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1. Kwong LN, Dove WF: APC and its modifiers in colon cancer. Adv Exp Med Biol; 2009;656:85-106
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  • [Title] APC and its modifiers in colon cancer.
  • Colon cancer closely follows the paradigm of a single "gatekeeper gene."
  • Mutations inactivating the APC (adenomatous polyposis coli) gene are found in approximately 80% of all human colon tumors and heterozygosity for such mutations produces an autosomal dominant colon cancer predisposition in humans and in murine models.
  • However, this tight association between a single genotype and phenotype belies a complex association of genetic and epigenetic factors that together generate the broad phenotypic spectrum ofboth familial and sporadic colon cancers.
  • In this Chapter, we give a general overview of the structure, function and outstanding issues concerning the role of Apc in human and experimental colon cancer.
  • The availability of increasingly close models for human colon cancer in genetically tractable animal species enables the discovery and eventual molecular identification of genetic modifiers of the Apc-mutant phenotypes, connecting the central role of Apc in colon carcinogenesis to the myriad factors that ultimately determine the course of the disease.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli Protein / genetics. Colorectal Neoplasms / genetics. Genes, APC

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  • (PMID = 19928355.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA063677; United States / NCI NIH HHS / CA / R37 CA063677
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
  • [Number-of-references] 174
  • [Other-IDs] NLM/ NIHMS490160; NLM/ PMC3754875
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2. Ciznadija D, Tothill R, Waterman ML, Zhao L, Huynh D, Yu RM, Ernst M, Ishii S, Mantamadiotis T, Gonda TJ, Ramsay RG, Malaterre J: Intestinal adenoma formation and MYC activation are regulated by cooperation between MYB and Wnt signaling. Cell Death Differ; 2009 Nov;16(11):1530-8
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  • [Title] Intestinal adenoma formation and MYC activation are regulated by cooperation between MYB and Wnt signaling.
  • Aberrant Wnt signaling mediated by mutations affecting APC (adenomatous polyposis coli) or beta-catenin initiates the majority of human colorectal cancers (CRC) and drives tumorigenesis through the activation of specific genes such as MYC.
  • We report here a novel association whereby another oncogenic transcription factor, MYB/c-Myb, is necessary for intestinal adenoma development directed by activated Wnt signaling.
  • APC(Min/+) mice in which c-myb is haploinsufficient survive longer than wild-type APC(Min/+) animals due to a delay in adenoma formation.
  • Intestinal adenomas from APC(Min/+) mice were assessed and found to have high levels of c-myc gene expression.
  • We explored the relationship between activated Wnt signaling and MYB in regulating MYC and found activated beta-catenin in combination with MYB induces robust upregulation of MYC promoter activity, as well as endogenous MYC mRNA and protein expression, in human cells.
  • [MeSH-major] Adenoma / metabolism. Colorectal Neoplasms / metabolism. Proto-Oncogene Proteins c-myb / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Alleles. Animals. Cell Line. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. RNA Interference. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Signal Transduction. Up-Regulation. beta Catenin / metabolism

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  • (PMID = 19609274.001).
  • [ISSN] 1476-5403
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Wnt Proteins; 0 / beta Catenin
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3. Voutsadakis IA: The ubiquitin-proteasome system in colorectal cancer. Biochim Biophys Acta; 2008 Dec;1782(12):800-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The proteasome is a multiprotein complex that regulates the stability of hundreds of cellular proteins and thus, it is implicated in virtually all cellular functions.
  • Most of the time, to be recognized and processed by the proteasome, a protein has to be linked to a chain of ubiquitin molecules.
  • In colorectal epithelium, UPS plays a role in the regulation of the Wnt/beta-catenin/APC/TCF4 signaling which regulates proliferation of colorectal epithelial cells in the bottom of the crypts and the inhibition of this proliferation as cells move towards colon villi tips.
  • In most colorectal cancers APC (Adenomatous Polyposis Coli) disabling mutations interfere with the ability of the proteasome to degrade beta-catenin leading to uninhibited cell proliferation.

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  • (PMID = 18619533.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Proteasome Inhibitors; 0 / Ubiquitin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 123
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4. Narayan S, Jaiswal AS, Balusu R: Tumor suppressor APC blocks DNA polymerase beta-dependent strand displacement synthesis during long patch but not short patch base excision repair and increases sensitivity to methylmethane sulfonate. J Biol Chem; 2005 Feb 25;280(8):6942-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor suppressor APC blocks DNA polymerase beta-dependent strand displacement synthesis during long patch but not short patch base excision repair and increases sensitivity to methylmethane sulfonate.
  • In the present investigation, we report a previously unsuspected function of the tumor suppressor protein, APC (adenomatous polyposis coli), in the regulation of base excision repair (BER).
  • We identified a proliferating cell nuclear antigen-interacting protein-like box sequence in APC that binds DNA polymerase beta and blocks DNA polymerase beta-mediated strand-displacement synthesis in long patch BER without affecting short patch BER.
  • We further showed that the colon cancer cell line expressing the wild-type APC gene was more sensitive to a DNA-methylating agent due to decreased DNA repair by long patch BER than the cell line expressing the mutant APC gene lacking the proliferating cell nuclear antigen-interacting protein-like box.
  • Experiments based on RNA interference showed that the wild-type APC gene expression is required for DNA methylation-induced sensitivity of colon cancer cells.
  • Thus, APC may play a critical role in determining utilization of long versus short patch BER pathways and affect the susceptibility of colon cancer cells to carcinogenic and chemotherapeutic agents.

