. Virchows Arch; 2007 Mar;450(3):311-9
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  • This study was done to characterize base excision repair (BER) genes and adenomatous polyposis coli (APC) alterations in the tumorigenesis of multiple colorectal adenomas in Korean patients.
  • The G:C>T:A transversion or attenuated familial adenomatous polyposis (AFAP) mutations of APC was identified in the specific genotypes of BER variants.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Biomarkers, Tumor / genetics. Colorectal Neoplasms / genetics. Mutation. Neoplasms, Multiple Primary / genetics
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Adult. Aged. Aged, 80 and over. DNA Glycosylases / genetics. DNA Glycosylases / metabolism. DNA Mismatch Repair. DNA Mutational Analysis. DNA Repair Enzymes / genetics. DNA Repair Enzymes / metabolism. DNA-(Apurinic or Apyrimidinic Site) Lyase / genetics. DNA-(Apurinic or Apyrimidinic Site) Lyase / metabolism. Female. Humans. Male. Middle Aged. Mitochondrial Proteins / genetics. Mitochondrial Proteins / metabolism. N-Glycosyl Hydrolases / genetics. N-Glycosyl Hydrolases / metabolism. Neoplasm Staging. Phosphoric Monoester Hydrolases / genetics. Phosphoric Monoester Hydrolases / metabolism. Polymorphism, Single Nucleotide. Prospective Studies

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  • (PMID = 17252231.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mitochondrial Proteins; EC 3.1.3.2 / Phosphoric Monoester Hydrolases; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / N-Glycosyl Hydrolases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.2.2.- / oxoguanine glycosylase 1, human; EC 3.6.1.55 / 8-oxodGTPase; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase; EC 6.5.1.- / DNA Repair Enzymes
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88. Wang Y, Zhang D, Zheng W, Luo J, Bai Y, Lu Z: Multiple gene methylation of nonsmall cell lung cancers evaluated with 3-dimensional microarray. Cancer; 2008 Mar 15;112(6):1325-36
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  • RESULTS: Methylation frequencies in the tumor samples were detected in 18% of samples for the breast cancer 1 gene BRCA1, in 43% of samples for the tissue inhibitor of metalloproteinase 3 gene TIMP-3, in 38% of samples for the cyclin-dependent kinase inhibitor 4A gene p16INK4a, in 54% of samples for the cadherin 13 gene CDH13, in 50% of samples for the death-associated protein kinase gene DAPK, in 11% of samples for the E-cadherin gene ECAD, in 25% of samples for the insulin-like growth factor binding protein 7 gene IGFBP7, in 18% of samples for the Ras association domain family 1 gene RASSF1, in 68% of samples for the adenomatous polyposis coli gene APC, in 7% of samples for the cyclin-dependent kinase inhibitor gene p15, in 18% of samples for the CD44 cell adhesion molecule gene, in 29% of samples for the human Mut-L homolog gene hMLH, in 32% of samples for the human telomerase reverse transcriptase gene hTERT, in 64% of samples for the calcitonin gene-related polypeptide alpha gene CALCA, and in 54% of samples for the estrogen receptor gene ER; however, methylation was not observed in the majority of corresponding nonmalignant tissues.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / secondary. Apoptosis Regulatory Proteins / genetics. Cadherins / genetics. Calcium-Calmodulin-Dependent Protein Kinases / genetics. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / secondary. Case-Control Studies. CpG Islands. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Death-Associated Protein Kinases. Female. Humans. In Situ Hybridization. Insulin-Like Growth Factor Binding Proteins / genetics. Lung / metabolism. Lung / pathology. Male. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Tissue Inhibitor of Metalloproteinase-3 / genetics. Ubiquitin-Protein Ligases / genetics

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  • [Copyright] Copyright (c) 2008 American Cancer Society.
  • (PMID = 18286531.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CDH17 protein, human; 0 / Cadherins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / H-cadherin; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / RNA, Messenger; 0 / TIMP3 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / insulin-like growth factor binding protein-related protein 1; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 6.3.2.- / BRAP protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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89. Frattini M, Carnevali I, Signoroni S, Balestra D, Moiraghi ML, Radice P, Varesco L, Gismondi V, Ballardini G, Sala P, Pierotti MA, Pilotti S, Bertario L: Cyclooxygenase-2 expression in FAP patients carrying germ line MYH mutations. Cancer Epidemiol Biomarkers Prev; 2005 Aug;14(8):2049-52
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  • Familial adenomatous polyposis (FAP) is an autosomal condition caused by inherited mutations in the adenomatous polyposis coli (APC) or in the MYH genes.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. DNA Glycosylases / genetics. Germ-Line Mutation / genetics. Prostaglandin-Endoperoxide Synthases / metabolism

