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1. 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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2. 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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  • (PMID = 16705313.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Neoplasm Proteins; 0 / Securin; 0 / TCF Transcription Factors; 0 / beta Catenin; 0 / pituitary tumor-transforming protein 1, human
  • [Other-IDs] NLM/ PMC2361298
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3. 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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4. Cetta F, Dhamo A, Malagnino G, Barellini L: Germ-line and somatic mutations of the APC gene and/or ss catenin gene in the occurrence of FAP associated thyroid carcinoma. World J Surg; 2007 Jun;31(6):1366-7; author reply 1368-9
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  • [MeSH-major] Adenocarcinoma, Papillary / genetics. Adenomatous Polyposis Coli / genetics. Genes, APC. Germ-Line Mutation / genetics. Mutation / genetics. Thyroid Neoplasms / genetics. beta Catenin / genetics

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  • [CommentOn] World J Surg. 2006 May;30(5):775-9 [16680592.001]
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  • (PMID = 17426899.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / beta Catenin
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5. 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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  • 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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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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  • 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. 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


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.
  • 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. 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


10. 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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11. 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.
  • 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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12. Will O, Carvajal-Carmona LG, Gorman P, Howarth KM, Jones AM, Polanco-Echeverry GM, Chinaleong JA, Günther T, Silver A, Clark SK, Tomlinson I: Homozygous PMS2 deletion causes a severe colorectal cancer and multiple adenoma phenotype without extraintestinal cancer. Gastroenterology; 2007 Feb;132(2):527-30
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  • BACKGROUND & AIMS: We report a patient of Indian descent with parental consanguinity, who developed 10 carcinomas and 35 adenomatous polyps at age 23 and duodenal adenocarcinoma at age 25.
  • PMS2 mutations-and perhaps other homozygous mismatch repair mutations-should be considered in any patient presenting with multiple gastrointestinal tumors, since our patient could not be distinguished clinically from cases with attenuated familial adenomatous polyposis or MUTYH-associated polyposis.
  • [MeSH-major] Adenomatous Polyps / genetics. Adenosine Triphosphatases / genetics. Colorectal Neoplasms / genetics. DNA Repair Enzymes / genetics. DNA-Binding Proteins / genetics. Gene Deletion. Homozygote. Intestinal Polyposis / genetics
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adult. DNA Glycosylases / genetics. Diagnosis, Differential. Duodenal Neoplasms / genetics. Fatal Outcome. Gene Expression Regulation, Neoplastic. Humans. Male. Microsatellite Instability. Mutation. Pedigree. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / genetics. Receptors, Transforming Growth Factor beta / genetics. Severity of Illness Index. ras Proteins

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  • (PMID = 17258725.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Transforming Growth Factor beta; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / PMS2 protein, human; EC 3.6.5.2 / ras Proteins; EC 6.5.1.- / DNA Repair Enzymes
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13. Meyer SE, Waltz SE, Goss KH: The Ron receptor tyrosine kinase is not required for adenoma formation in Apc(Min/+) mice. Mol Carcinog; 2009 Nov;48(11):995-1004
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  • Increased Ron expression positively correlates with tumor progression, and reduction of Ron levels in human colon adenocarcinoma cells reverses their tumorigenic properties.
  • Nearly all colon tumors demonstrate loss of the adenomatous polyposis coli (APC) tumor suppressor, an early initiating event, subsequently leading to beta-catenin stabilization.

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  • (PMID = 19452510.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA059268; United States / NCI NIH HHS / CA / R01 CA125379; United States / NCI NIH HHS / CA / CA 100002; United States / NCI NIH HHS / CA / R01 CA100002; United States / NCI NIH HHS / CA / T32 CA 59268
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.1.- / RON protein; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ NIHMS600186; NLM/ PMC4102426
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14. 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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  • 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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15. Zare M, Jazii FR, Alivand MR, Nasseri NK, Malekzadeh R, Yazdanbod M: Qualitative analysis of Adenomatous Polyposis Coli promoter: hypermethylation, engagement and effects on survival of patients with esophageal cancer in a high risk region of the world, a potential molecular marker. BMC Cancer; 2009;9:24
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  • [Title] Qualitative analysis of Adenomatous Polyposis Coli promoter: hypermethylation, engagement and effects on survival of patients with esophageal cancer in a high risk region of the world, a potential molecular marker.
  • Adenomatous Polyposis Coli (APC) promoter hypermethylation has been shown to be a suitable marker for both serum and solid tumors of adenocarcinoma of esophagus.