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  • (PMID = 15548520.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097031; United States / NCI NIH HHS / CA / R01 CA100247; United States / NCI NIH HHS / CA / R01-CA 097031; United States / NCI NIH HHS / CA / R01-CA 100247
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Peptide Fragments; 0 / Tumor Suppressor Proteins; 9007-49-2 / DNA; AT5C31J09G / Methyl Methanesulfonate; EC 2.7.7.- / DNA Polymerase beta
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5. Näthke I: Cytoskeleton out of the cupboard: colon cancer and cytoskeletal changes induced by loss of APC. Nat Rev Cancer; 2006 12;6(12):967-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytoskeleton out of the cupboard: colon cancer and cytoskeletal changes induced by loss of APC.
  • Mutation of APC (adenomatous polyposis coli) is a common factor in most colorectal cancers.
  • APC has many functions, the most prominent is its capacity to regulate beta-catenin-mediated gene transcription in response to Wnt signalling.
  • Loss of APC leads to deregulated beta-catenin and this is intimately linked with tumour formation.
  • However, recent evidence indicates that the interaction of APC with the cytoskeleton might also contribute to tumour initiation and progression.
  • How does APC interact with the cytoskeleton and how could this play a part in colorectal tumorigenesis?
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Colonic Neoplasms / metabolism. Cytoskeleton / metabolism. Genes, APC. Signal Transduction
  • [MeSH-minor] Apoptosis. Cell Differentiation. Cell Movement. Cell Proliferation. Cytoskeletal Proteins / metabolism. Gene Expression Regulation, Neoplastic. Humans. Intestinal Mucosa / metabolism. Mutation. beta Catenin / metabolism

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  • (PMID = 17093505.001).
  • [ISSN] 1474-175X
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cytoskeletal Proteins; 0 / beta Catenin
  • [Number-of-references] 86
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6. Major MB, Camp ND, Berndt JD, Yi X, Goldenberg SJ, Hubbert C, Biechele TL, Gingras AC, Zheng N, Maccoss MJ, Angers S, Moon RT: Wilms tumor suppressor WTX negatively regulates WNT/beta-catenin signaling. Science; 2007 May 18;316(5827):1043-6
eagle-i research resources. PMID 17510365 (Special Collections) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In colorectal cancer and melanoma, mutational disruption of proteins involved in the degradation of beta-catenin, the key effector of the WNT signaling pathway, results in stabilization of beta-catenin and, in turn, activation of transcription.
  • We have used tandem-affinity protein purification and mass spectrometry to define the protein interaction network of the beta-catenin destruction complex.
  • This assay revealed that WTX, a protein encoded by a gene mutated in Wilms tumors, forms a complex with beta-catenin, AXIN1, beta-TrCP2 (beta-transducin repeat-containing protein 2), and APC (adenomatous polyposis coli).
  • [MeSH-major] Signal Transduction. Tumor Suppressor Proteins / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / metabolism. Animals. Axin Protein. Cell Line. Cell Line, Tumor. Cell Nucleus / metabolism. Cytoplasm / metabolism. Genes, Wilms Tumor. Humans. Kidney Neoplasms / genetics. Protein Binding. Protein Interaction Mapping. Proteomics. RNA Interference. Recombinant Fusion Proteins / metabolism. Repressor Proteins / metabolism. Transduction, Genetic. Ubiquitin / metabolism. Ubiquitin-Protein Ligases / metabolism. Wilms Tumor / genetics. Xenopus Proteins. Zebrafish. beta-Transducin Repeat-Containing Proteins / metabolism