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  • (PMID = 16103460.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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90. Shao J, Washington MK, Saxena R, Sheng H: Heterozygous disruption of the PTEN promotes intestinal neoplasia in APCmin/+ mouse: roles of osteopontin. Carcinogenesis; 2007 Dec;28(12):2476-83
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  • Mutations of both regulatory subunit and catalytic subunit of PI3K have been demonstrated in colon cancers.
  • Number and size of intestinal tumors were significantly increased in mice bearing both adenomatous polyposis coli (APC) and PTEN mutations.
  • In colon cancer cells, gain-of-function mutation of PI3K robustly increased levels of OPN and treatment with OPN reduced growth factor deprivation-induced programmed cell death.
  • Thus, our results suggest that the PI3K pathway promotes the transformation of intestinal adenoma to adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Adenomatous Polyposis Coli / genetics. Colonic Neoplasms / pathology. Osteopontin / physiology. PTEN Phosphohydrolase / physiology

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  • (PMID = 17693663.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-065615; United States / NIDDK NIH HHS / DK / DK-64593
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Spp1 protein, mouse; 106441-73-0 / Osteopontin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
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91. Bouguen G, Manfredi S, Blayau M, Dugast C, Buecher B, Bonneau D, Siproudhis L, David V, Bretagne JF: Colorectal adenomatous polyposis Associated with MYH mutations: genotype and phenotype characteristics. Dis Colon Rectum; 2007 Oct;50(10):1612-7
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  • [Title] Colorectal adenomatous polyposis Associated with MYH mutations: genotype and phenotype characteristics.
  • RESULTS: MYH mutations were identified only in the group of patients with attenuated adenomatous polyposis with ten or more adenomatous polyps.
  • Three patients presented with a family history of adenomatous polyposis in siblings, without vertical transmission.
  • The median number of colorectal adenomatous polyps was 53 without preferential localization.
  • Colorectal cancer was associated with polyposis in seven patients.
  • CONCLUSIONS: MYH mutations have been observed in one-third of patients with attenuated polyposis.
  • The phenotype of the disease is similar to attenuated familial adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. DNA Glycosylases / genetics. Mutation / genetics

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  • (PMID = 17674103.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases
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92. Campos FG, Habr-Gama A, Kiss DR, da Silva EV, Rawet V, Imperiale AR, Perez R, da Silva JH, Sousa AH Jr, Gama-Rodrigues J: Adenocarcinoma after ileoanal anastomosis for familial adenomatous polyposis: review of risk factors and current surveillance apropos of a case. J Gastrointest Surg; 2005 May-Jun;9(5):695-702
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  • [Title] Adenocarcinoma after ileoanal anastomosis for familial adenomatous polyposis: review of risk factors and current surveillance apropos of a case.
  • Restorative proctocolectomy has become the most common surgical option for familial adenomatous polyposis (FAP) patients, based on the premise that it provides good functional results and reduces colorectal cancer risk.
  • Proctologic examination revealed an elevated mass 3 cm from the anal margin, which biopsy determined to be a mucinous adenocarcinoma.
  • Histologic analysis showed a 2.2 cm mucinous adenocarcinoma between the ileal and anal mucosa (T2N0Mx) and multiple tubular microadenomas in the ileal pouch.
  • [MeSH-major] Adenocarcinoma / etiology. Adenomatous Polyposis Coli / surgery. Anastomosis, Surgical / adverse effects. Anus Neoplasms / etiology. Colonic Pouches / adverse effects. Proctocolectomy, Restorative / adverse effects