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  • (PMID = 19149902.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC2637891
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16. Bellizzi AM, Kahaleh M, Stelow EB: The assessment of specimens procured by endoscopic ampullectomy. Am J Clin Pathol; 2009 Oct;132(4):506-13
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  • Familial adenomatous polyposis (FAP) status and the endoscopist's impression of completeness of removal were also ascertained.
  • The histologic features of the ampullectomy specimens were as follows: diagnosis (no diagnostic abnormality, 3; reactive, 8; adenoma, 26; adenocarcinoma, 7; other, 1); HGD, 1; submucosal ampullary gland/ductule involvement, 20; specimen integrity (intact, 22; fragmented, 23); and margin status (positive, 20; negative, 2; could not be assessed, 12).
  • [MeSH-minor] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / pathology. Adult. Aged. Aged, 80 and over. Cholangiopancreatography, Endoscopic Retrograde. Female. Humans. Male. Middle Aged

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  • (PMID = 19762527.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. 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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18. 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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19. 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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20. 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 -> 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.
  • [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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21. Logani S, Oliva E, Arnell PM, Amin MB, Young RH: Use of novel immunohistochemical markers expressed in colonic adenocarcinoma to distinguish primary ovarian tumors from metastatic colorectal carcinoma. Mod Pathol; 2005 Jan;18(1):19-25
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  • [Title] Use of novel immunohistochemical markers expressed in colonic adenocarcinoma to distinguish primary ovarian tumors from metastatic colorectal carcinoma.
  • Recently, three immunohistochemical markers CDX2, a homeobox gene encoding an intestine-specific transcription factor; alpha-methylacyl-CoA racemase (AMACR/P504S), a mitochondrial and peroxisomal enzyme with fairly restricted expression in selective tumors and beta-catenin, an adenomatous polyposis coli (APC) mutation product resulting in activation of the Wnt pathway, have been reported to have specific and sensitive expression in colorectal carcinomas.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers / analysis. Colonic Neoplasms / pathology. Colorectal Neoplasms / secondary. Ovarian Neoplasms / pathology

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  • (PMID = 15389251.001).
  • [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 / Biomarkers; 0 / CDX2 protein, human; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Homeodomain Proteins; 0 / Trans-Activators; 0 / beta Catenin; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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22. 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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23. 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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  • 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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24. Irabor D, Adedeji OA: Colorectal cancer in Nigeria: 40 years on. A review. Eur J Cancer Care (Engl); 2009 Mar;18(2):110-5
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  • This paper is a review of work done on colorectal cancer in Nigeria over the last 40 years showing geographic spread, age and sex ratios, predominant histopathology and paucity of polyposis coli syndromes.
  • There seems to be quite a significant incidence of mucin-secreting adenocarcinoma subgroups which are said to carry a worse prognosis.
  • Almost all the authors have stated the rarity of polyposis coli syndromes; a few have looked into the possibility of mismatch repair mutations as an aetiological factor.

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  • (PMID = 19267725.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 41
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25. 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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  • 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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26. 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.
  • [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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27. 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.
  • [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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28. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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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29. 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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  • [ErratumIn] Int J Colorectal Dis. 2007 Mar;22(3):339
  • [RepublishedIn] Int J Colorectal Dis. 2006 Jan;21(1):79-83 [16676398.001]
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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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30. 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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31. Benito M, Díaz-Rubio E: Molecular biology in colorectal cancer. Clin Transl Oncol; 2006 Jun;8(6):391-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • High-penetrance mutations confer predisposition to colorectal cancer mainly in Lynch syndrome (which involves mutations in mismatch-repair genes) and in familial adenomatous polyposis (which involves mutations in the APC tumour suppressor).
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / genetics. Adenoma / epidemiology. Adenoma / genetics. Adenomatous Polyposis Coli / epidemiology. Adenomatous Polyposis Coli / genetics. Base Pair Mismatch. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / epidemiology. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA Repair / genetics. Disease Progression. Ethnic Groups / genetics. Genes, APC. Genes, Tumor Suppressor. Genetic Predisposition to Disease. Genetic Testing. Germ-Line Mutation. Humans. Incidence. Mutation. Penetrance. Peutz-Jeghers Syndrome / epidemiology. Peutz-Jeghers Syndrome / genetics

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  • (PMID = 16790391.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 9
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32. 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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  • Colonic tissues representing colitis, adenomatous polyposis, tubulovillous adenoma, and mucoid/adeno-carcinomas were processed for immunohistochemistry using an antibody specific for human TFF3.
  • 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.
  • [MeSH-major] Adenocarcinoma, Mucinous / chemistry. Adenoma, Villous / chemistry. Adenomatous Polyposis Coli / chemistry. Colitis / metabolism. Colonic Neoplasms / chemistry. Peptides / analysis