7. Fernández-Suárez A, Cordero Fernández C, García Lozano R, Pizarro A, Garzón M, Núñez Roldán A: Clinical and ethical implications of genetic counselling in familial adenomatous polyposis. Rev Esp Enferm Dig; 2005 Sep;97(9):654-65
MedlinePlus Health Information. consumer health - Genetic Counseling.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and ethical implications of genetic counselling in familial adenomatous polyposis.
  • The association of specific genetic disturbances with the development of hereditary cancer helps us to understand the risk of suffering from it, the possibility of an earlier diagnosis, and the treatment and prevention of this disease.
  • Familial adenomatous polyposis (FAP) is a pre-neoplastic syndrome characterized by the presence of hundreds of adenomatous polyps in the colon, which develop into a carcinoma.
  • FAP can be diagnosed using sequencing techniques to detect mutations in the germinal line of the APC (adenomatous polyposis coli) gene.
  • The genetic diagnostic approach in families with FAP, previously followed up in the Gastrointestinal Clinic, has both advantages and disadvantages, and places us nearer the disease and patient.
  • Disclosing the results of this genetic test entails relevant problems in clinical practice, which affect the health field and raise legal and ethical issues, along with the familial, occupational, and social implications that knowing the genetic status can have on the patient.
  • Specialized multidisciplinary units are necessary for the management of patients with FAP undergoing analysis and appropriate genetic counselling, thus providing an individualized service.
  • The creation of FAP registers and protocols for this healthcare process should optimize the management of these patients and their families.
  • [MeSH-major] Adenomatous Polyposis Coli / prevention & control. Genetic Counseling
  • [MeSH-minor] Adolescent. Adult. Child. Genes, APC. Genetic Testing. Humans

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  • (PMID = 16266238.001).
  • [ISSN] 1130-0108
  • [Journal-full-title] Revista española de enfermedades digestivas : organo oficial de la Sociedad Española de Patología Digestiva
  • [ISO-abbreviation] Rev Esp Enferm Dig
  • [Language] eng; spa
  • [Publication-type] Journal Article
  • [Publication-country] Spain
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8. Sheng JQ, Cui WJ, Fu L, Jin P, Han Y, Li SJ, Fan RY, Li AQ, Zhang MZ, Li SR: APC gene mutations in Chinese familial adenomatous polyposis patients. World J Gastroenterol; 2010 Mar 28;16(12):1522-6
Genetic Alliance. consumer health - Familial Polyposis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] APC gene mutations in Chinese familial adenomatous polyposis patients.
  • AIM: To study the characteristics of APC (adenomatous polyposis coli) gene germline mutation in Chinese patients with familial adenomatous polyposis (FAP).
  • METHODS: APC gene from 14 FAP families was amplified by polymerase chain reaction (PCR) and underwent direct sequencing to determine the micromutation type.
  • For the samples without micromutation, the large fragment deletion of APC gene was examined by multiplex ligation-dependent probe amplification (MLPA).
  • Large fragment deletions were detected by MLPA in 2 families.
  • The total mutation detection rate of micromutations and large fragment deletions was 78.6% (11/14).
  • CONCLUSION: The detection rate of APC gene germline mutation can be improved by direct sequencing combined with MLPA large fragment deletion detection.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Mutation
  • [MeSH-minor] Adolescent. Adult. Asian Continental Ancestry Group / genetics. Child. China / epidemiology. Codon, Nonsense. DNA Mutational Analysis. Exons. Female. Frameshift Mutation. Gene Deletion. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Male. Middle Aged. Pedigree. Risk Factors. Young Adult

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  • (PMID = 20333795.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Codon, Nonsense
  • [Other-IDs] NLM/ PMC2846260
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9. Goldstein NS: Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification. Am J Clin Pathol; 2006 Jan;125(1):146-53
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification.
  • This review addresses the genetic mutations and cell signaling pathway alterations in colorectal premalignant polyps, focusing on the link between molecular changes and morphologic features.
  • Biallelic APC (adenomatous polyposis coli) mutations are directly responsible for the specific and characteristic cytologic features of dysplastic cells in conventional tubular adenomas.
  • Intracellular butyrate inhibits histone deacetylase, allowing histone hyperacetylation and, eventually, transcriptional activation of specific genes.
  • Decreased p21(WAF1/CIP1) and activation of the mitogen-activated protein kinase pathway may be the key intermediary alterations.
  • Progressive loss of cell cycle control and decreased and altered cytoplasmic differentiation produce the characteristic constellation of morphologic changes of SSAs and traditional serrated adenomas.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Colonic Polyps / pathology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / physiology. Carrier Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Nuclear Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics

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  • (PMID = 16483003.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  • [Number-of-references] 123
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10. Joyce T, Pintzas A: Microarray analysis to reveal genes involved in colon carcinogenesis. Expert Opin Pharmacother; 2007 May;8(7):895-900
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microarray analysis to reveal genes involved in colon carcinogenesis.
  • Sporadic colon cancer is a major cause of death throughout the world.
  • Multistage development of the disease has been associated with remarkable genetic events, mainly at the level of oncogenes and oncosuppressor genes, most notably APC (adenomatous polyposis coli), ras and p53.
  • Despite all of these efforts, the development of a sensitive and convenient diagnostic system for detecting colorectal cancers at the early stage is still in progress.
  • In recent years, cDNA and oligonucleotide microarray technologies have made the analysis of gene expression profiles of colorectal tumours at the genomic level possible and have identified signatures of gene expression associated with pre-cancerous phenotypes, cancers of the early stage and/or metastatic cancer.
  • The contribution of this powerful technology in identification of novel important genes for prognosis, diagnosis and therapy of sporadic colorectal will be discussed.