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  • (PMID = 15862266.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 46
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93. Brosens LA, Iacobuzio-Donahue CA, Keller JJ, Hustinx SR, Carvalho R, Morsink FH, Hylind LM, Offerhaus GJ, Giardiello FM, Goggins M: Increased cyclooxygenase-2 expression in duodenal compared with colonic tissues in familial adenomatous polyposis and relationship to the -765G -&gt; C COX-2 polymorphism. Clin Cancer Res; 2005 Jun 1;11(11):4090-6
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  • [Title] Increased cyclooxygenase-2 expression in duodenal compared with colonic tissues in familial adenomatous polyposis and relationship to the -765G -> C COX-2 polymorphism.
  • BACKGROUND: Colorectal cancers arising in patients with familial adenomatous polyposis (FAP) can be largely prevented by polyp surveillance and prophylactic colectomy.
  • As a result, duodenal adenocarcinoma has become a leading cause of death in patients with FAP.
  • Cyclooxygenase 2 (COX-2) inhibition is effective against colorectal polyposis in FAP, but is less effective in treating duodenal polyps.
  • METHODS: The study population included 36 FAP patients with colonic adenomas, 22 FAP patients with duodenal adenomas, 22 patients with sporadic duodenal adenomas, and 17 patients with sporadic duodenal adenocarcinoma.
  • CONCLUSIONS: High COX-2 expression in the normal and adenomatous duodenal mucosa of patients with FAP may explain the poorer response of these neoplasms to chemoprevention with COX-2 inhibitors.
  • [MeSH-major] Adenoma / pathology. Adenomatous Polyposis Coli / pathology. Colonic Neoplasms / pathology. Duodenal Neoplasms / pathology. Polymorphism, Single Nucleotide. Prostaglandin-Endoperoxide Synthases / genetics

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  • (PMID = 15930344.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / PHS HHS / / 51085; United States / PHS HHS / / 63721; United States / NCI NIH HHS / CA / CA 53801; United States / NCI NIH HHS / CA / P50 CA 93-16; United States / NCI NIH HHS / CA / P50 CA62924
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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94. Ramírez-Tapia D, Jalife-Montaño A, Domínguez-Meléndez KE, Vargas-Domínguez A, Ortega-León LH, Rodríguez-Baez A: [Familial adenomatous polyposis: case report of male twins]. Cir Cir; 2008 Mar-Apr;76(2):173-6
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  • [Title] [Familial adenomatous polyposis: case report of male twins].
  • [Transliterated title] Poliposis adenomatosa familiar: presentación de dos casos en gemelos masculinos idénticos.
  • BACKGROUND: One hundred percent of the cases of familial adenomatous polyposis (FAP) will develop carcinoma; therefore, the necessity of diagnosis at an early age with immediate therapy is essential.
  • The second twin was operated on at the age of 33 years and was already a carrier of a well differentiated rectal adenocarcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli. Diseases in Twins


95. Jannasch O, Dombrowski F, Lippert H, Meyer F: Rare coincidence of familial adenomatous polyposis and a retroperitoneal fibromyxoid sarcoma: report of a case. Dis Colon Rectum; 2008 Apr;51(4):477-81
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  • [Title] Rare coincidence of familial adenomatous polyposis and a retroperitoneal fibromyxoid sarcoma: report of a case.
  • PURPOSE: Familial adenomatous polyposis is an autosomal-dominant inherited disease with development of as many as thousands of adenomas within colon and rectum.
  • All untreated patients will develop colorectal adenocarcinoma.
  • An association of familial adenomatous polyposis and sarcomas was reported in a few cases only.
  • METHODS: We present the exceptional case of a 24-year-old male with genetically verified familial adenomatous polyposis (deletion of 10 base pairs at position 228-237 of exon 15A).
  • CONCLUSIONS: To our knowledge, this is the first reported case of familial adenomatous polyposis with metachronous retroperitoneal fibromyxoid sarcoma.
  • In addition to more common semimalignant retroperitoneal desmoid tumors in familial adenomatous polyposis patients, a malignant soft-tissue tumor also has to be considered for differential diagnosis.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Fibrosarcoma / complications. Retroperitoneal Neoplasms / complications