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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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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. 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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  • (PMID = 15827855.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
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35. 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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36. Zhou JN, Chen SQ, Zhang XM, Zhou X, Zhu M, Feng B, Li JT, Ma GJ, Zhang YY: [A novel APC gene germline mutation in a familial adenomatous polyposis pedigree]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2006 Aug;23(4):388-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A novel APC gene germline mutation in a familial adenomatous polyposis pedigree].
  • OBJECTIVE: To detect the adenomatous polyposis coli (APC) gene germline mutation in the proband and her family members with familial adenomatous polyposis (FAP).
  • This mutation manifested an aggressive form of FAP with early onset of colorectal adenocarcinoma and colonic adenoma.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli Protein / genetics. Germ-Line Mutation

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  • (PMID = 16883523.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
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37. Castellví-Bel S, Castells A: [Genetic and molecular biology techniques for the analysis of hereditary colorectal cancer]. Gastroenterol Hepatol; 2005 Jun-Jul;28(6):354-60
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  • The knowledge acquired in genetics and molecular biology over the last 2 decades has led to advances in the molecular diagnosis of some diseases, among them hereditary forms of colorectal cancer such as hereditary non-polyposis colorectal cancer and familial adenomatous polyposis.
  • [MeSH-major] Adenocarcinoma / genetics. Colorectal Neoplasms / genetics. Genetics, Medical / methods. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / genetics. Algorithms. Colonic Polyps / diagnosis. Colonic Polyps / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA Mutational Analysis. DNA Repair / genetics. Genes, APC. Genetic Counseling. Genetic Predisposition to Disease. Hamartoma / diagnosis. Hamartoma / genetics. Humans

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  • (PMID = 15989818.001).
  • [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
  • [Number-of-references] 29
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38. 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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39. Reedijk M, Odorcic S, Zhang H, Chetty R, Tennert C, Dickson BC, Lockwood G, Gallinger S, Egan SE: Activation of Notch signaling in human colon adenocarcinoma. Int J Oncol; 2008 Dec;33(6):1223-9
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  • [Title] Activation of Notch signaling in human colon adenocarcinoma.
  • Studies in mice have also shown that Notch signaling is required for adenoma formation in response to elevated Wnt-pathway signaling that occurs in the APCMin mouse model of human adenomatous polyposis coli.

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  • (PMID = 19020755.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U24 CA074783; United States / NCI NIH HHS / CA / RFA#CA-96-011; United States / NCI NIH HHS / CA / U01 CA074783-06; United States / NCI NIH HHS / CA / CA074783-06; United States / NCI NIH HHS / CA / CA074783-05; United States / NCI NIH HHS / CA / U01 CA074783-05; United States / NCI NIH HHS / CA / U01 CA074783
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Calcium-Binding Proteins; 0 / Homeodomain Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NOTCH1 protein, human; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Receptors, Notch; 134324-36-0 / Serrate proteins; 149348-15-2 / HES1 protein, human; EC 2.4.- / Glycosyltransferases; EC 2.4.1.- / LFNG protein, human
  • [Other-IDs] NLM/ NIHMS139694; NLM/ PMC2739737
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40. 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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41. 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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42. 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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43. 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


44. 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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45. Schuetze D, Hoschar AP, Seethala RR, Assaad A, Zhang X, Hunt JL: The T1799A BRAF mutation is absent in cribriform-morular variant of papillary carcinoma. Arch Pathol Lab Med; 2009 May;133(5):803-5
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  • It has been associated with familial adenomatous polyposis, though it can also occur sporadically.
  • DESIGN: Four cases of CMVPTC (1 associated with familial adenomatous polyposis and the others apparently sporadic) were identified from the files of 3 large centers.
  • [MeSH-major] Adenocarcinoma, Papillary / genetics. Point Mutation. Proto-Oncogene Proteins B-raf / genetics. Thyroid Neoplasms / genetics
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. DNA Mutational Analysis. DNA, Neoplasm / analysis. Humans

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  • (PMID = 19415957.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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46. 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].
  • 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


47. 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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48. 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