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  • (PMID = 17472535.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 27
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11. Goodin GS, McCarville MB, Thibodeau SN, Skapek SX, Khoury JD, Spunt SL: Prolactinoma as the first manifestation of Gardner's syndrome. Pediatr Blood Cancer; 2008 Feb;50(2):409-12
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactinoma as the first manifestation of Gardner's syndrome.
  • Familial adenomatous polyposis (FAP) is an inherited condition causing numerous adenomatous colorectal polyps and a markedly elevated risk of colon cancer.
  • FAP may be associated with various extracolonic manifestations such as desmoid fibromatosis and osteomas (termed Gardner's syndrome) and brain tumors, usually medulloblastoma or glioma [termed Brain Tumor Polyposis (BTP) syndrome type 2].
  • We describe a pediatric patient who initially presented with prolactinoma and later was found to have Gardner's syndrome.
  • A germline mutation of the APC (adenomatous polyposis coli) gene was identified.
  • Our case illustrates the association between prolactinoma and FAP, which may represent a rare subtype of Gardner's and BTP syndromes.
  • [MeSH-major] Gardner Syndrome / genetics. Prolactinoma / genetics
  • [MeSH-minor] Child. Genes, APC. Humans. Male. Mutation

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 16862550.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 23099; United States / NCI NIH HHS / CA / P30 CA 21765
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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12. Behrens J: The role of the Wnt signalling pathway in colorectal tumorigenesis. Biochem Soc Trans; 2005 Aug;33(Pt 4):672-5
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Mutations in the tumour suppressor APC (adenomatous polyposis coli) genes occur early in the development of CRC and lead to the stabilization of the Wnt pathway component beta-catenin and to the constitutive activation of Wnt signalling.
  • [MeSH-minor] Genes, APC. Humans. Protein-Tyrosine Kinases / genetics. Signal Transduction / genetics

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  • (PMID = 16042571.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 50
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13. Siriwardena BS, Kudo Y, Ogawa I, Tilakaratne WM, Takata T: Aberrant beta-catenin expression and adenomatous polyposis coli gene mutation in ameloblastoma and odontogenic carcinoma. Oral Oncol; 2009 Feb;45(2):103-8
Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant beta-catenin expression and adenomatous polyposis coli gene mutation in ameloblastoma and odontogenic carcinoma.
  • The Wnt pathway is involved in carcinogenesis and three regulatory genes of the Wnt pathway, APC (adenomatous polyposis coli), beta-catenin and Axin are frequently mutated in some primary human cancers.
  • This study was conducted to clarify the relation of beta-catenin accumulation and the mutation of the CTNNB1 (beta-catenin) gene with the mutation of APC gene in the process of development of odontogenic tumors including ameloblastoma and odontogenic carcinoma (OC).
  • beta-Catenin accumulation was examined by immunohistochemistry in formalin-fixed, paraffin-embedded samples of six ameloblastomas and eight OCs.
  • We also performed a mutation analysis of CTNNB1 and APC to examine the cause of beta-catenin accumulation.
  • CTNNB1 mutation was only found in one OC case, whereas three of six (50%) ameloblastoma cases and two out of eight (25%) OC cases had APC mutations within the mutational cluster region.
  • Our findings suggest that aberrant beta-catenin expression and APC missense mutation may play an important role for the pathogenesis of epithelial odontogenic tumors.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Carcinoma, Squamous Cell / metabolism. Mutation. Odontogenic Tumors / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adult. Ameloblastoma / genetics. Ameloblastoma / metabolism. Ameloblastoma / pathology. Cytoplasm / metabolism. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Genes, APC. Humans. Immunohistochemistry. Male. Middle Aged. Molecular Sequence Data

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  • (PMID = 18486530.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CTNNB1 protein, human; 0 / DNA, Neoplasm; 0 / beta Catenin
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14. Cordero J, Vidal M, Sansom O: APC as a master regulator of intestinal homeostasis and transformation: from flies to vertebrates. Cell Cycle; 2009 Sep 15;8(18):2926-31
FlyBase. FlyBase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] APC as a master regulator of intestinal homeostasis and transformation: from flies to vertebrates.
  • The mammalian intestinal epithelium is one of the most actively self-renewing tissues, which is constantly replenished by pluripotent intestinal stem cells (ISCs).
  • Indeed, many of the molecular pathways that regulate normal intestinal homeostasis appear involved in colorectal carcinogenesis.
  • Inactivating mutations of the APC (Adenomatous Polyposis Coli) gene is a hallmark of colorectal cancer.
  • The main tumor suppressive function of Apc is to negatively regulate Wnt signaling.
  • Targeted deletion of Apc in the murine intestine, and more recently in the zebrafish gut, recapitulate many aspects of the human disease.
  • Work in Drosophila now reveals that the role of APC in the intestine is ancient and highly conserved across species.
  • In support of these findings, we present data which suggests that APC1 may be a marker for adult ISCs in Drosophila and is required specifically within the ISCs to regulate intestinal homeostasis.
  • Here we discuss the similarities and differences between these model organisms in regards to the role of Wnt signaling and APC in intestinal homeostasis and transformation.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Cell Transformation, Neoplastic. Drosophila Proteins / physiology. Homeostasis. Intestines / physiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Animals. Drosophila. Pluripotent Stem Cells. Signal Transduction. Wnt Proteins