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  • (PMID = 18180996.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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96. Linehan G, Cahill RA, Kalimuthu SN, O'Connell F, Redmond HP, Kirwan WO: Adenocarcinoma arising in the ileoanal pouch after restorative proctocolectomy for familial adenomatous polyposis. Int J Colorectal Dis; 2008 Mar;23(3):329-30
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  • [Title] Adenocarcinoma arising in the ileoanal pouch after restorative proctocolectomy for familial adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma / etiology. Adenomatous Polyposis Coli / surgery. Anus Neoplasms / etiology. Colonic Pouches / adverse effects. Proctocolectomy, Restorative / adverse effects


97. Hewavisenthi SJ, Deen KI: Synchronous colorectal adenocarcinoma arising in a patient with serrated adenomatous polyposis. Ceylon Med J; 2005 Jun;50(2):91-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synchronous colorectal adenocarcinoma arising in a patient with serrated adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Colorectal Neoplasms / pathology

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  • (PMID = 16114779.001).
  • [ISSN] 0009-0875
  • [Journal-full-title] The Ceylon medical journal
  • [ISO-abbreviation] Ceylon Med J
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Sri Lanka
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98. Kyrgidis A, Kountouras J, Zavos C, Chatzopoulos D: New molecular concepts of Barrett's esophagus: clinical implications and biomarkers. J Surg Res; 2005 May 15;125(2):189-212
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  • Given that BE is the only known precursor to esophageal adenocarcinoma (EA), a systematic endoscopic biopsy protocol can detect EAs at an early stage.
  • High plasma adenomatous polyposis coli levels correlate with reduced patient survival. p53 expression allows patient risk for EA stratification.
  • [MeSH-major] Adenocarcinoma. Barrett Esophagus. Biomarkers, Tumor / blood. Esophageal Neoplasms. Gastroesophageal Reflux / complications
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / blood. Biomarkers / blood. Cadherins / metabolism. Clinical Trials as Topic. Colorectal Neoplasms / complications. Cyclin D1 / metabolism. Cyclooxygenase 2. Endoscopy, Gastrointestinal. Gene Expression Regulation, Neoplastic. Humans. Membrane Proteins. NF-kappa B / metabolism. Prostaglandin-Endoperoxide Synthases / metabolism. Receptor, ErbB-2 / metabolism. Risk Factors. Survival Rate. Tumor Suppressor Protein p53 / metabolism. Up-Regulation


99. Smith GV, Feakins R, Farthing MJ, Ballinger A: Cyclooxygenase 2, p53, beta-catenin, and APC protein expression in gastric adenomatous polyps. Am J Clin Pathol; 2005 Mar;123(3):415-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase 2, p53, beta-catenin, and APC protein expression in gastric adenomatous polyps.
  • Gastric adenomatous polyps are rare findings in upper gastrointestinal endoscopy; however, they are associated strongly with malignant transformation.
  • In the present study, we immunohisto-chemically assessed the expression of cyclooxygenase (COX)-2, beta-catenin, p53, and adenomatous polyposis coli (APC) in paraffin-embedded specimens of 14 gastric adenomas.
  • Control samples of normal gastric tissue and gastric adenocarcinoma also were analyzed.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Adenomatous Polyps / metabolism. Cytoskeletal Proteins / metabolism. Prostaglandin-Endoperoxide Synthases / metabolism. Stomach Neoplasms / metabolism. Trans-Activators / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15716238.001).
  • [ISSN] 0002-9173
  • [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 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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100. Parés D, García-Ruiz A, Biondo S, Blanco I, Llort G, Arriol E, de Oca J, del Río C, Osorio A, Navarro M, Martí-Ragué J, Jaurrieta E: [Current status of follow-up of the upper digestive tract in familial adenomatous polyposis]. Gastroenterol Hepatol; 2006 Jan;29(1):15-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Current status of follow-up of the upper digestive tract in familial adenomatous polyposis].
  • [Transliterated title] Estado actual del seguimiento del área gastroduodenal en la poliposis adenomatosa familiar.
  • Familiar adenomatous polyposis (FAP) is a hereditary disease characterized by the development of multiple adenomatous polyps in the gastrointestinal tract and colorectal cancer in practically all patients who do not receive appropriate treatment.
  • In the present article, we report a case of a gastric adenocarcinoma detected during the follow-up of a patient diagnosed with FAP, as well as a review of the literature on this subject.
  • [MeSH-major] Adenocarcinoma / etiology. Adenomatous Polyposis Coli / complications. Stomach Neoplasms / etiology






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