49. Lee SH, Ahn BK, Chang HK, Baek SU: Adenocarcinoma in ileal pouch after proctocolectomy for familial adenomatous polyposis: report of a case. J Korean Med Sci; 2009 Oct;24(5):985-8
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  • [Title] Adenocarcinoma in ileal pouch after proctocolectomy for familial adenomatous polyposis: report of a case.
  • Restorative proctocolectomy with ileal pouch-anal anastomosis is one of the surgical treatments of choice for patients with familial adenomatous polyposis.
  • Although the risk of cancer developing in an ileal pouch is not yet clear, a few cases of adenocarcinoma arising in an ileal pouch have been reported.
  • We report a case of adenocarcinoma in ileal pouch after proctocolectomy with ileal pouch-anal anastomosis.
  • A 56-yr-old woman was diagnosed as having familial adenomatous polyposis.
  • Endoscopic biopsies revealed adenocarcinoma at the ileal pouch.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenomatous Polyposis Coli / surgery. Colonic Pouches / pathology. Colorectal Neoplasms / diagnosis. Proctocolectomy, Restorative

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  • (PMID = 19795007.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2752792
  • [Keywords] NOTNLM ; Adenocarcinoma / Adenomatous Polyposis Coli / Ileal Pouches
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50. 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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51. 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


52. 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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53. Pan SY, Xie EF, Shu YQ, Gao L, Zhang LX, Chen D, Chen JB, Zhao WJ, Mu Y, Zhang JN: [Methylation quantification of adenomatous polyposis coli (APC) gene promoter in plasma of lung cancer patients]. Ai Zheng; 2009 Apr;28(4):384-9
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  • [Title] [Methylation quantification of adenomatous polyposis coli (APC) gene promoter in plasma of lung cancer patients].
  • BACKGROUND AND OBJECTIVE: The protein encoded by adenomatous polyposis coli (APC) gene participates in the signaling transduction pathway.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. DNA Methylation. Genes, APC. Lung Neoplasms / genetics. Promoter Regions, Genetic
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / genetics. Adult. Aged. Base Sequence. Carcinoma, Squamous Cell / blood. Carcinoma, Squamous Cell / genetics. DNA, Neoplasm / genetics. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Polymerase Chain Reaction / methods

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  • (PMID = 19622298.001).
  • [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 / DNA, Neoplasm
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54. 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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55. 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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56. Kucherlapati MH, Lee K, Nguyen AA, Clark AB, Hou H Jr, Rosulek A, Li H, Yang K, Fan K, Lipkin M, Bronson RT, Jelicks L, Kunkel TA, Kucherlapati R, Edelmann W: An Msh2 conditional knockout mouse for studying intestinal cancer and testing anticancer agents. Gastroenterology; 2010 Mar;138(3):993-1002.e1
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  • Resulting adenomas and adenocarcinomas had somatic truncation mutations to the adenomatous polyposis coli (Apc) gene.

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 19931261.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES11040; United States / NCI NIH HHS / CA / U01 CA084301; United States / NCI NIH HHS / CA / CA13330; United States / NCI NIH HHS / CA / CA084301-11; United States / NCI NIH HHS / CA / R01 CA093484; United States / NCI NIH HHS / CA / CA013330-37S49022; United States / NIEHS NIH HHS / ES / Z01 ES065089; United States / NCI NIH HHS / CA / R01 CA076329; United States / Intramural NIH HHS / / Z01 ES065089-12; United States / NCI NIH HHS / CA / R01 CA076329-12; United States / NCI NIH HHS / CA / CA084301; United States / NCI NIH HHS / CA / P30 CA013330-37S49022; United States / NCI NIH HHS / CA / R01 CA093484-08; United States / NCI NIH HHS / CA / U01 CA084301-11; United States / NIEHS NIH HHS / ES / U01 ES011040-06; United States / NIEHS NIH HHS / ES / U01 ES011040; United States / NCI NIH HHS / CA / CA93484; United States / NCI NIH HHS / CA / P30 CA013330; United States / NCI NIH HHS / CA / CA093484-08; United States / NCI NIH HHS / CA / CA76329; United States / NCI NIH HHS / CA / CA076329-12; United States / NIEHS NIH HHS / ES / ES011040-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Microfilament Proteins; 0 / Organoplatinum Compounds; 0 / villin; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.6.1.3 / Msh2 protein, mouse; EC 3.6.1.3 / MutS Homolog 2 Protein; Q20Q21Q62J / Cisplatin; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ NIHMS159931; NLM/ PMC2862591
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57. Kim JY, Beart RW, Shibata D: Stability of colon stem cell methylation after neo-adjuvant therapy in a patient with attenuated familial adenomatous polyposis. BMC Gastroenterol; 2005 Jun 07;5:19
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  • [Title] Stability of colon stem cell methylation after neo-adjuvant therapy in a patient with attenuated familial adenomatous polyposis.
  • CASE PRESENTATION: A 22 year-old male with attenuated familial adenomatous polyposis received neo-adjuvant chemotherapy and radiation prior to surgery for rectal adenocarcinoma.