  • COS Scholar Universe. author profiles.
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  • (PMID = 19657225.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United Kingdom / National Centre for the Replacement, Refinement and Reduction of Animals in Research / / NC3RS/ G1000078/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / APC1 (adenomatous polyposis coli) protein, Drosophila; 0 / Adenomatous Polyposis Coli Protein; 0 / Drosophila Proteins; 0 / Tumor Suppressor Proteins; 0 / Wnt Proteins
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15. Collin L, Schlessinger K, Hall A: APC nuclear membrane association and microtubule polarity. Biol Cell; 2008 Apr;100(4):243-52
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] APC nuclear membrane association and microtubule polarity.
  • RESULTS: We previously showed, using primary fibroblasts and astrocytes in in vitro scratch-induced migration assays, that the accumulation of APC (adenomatous polyposis coli; the APC tumour suppressor protein) at microtubule plus-ends promotes their association with the plasma membrane at the leading edge.
  • CONCLUSIONS: We find that APC, through a direct interaction with the NPC (nuclear pore complex) protein Nup153 (nucleoporin 153), promotes the association of microtubules with the nuclear membrane.

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  • (PMID = 18042042.001).
  • [ISSN] 1768-322X
  • [Journal-full-title] Biology of the cell
  • [ISO-abbreviation] Biol. Cell
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / NUP153 protein, human; 0 / Nuclear Pore Complex Proteins
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16. Figer A, Shacham-Shmueli E, Liberman E, Sagiv E, Hall MJ, Dolkart O, Kazanov D, Kraus S, Neugut AI, Inbar M, Arber N: Effect of the I1307K polymorphism in APC confers a higher risk for polyp recurrence in Jewish Ashkenazi carriers. J Clin Oncol; 2009 May 20;27(15_suppl):e22003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of the I1307K polymorphism in APC confers a higher risk for polyp recurrence in Jewish Ashkenazi carriers.
  • : e22003 Background: The I1307K adenomatous polyposis coli gene variant, prevalent among Ashkenazi Jews, may increase risk for colorectal neoplasia [colorectal cancer (CRC) and CR adenoma].
  • Germline genetic analysis for the APC I1307K variant was performed using real-time PCR for DNA extracted from peripheral mononuclear cells.
  • Among Ashkenazi Jews, the I1307K variant was significantly more prevalent among persons with a personal or family history (1<sup>st</sup> degree) of CR neoplasia (p=0.01) as compared to Ashkenazi Jews with no family history.
  • The histopathological features of adenomas and cancers did not differ between carriers and non-carriers.
  • CONCLUSIONS: In the general population, the APC I1307K variant does not change the risk or prognosis of colorectal neoplasia in carriers and does not necessarily change their clinical practice.
  • Nevertheless, the variant, which is more prevalent among high risk individuals of Ashkenazi Jewish origin, is an important risk factor for the assessment of recurrence of neoplasia as it confers a higher risk for polyp recurrence in this population.

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  • (PMID = 27963171.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Constantinidou A, Scurr M, Jones R, Al-Muderis O, Judson I: Treatment of aggressive fibromatosis with pegylated liposomal doxorubicin: The Royal Marsden Hospital experience. J Clin Oncol; 2009 May 20;27(15_suppl):10519

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 10519 Background: Aggressive fibromatosis (AF) or desmoid tumors are monoclonal proliferations which are locally invasive but do not metastasise.
  • Sporadic tumors are usually associated with mutations in the beta-catenin gene CTNNB1whereas those occurring in the context of familial adenomatous polyposis usually have inactivating mutations in APC.
  • When surgery and radiotherapy are not applicable or fail to control the disease, systemic treatment with anti-oestrogens, non steroidal anti-inflammatory drugs (NSAIDs) and chemotherapy can be used.
  • RESULTS: The female/male ratio was 9:1 and the median age at presentation was 39.5 years (range 18-53).
  • For the nine patients who have completed treatment the median number of C cycles was 6 (range 4-6).
  • Objective response according to RECIST was achieved in 4/10 patients and in 5 patients the best response was stable disease.