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  • (PMID = 15941485.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R21 DK061140; United States / NIDDK NIH HHS / DK / DK61140
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1164411
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58. Iwamoto M, Hoffenberg EJ, Carethers JM, Doctolero R, Tajima A, Sugano K, Franklin WA, Ahnen DJ: Nuclear accumulation of beta-catenin occurs commonly in the epithelial cells of juvenile polyps. Pediatr Res; 2005 Jan;57(1):4-9; discussion 1-3
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  • In the two conditions juvenile polyps (JPs) and juvenile polyposis coli (JPC), colonic polyps may have overlapping histologic and phenotypic appearance, but JPC confers a significant risk for colon adenocarcinoma.
  • Although not thought to contain adenomatous polyposis coli (APC) mutations, the status of beta-catenin and full-length APC protein expression in JPs is not known.

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  • [CommentIn] Pediatr Res. 2005 Jan;57(1):1-3 [15557110.001]
  • (PMID = 15557107.001).
  • [ISSN] 0031-3998
  • [Journal-full-title] Pediatric research
  • [ISO-abbreviation] Pediatr. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090231-04; United States / NCI NIH HHS / CA / R01 CA090231; United States / NCI NIH HHS / CA / CA88007; United States / NCI NIH HHS / CA / CA090231-04; United States / NCI NIH HHS / CA / CA90231
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / Transforming Growth Factor beta; 0 / beta Catenin
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59. Restucci B, Maiolino P, Martano M, Esposito G, De Filippis D, Borzacchiello G, Lo Muzio L: Expression of beta-catenin, E-cadherin and APC in canine mammary tumors. Anticancer Res; 2007 Sep-Oct;27(5A):3083-9
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  • [MeSH-major] Adenocarcinoma / metabolism. Adenomatous Polyposis Coli Protein / biosynthesis. Cadherins / biosynthesis. Dog Diseases / metabolism. Mammary Neoplasms, Animal / metabolism. beta Catenin / biosynthesis

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  • (PMID = 17970048.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cadherins; 0 / beta Catenin
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60. Gatalica Z, Torlakovic E: Pathology of the hereditary colorectal carcinoma. Fam Cancer; 2008;7(1):15-26
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  • 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.
  • 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.
  • [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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61. Hirokawa M, Maekawa M, Kuma S, Miyauchi A: Cribriform-morular variant of papillary thyroid carcinoma--cytological and immunocytochemical findings of 18 cases. Diagn Cytopathol; 2010 Dec;38(12):890-6
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  • We believe that cytologic diagnosis of CMV-PTC is possible and it may lead to the early detection of polyposis coli.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Papillary / pathology. Thyroid Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
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  • [Copyright] Copyright © 2010 Wiley-Liss, Inc.
  • (PMID = 20091902.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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62. 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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  • Familial adenomatous polyposis (FAP) subjects, carrying germ-line mutations in the APC gene, are at high risk of CRC.
  • [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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63. Ruys AT, Alderlieste YA, Gouma DJ, Dekker E, Mathus-Vliegen EM: Jejunal cancer in patients with familial adenomatous polyposis. Clin Gastroenterol Hepatol; 2010 Aug;8(8):731-3
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  • [Title] Jejunal cancer in patients with familial adenomatous polyposis.
  • BACKGROUND & AIMS: Familial adenomatous polyposis (FAP) is an inherited disease affecting approximately 1:10,000 newborns, characterized by the formation of numerous adenomas in the digestive tract.
  • CONCLUSIONS: Jejunal adenomas in FAP patients are reported occasionally and can progress into adenocarcinoma with a poor prognosis.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Adenomatous Polyposis Coli / complications. Jejunal Neoplasms / diagnosis


64. 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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  • Number and size of intestinal tumors were significantly increased in mice bearing both adenomatous polyposis coli (APC) and PTEN mutations.
  • 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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65. 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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66. Cai JC, Liu D, Zhang HP, Zhong S, Xia NS: [Promoter methylation of several tumor suppressor genes in human gastric adenocarcinoma]. Zhonghua Yi Xue Za Zhi; 2007 Apr 10;87(14):978-81
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  • [Title] [Promoter methylation of several tumor suppressor genes in human gastric adenocarcinoma].
  • OBJECTIVE: To study the promoter methylation of several tumor suppressor genes in human gastric foveolar epithelia (GFE) of chronic gastritis, adjacent GFE of gastric adenocarcinoma (GAC) and GAC.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Genes, Tumor Suppressor. Promoter Regions, Genetic. Stomach Neoplasms / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adenomatous Polyposis Coli Protein / genetics. Adult. Aged. Aged, 80 and over. Cadherins / genetics. Cadherins / metabolism. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Nuclear Proteins / genetics. Polymerase Chain Reaction / methods. Tumor Suppressor Proteins / genetics