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  • (PMID = 27963658.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Labianca R, Mandalà M, Barni S, Falanga A: Acquired and inherited risk factors for the developing of venous thromboembolism in cancer patients receiving adjuvant chemotherapy: A prospective trial. J Clin Oncol; 2009 May 20;27(15_suppl):9572

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We prospectively evaluated the effect of acquired (i.e. age, chemotherapy, tumor hystotype, history of thrombosis, body mass index and smoke) and inherited risk factors (i.e. antithrombin, protein C, protein S, homocysteine, activated protein C [APC] resistance, factor V Leiden [FVL] and Prothrombin [PT] mutations).
  • At multivariate analysis thrombocytosis (HR 2.8; 95% CI, 1.13-7.30, P< 0.026) and a previous episode of thrombosis (HR 12.4; 95% CI, 2.48-62.6, P< 0.0026) were significantly associated to the development of VTE .

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  • (PMID = 27963660.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. van der Bol JM, Verweij J, de Jong FA, Loos WJ, Lam MH, van Meerten E, Mathijssen RH: Effects of omeprazole on the pharmacokinetics and toxicities of irinotecan in cancer patients: A prospective open-label cross-over drug-interaction study. J Clin Oncol; 2009 May 20;27(15_suppl):2502

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2502 Background: The proton pump inhibitor omeprazole (Losec) is one of the most extensively prescribed medications worldwide and within its class, omeprazole is most frequently associated with drug interactions.
  • Plasma samples were obtained up to 55 hours after infusion and analyzed for irinotecan, and its metabolites SN-38, SN-38 glucuronide (SN-38G), NPC, and APC by reversed-phase high-performance liquid chromatography with fluorescence detection.
  • RESULTS: The mean AUCs of irinotecan and all metabolites were not significantly different between both courses (p>.151; see table).
  • The nadir ANC and WBC and the percentage decrease in ANC and WBC from baseline were not different between both courses (p>.529).
  • CONCLUSIONS: Omeprazole 40 mg did not alter the pharmacokinetics and toxicities of irinotecan.

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  • (PMID = 27961961.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Castellsague E, González S, Blanco I, Guinó E, Lázaro C, Gruber S, Capella G: APC germ-line allele-specific expression in familial adenomatous polyposis. J Clin Oncol; 2009 May 20;27(15_suppl):e22037

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] APC germ-line allele-specific expression in familial adenomatous polyposis.
  • : e22037 Background: About 13% of Familial Adenomatous Polyposis (FAP) families and 70% of Attenuated FAP families remain with unknown molecular pathogenic cause after APC and MYH mutational analyses.
  • The aim of the study was to determine the presence of germline ASE in the APC gene in FAP and AFP with and without detectable APC or MYH mutations.
  • METHODS: Germline RNA from fresh frozen and/or cultured lymphocytes of 17 APC/MYH-negative Polyposis (7 FAP, 10 AFAP) families (21 individuals) and 35 APC-mutated Polyposis (30 FAP, 5 AFAP) families (60 individuals) was analyzed.
  • ASE was investigated by single nucleotide primer extension (SNuPE) of rs2229992 APC coding SNP.
  • We found that 17% (3 of 17) APC/MYH(-) FAP and AFAP families showed ASE (range=1.17-1.39) and ASE co-segregated with disease.
  • Eleven of 35 (31%) APC-FAP/AFAP harbored ASE (range=1.20-7.76), and the mutant allele was underexpressed in each case.
  • CONCLUSIONS: APC ASE is present in a significant proportion (17%) of APC/MYH(-) FAP or AFAP.
  • ASE, due to nonsense-mediated decay (NMD), is present in APC-FAP and is associated with specific mutation location, similar to reports for other hereditary syndromes.

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  • (PMID = 27963154.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Riess H, Pelzer U, Deutschinoff G, Opitz B, Stauch M, Reitzig P, Hahnfeld S, Hilbig A, Stieler J, Oettle H: A prospective, randomized trial of chemotherapy with or without the low molecular weight heparin (LMWH) enoxaparin in patients (pts) with advanced pancreatic cancer (APC): Results of the CONKO 004 trial. J Clin Oncol; 2009 May 20;27(15_suppl):LBA4506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A prospective, randomized trial of chemotherapy with or without the low molecular weight heparin (LMWH) enoxaparin in patients (pts) with advanced pancreatic cancer (APC): Results of the CONKO 004 trial.