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  • (PMID = 17650424.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Cadherins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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67. Buecher B, Baert-Desurmont S, Leborgne J, Humeau B, Olschwang S, Frébourg T: Duodenal adenocarcinoma and Mut Y human homologue-associated polyposis. Eur J Gastroenterol Hepatol; 2008 Oct;20(10):1024-7
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  • [Title] Duodenal adenocarcinoma and Mut Y human homologue-associated polyposis.
  • Mut Y human homologue-associated polyposis is a recently described colorectal adenomatous polyposis with an autosomal recessive mode of inheritance.
  • Several extracolonic manifestations have been reported in patients affected by Mut Y human homologue-associated polyposis (MAP).
  • Among these, duodenal polyposis, a highly prevalent manifestation of Adenomatous Polyposis Coli related familial adenomatous polypyposis, is undoubtedly part of the clinical spectrum of the disease.
  • The true association of other clinical manifestations with MAP remains questionable.We report the observation of two patients affected by MAP who developed an adenocarcinoma of the duodenum in the context of duodenal polyposis.
  • These observations emphasize the malignant potential of MAP-associated duodenal polyposis and the need to enroll these patients into an upper gastrointestinal surveillance programme.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms / genetics. DNA Glycosylases / genetics. Duodenal Neoplasms / genetics. Mutation, Missense

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  • (PMID = 18787472.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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68. 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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69. 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


70. Wu R, Hendrix-Lucas N, Kuick R, Zhai Y, Schwartz DR, Akyol A, Hanash S, Misek DE, Katabuchi H, Williams BO, Fearon ER, Cho KR: Mouse model of human ovarian endometrioid adenocarcinoma based on somatic defects in the Wnt/beta-catenin and PI3K/Pten signaling pathways. Cancer Cell; 2007 Apr;11(4):321-33
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  • [Title] Mouse model of human ovarian endometrioid adenocarcinoma based on somatic defects in the Wnt/beta-catenin and PI3K/Pten signaling pathways.
  • One histologic subtype of ovarian carcinoma, ovarian endometrioid adenocarcinoma (OEA), frequently harbors mutations that constitutively activate Wnt/beta-catenin-dependent signaling.
  • [MeSH-minor] Adenocarcinoma, Clear Cell / genetics. Adenocarcinoma, Clear Cell / metabolism. Adenocarcinoma, Clear Cell / pathology. Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / physiology. Animals. Carcinoma, Endometrioid / genetics. Carcinoma, Endometrioid / metabolism. Carcinoma, Endometrioid / pathology. Cystadenocarcinoma, Serous / genetics. Cystadenocarcinoma, Serous / metabolism. Cystadenocarcinoma, Serous / pathology. Epithelium / metabolism. Epithelium / pathology. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Mice. Mutation. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Ovary / metabolism. Ovary / pathology. Survival Rate. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism


71. 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


72. 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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73. 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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74. 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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75. Kim JC, Cho YK, Roh SA, Yu CS, Gong G, Jang SJ, Kim SY, Kim YS: Individual tumorigenesis pathways of sporadic colorectal adenocarcinomas are associated with the biological behavior of tumors. Cancer Sci; 2008 Jul;99(7):1348-54
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  • Individual steps in the tumorigenesis pathway, that is, adenomatosis polyposis coli (APC), Wnt-activated, base excision repair mutations, mismatch repair defects, RAF-mediated, transforming growth factor (TGF)-beta-suppressed, bone morphogenic protein (BMP)-suppressed, and p53 alterations, were examined in terms of genetic and epigenetic changes, as well as protein expression.
  • [MeSH-major] Adenocarcinoma / etiology. Colorectal Neoplasms / etiology

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  • [ErratumIn] Cancer Sci. 2008 Jul;99(7):1499
  • (PMID = 18422752.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.1 / raf Kinases
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76. 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


77. 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.
  • 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


78. Bishnupuri KS, Luo Q, Korzenik JR, Henderson JO, Houchen CW, Anant S, Dieckgraefe BK: Dysregulation of Reg gene expression occurs early in gastrointestinal tumorigenesis and regulates anti-apoptotic genes. Cancer Biol Ther; 2006 Dec;5(12):1714-20
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  • Using real time RT-PCR, we measured expression of Reg genes in human colorectal adenocarcinoma specimens, colon adenocarcinoma cell lines and adenomas from multiple intestinal neoplasia (min) mice heterozygous for a germ-line mutation of the adenomatous polyposis coli (APC) gene.
  • Addition of exogenous recombinant human Reg IV to human colon adenocarcinoma cells significantly increased Bcl-2 and Bcl-xL expression and induced resistance to ionizing radiation.
  • [MeSH-major] Adenocarcinoma / genetics. Apoptosis / genetics. Colonic Neoplasms / genetics. Colorectal Neoplasms / genetics. Lithostathine / genetics

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  • [CommentIn] Cancer Biol Ther. 2007 Jan;6(1):123-4 [17297304.001]
  • (PMID = 17106246.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109269; United States / NIDDK NIH HHS / DK / DK060106; United States / NIDDK NIH HHS / DK / DK62265; United States / NIDDK NIH HHS / DK / P30 DK52574
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / DNA Primers; 0 / Lithostathine; 0 / REG1A protein, human; 0 / bcl-X Protein
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79. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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80. Rio Frio T, Lavoie J, Hamel N, Geyer FC, Kushner YB, Novak DJ, Wark L, Capelli C, Reis-Filho JS, Mai S, Pastinen T, Tischkowitz MD, Marcus VA, Foulkes WD: Homozygous BUB1B mutation and susceptibility to gastrointestinal neoplasia. N Engl J Med; 2010 Dec 30;363(27):2628-37
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  • A patient received a diagnosis of adenocarcinoma of the ampulla of Vater at 34 years of age.
  • Our findings expand the phenotype associated with BUB1B mutations and the mosaic variegated aneuploidy syndrome to include common adult-onset cancers and provide evidence for the interdependency of the APC protein (encoded by the adenomatous polyposis coli gene) and the BUBR1 protein (encoded by BUB1B) in humans. (Funded by the Turner Family Cancer Research Fund and others.).
  • [MeSH-minor] Adenocarcinoma / genetics. Adenoma / genetics. Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Aged. Chromosome Disorders / genetics. DNA Mutational Analysis. Female. Genomic Instability. Homozygote. Humans. Karyotyping. Male. Mosaicism. Oligonucleotide Array Sequence Analysis. Pedigree. Phenotype. Spindle Apparatus


81. 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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82. 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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  • 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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83. 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


84. 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.
  • 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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85. Shinmura K, Suzuki M, Yamada H, Tao H, Goto M, Kamo T, Nagura K, Kageyama S, Kato M, Ogawa S, Maekawa M, Takamochi K, Suzuki K, Nakamura T, Sugimura H: Characterization of adenocarcinoma of the lung in a familial adenomatous polyposis patient. Pathol Int; 2008 Nov;58(11):706-12
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  • [Title] Characterization of adenocarcinoma of the lung in a familial adenomatous polyposis patient.
  • The incidence of several extracolonic tumors, such as duodenal carcinoma, is higher in familial adenomatous polyposis (FAP) patients than in the general population, but there is little information about lung carcinoma in FAP.
  • Pathohistological analysis of the lung tumor demonstrated mixed adenocarcinoma consisting of a papillary adenocarcinoma component and a bronchioloalveolar carcinoma component.
  • The present results suggest that the chromosomal copy number alterations detected on SNP microarray were involved in the carcinogenesis of the adenocarcinoma of the lung in the present FAP patient.
  • [MeSH-major] Adenocarcinoma, Bronchiolo-Alveolar / pathology. Adenocarcinoma, Papillary / pathology. Adenomatous Polyposis Coli / pathology. Lung Neoplasms / pathology


86. 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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  • [Title] [Current status of follow-up of the upper digestive tract in familial adenomatous polyposis].
  • 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


87. 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).
  • [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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88. Croitoru ME, Cleary SP, Berk T, Di Nicola N, Kopolovic I, Bapat B, Gallinger S: Germline MYH mutations in a clinic-based series of Canadian multiple colorectal adenoma patients. J Surg Oncol; 2007 May 1;95(6):499-506
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  • METHODS: We screened for germline MYH mutations (by dHPLCO) in 20 clinic-based multiple adenoma patients who were adenomatous polyposis coli (APC) mutation-negative.
  • [MeSH-major] Adenoma / genetics. Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms / genetics. DNA Glycosylases / genetics. Germ-Line Mutation
  • [MeSH-minor] Adenocarcinoma / genetics. Adult. Aged. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Genetic Predisposition to Disease. Heterozygote. Humans. Male. Middle Aged. Pedigree

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  • [Copyright] Copyright 2007 Wiley-Liss, Inc.
  • (PMID = 17219385.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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89. 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.
  • 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.