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  • (PMID = 27960826.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Azuara D, Rodriguez-Moranta F, Soriano-Izquierdo A, Guardiola J, de Oca J, Biondo S, Blanco I, Esteller M, Capella G: Evaluation of stool melting curve analysis of methylated CpG island promoters as an alternative for early noninvasive diagnosis of colorectal tumors. J Clin Oncol; 2009 May 20;27(15_suppl):e15036

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of stool melting curve analysis of methylated CpG island promoters as an alternative for early noninvasive diagnosis of colorectal tumors.
  • : e15036 Background: Previous studies have shown that assessment of promoter hypermethylation of a limited number of genes in tumor biopsies may identify all colorectal tumors analyzed.
  • The aim of the present study was to assess the clinical usefulness of a panel of methylation biomarkers in stool DNA in the diagnosis of colorectal tumors using Methylation Curve (MC) analyses, a technique that simultaneously analyze all CpG residues within a promoter.
  • METHODS: Promoter methylation status of 5 tumor-related genes (RARB2, p16<sup>INK4a</sup>, MGMT, p14<sup>ARF</sup> and APC) was analyzed in DNA stool samples and corresponding tissues in an initial set of 12 newly diagnosed patients with primary colorectal carcinomas and 20 with colorectal adenomas using Methylation-specific PCR (MSP).
  • Results were validated in a set of 88 patients (20 healthy subjects, 17 inflammatory bowel disease, 23 adenomas, 28 carcinomas) using MC analyses.
  • Analytical sensitivity of MC was 5% of methylated alleles for p16<sup>INK4a</sup>, p14<sup>ARF</sup>, RARB2 and APC and 10% for MGMT.
  • CONCLUSIONS: Melting Curve analysis of a panel of methylation markers in stool DNA is a good alternative for the early non-invasive diagnosis of colorectal tumors.

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  • (PMID = 27964470.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Cescon DW, Canil C, Le LW, Tannock IF: Use of the Prostate Cancer-specific Quality of Life Instrument (PROSQOLI) in clinical practice. J Clin Oncol; 2009 May 20;27(15_suppl):e20569

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e20569 Background: Improvement of quality of life (QOL) is a major therapeutic goal for men with advanced prostate cancer (APC).
  • The PROSQOLI consists of a series of 9 linear analog self-assessment (LASA) scales that evaluate pain, fatigue, appetite, constipation and other symptoms, and overall well-being; it was designed and validated for use in patients with APC.
  • Here we evaluate the use of a computer-based version of the PROSQOLI in routine clinical practice for its ability to stimulate recognition of symptoms and for its impact on clinical decision-making.
  • METHODS: Consenting patients with APC completed a touch screen version of the PROSQOLI before seeing the doctor at visits to the outpatient clinic.
  • In phase I of the study physicians did not have access to this information; in phase II physicians were provided with results of the PROSQOLI and its changes from previous visits.
  • Rates of documentation did not differ between study phases.
  • Prostate cancer-specific symptoms were poorly documented in clinical notes; improved recording of symptoms might be facilitated by the use of a tool such as the electronic touch-screen PROSQOLI.

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  • (PMID = 27961125.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Obrador-Hevia A, Chin F, Gonzalez S, Vilardell F, Cordero D, Greenson J, Moreno V, Caldas C, Capella G: Wnt signaling somatic alterations in apc-associated fap adenomas. J Clin Oncol; 2009 May 20;27(15_suppl):e22046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wnt signaling somatic alterations in apc-associated fap adenomas.
  • : e22046 Background: APC mutations are believed to constitutively activate the wnt pathway in colorectal tumors.
  • Our goal was to comprehensively characterize Wnt signaling components in a set of APC-associated FAP tumors both at the DNA and RNA levels.
  • METHODS: Sixty adenomas from FAP cases harboring pathogenic APC mutations were included (10 adenomas and 1 normal mucosa per case).
  • Somatic APC and KRAS alterations, β-catenin immunostaining and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analyzed. aCGH was also assessed in 26 FAP adenomas and 24 additional paired normal-adenoma-carcinoma samples.
  • RESULTS: A second APC alteration was present in 30 (50%) of adenomas (26 LOH and 4 point mutations).
  • LOH was only occasionally associated with loss of genetic material.
  • In 3 of 6 cases APC mRNA was overexpressed in macroscopically normal mucosa.
  • In these cases diminished APC levels mRNA were observed in 11 of 30 adenomas analyzed..
  • In the remaining 3 cases APC mRNA was already underexpressed in normal mucosa with only 3 of 30 adenomas showing further underexpression.
  • In FAP normal mucosae MYC was overexpressed (logratio range: 3.37-5.66).
  • All adenomas showed further MYC (logratio range: 1.78-2.92) and AXIN2 overexpression (logratio range: 1.62-4.65), corregulating with APC mRNA levels (r=0.31 for MYC; r=0.59 for AXIN2).
  • DNA changes were more often detected in areas containing wnt genes when FAP and sporadic tumors were jointly analyzed (p=0.02).
  • CONCLUSIONS: Wnt pathway is altered, at the DNA and/or RNA level, in all APC mutant FAP tumors.
  • MYC overexpression is a universal event that correlates with APC and AXIN2 expression levels as well as bcatenin nuclear accumulation.