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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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90. Kountouras J, Zavos C, Chatzopoulos D: New concepts of molecular biology on gastric carcinogenesis. Hepatogastroenterology; 2005 Jul-Aug;52(64):1305-12
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  • Gastric cancer not located in the cardia still remains the second most common cancer worldwide, whereas adenocarcinoma of the cardia and gastroesophageal junction has been rapidly rising over the past two decades.
  • The most common genetic abnormalities in gastric cancer tend to be loss of heterozygosity of tumor suppressor genes, particularly of p53 or "Adenomatous Polyposis Coli" gene.


91. 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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92. Ouaïssi M, Sielezneff I, Alves A, Pirro N, Heyries L, Robitail S, Consentino B, Payan MJ, Valleur P, Panis Y, Sastre B: [Long term outcome following 26 surgical ampullectomies]. Ann Chir; 2006 May;131(5):322-7
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  • Of the 26 patients, 8 had familial adenomatous polyposis (FAP).
  • [MeSH-minor] Adenocarcinoma / surgery. Adenoma / surgery. Adenomatous Polyposis Coli / surgery. Adult. Aged. Carcinoma in Situ / surgery. Cause of Death. Common Bile Duct Diseases / surgery. Female. Follow-Up Studies. Granuloma, Plasma Cell / surgery. Humans. Longitudinal Studies. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Retrospective Studies. Somatostatinoma / surgery. Survival Rate. Treatment Outcome

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  • (PMID = 16615931.001).
  • [ISSN] 0003-3944
  • [Journal-full-title] Annales de chirurgie
  • [ISO-abbreviation] Ann Chir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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93. 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


94. 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


95. 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


96. 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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  • Patients with polyposis syndromes were excluded the analysis.
  • [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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97. Goto A, Nakajima J, Hara K, Niki T, Fukayama M: Lung adenocarcinoma associated with familial adenomatous polyposis. Clear cell carcinoma with beta-catenin accumulation accompanied by atypical adenomatous hyperplasia. Virchows Arch; 2005 Jan;446(1):73-7
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  • [Title] Lung adenocarcinoma associated with familial adenomatous polyposis. Clear cell carcinoma with beta-catenin accumulation accompanied by atypical adenomatous hyperplasia.
  • A 46-year-old man presented with a lung tumor 17 years after a subtotal colectomy and 13 years after a partial duodenectomy for familial adenomatous polyposis (FAP).
  • Pathological analysis of the lung tumor demonstrated adenocarcinoma with clear cells and a papillary structure, accompanied by tiny tumorous nodules in the background lung parenchyma.
  • Many of the nodules were multifocal adenocarcinoma; however, some of the nodules demonstrated atypical adenomatous hyperplasia (AAH).
  • This is the first case report of a lung adenocarcinoma accompanied by AAH in a FAP patient.
  • Immunohistochemical and loss of heterozygosity studies revealed unique features of the lesions reflecting a disruption of the adenomatous poliposis coli-beta-catenin pathway.
  • [MeSH-major] Adenocarcinoma / pathology. Adenomatous Polyposis Coli / complications. Cytoskeletal Proteins / metabolism. Lung Neoplasms / pathology. Trans-Activators / metabolism

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  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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98. Li M, Edamatsu H, Kitazawa R, Kitazawa S, Kataoka T: Phospholipase Cepsilon promotes intestinal tumorigenesis of Apc(Min/+) mice through augmentation of inflammation and angiogenesis. Carcinogenesis; 2009 Aug;30(8):1424-32
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  • Apc(Min/+) mice, carrying an inactivated allele of the adenomatous polyposis coli gene, are widely used as an animal model for human colorectal tumorigenesis, where tumor environment, such as inflammation, is known to play a critical role in tumor progression.
  • [MeSH-minor] Adenocarcinoma / blood supply. Adenocarcinoma / etiology. Adenocarcinoma / pathology. Adenoma / blood supply. Adenoma / etiology. Adenoma / pathology. Animals. Apoptosis. Blotting, Western. Carcinogens / toxicity. Cell Proliferation. Female. Immunoenzyme Techniques. Male. Mice. Mice, Inbred C57BL. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tetradecanoylphorbol Acetate / toxicity. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19458037.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 3.1.4.11 / Phosphoinositide Phospholipase C; EC 3.1.4.11 / phospholipase C epsilon; NI40JAQ945 / Tetradecanoylphorbol Acetate
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99. 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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100. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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