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  • (PMID = 27963228.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Colucci G, Labianca R, Di Costanzo F, Gebbia V, Cartenì G, Massidda B, Frontini L, Falconi M, Gallo C, Di Maio M: A randomized trial of gemcitabine (G) versus G plus cisplatin in chemotherapy-naive advanced pancreatic adenocarcinoma: The GIP-1 (Gruppo Italiano Pancreas- GOIM/GISCAD/GOIRC) study. J Clin Oncol; 2009 May 20;27(15_suppl):4504

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 4504 Background: Single-agent gemcitabine (G) remains standard treatment for advanced pancreatic adenocarcinoma (APC).
  • In Arm B, P 25 mg/m2 weekly (with the exception of day 22) was added to G, same dose used in Arm A (Colucci et al, Cancer 2002; 94:902-10).
  • After a median follow-up of 38.2 months and 357 deaths, median OS was 8.3 vs 7.2 months in arm A and B, respectively (HR 1.10, 95% CI 0.89-1.35, p=0.38).
  • Median PFS was 3.9 vs 3.8 months in arm A and B, respectively (HR 0.97, 95% CI 0.80-1.19, p=0.80).
  • ORR was 10.1% in arm A and 12.9% in B (p=0.37).
  • CONCLUSIONS: Weekly combination of P and G, compared to single-agent G as 1st-line treatment of APC, failed to demonstrate any improvement in OS, PFS, ORR and clinical benefit.

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  • (PMID = 27962688.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Baden J, Markiewicz J, Painter J, Jones J, Curtin K, Canning S, Quijano J, Guinto W, Wang Y, Green G: Informative rate and reproducibility of the investigational GeneSearch ProCaM assay in a multicenter laboratory setting. J Clin Oncol; 2009 May 20;27(15_suppl):e22038

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The investigational ProCaM assay detects CpG island methylation within the promoter regions of three markers (GSTP1, RARß2, and APC) that are indicative of the presence of prostate cancer.
  • METHODS: Assay reproducibility: 8 operators from 4 external clinical laboratories tested a panel comprised of a negative panel member (NM2C5 cells) for the internal control (ß-Actin), a high positive and low positive panel members (LNCaP cells) for all 3 markers and ß-Actin.
  • The overall intersite %CV and SD values for Cts were = 9.2% and 1.49%, respectively.
  • The percent agreement with qualitative (positive/negative) outcome for High, Low, and Negative panel members was = 98% for GSTP1, RARß2, APC, and ß-Actin.
  • Using the result categories of negative and positive with identical cutoffs for GSTP1, RARß2, APC for samples with >5 ssDNA copies 98% concordance was observed for all 3 lots evaluated.

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  • (PMID = 27963156.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Lai R Sr, Feng L, Liu L, Xie L, Wu X, Zhang S, Tang X, Geng J, Chen T: The clinical pathogensis significance associated with mutation of APC MCR in colorectal neoplasms. J Clin Oncol; 2009 May 20;27(15_suppl):e15119

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical pathogensis significance associated with mutation of APC MCR in colorectal neoplasms.
  • : e15119 Background: To explore the clinical pathogensis evalution of codon 1493,1367 and 1328 mutations in MCR (mutation cluster region) of exon 15 of APC (Adenomatous polyposis coli) gene in cases of colorectal neoplasm and the family history.
  • METHODS: The specimens from 21 colorectal adenoma specimens groups,16 colorectal carcinoma groups, 20 healthy germline groups with positive familial history and 8 healthy germline groups without familial history.
  • MCR of APC gene were extracted and specificly amplified, then sequenced by sequencer, the codon mutations were analyzed between the 4 groups and various genotypes tested with Chi-square.
  • The allele mutations were checked out four genotypes such as 4478(G→A), 41/69(59.4%); 4478(G/A), 22/69(31.9%); 4096(C/T), 1/69 (1.4%) and 3979(C/T), 5/69(7.2%); but the significant groups status (P<0.05) were shown between the adenoma and nonfamily history group on the analysis of 4478(G→A) and (G/A), also the significant differences were tested between the with and without family history on the analysis of 4478(G→A).
  • The significant differences (P<0.05) in pathogensis mutant phenotypes were involved between 4478(G→A) with 4478(G/A), 4096(C/T) and 3979(C/T), respectively; also showed between 4478(G/A) with 4096(C/T) and 3979(C/T); but not between 4096(C/T) and 3979(C/T) (P>0.05).
  • CONCLUSIONS: In our data, the highest mutant frequency 4478(G→A) of 1493(ACG>ACA) presented to the significant phenotype of positive history and adenoma, but 4478 (G/A) were associated with colorectal adenocancer, which was discovered in the different effect to candidators despite the same synonymous mutation.
  • In researches, APC MCR codon 1367 and 1328 genotyping were significantly presented in the colorectal cancergenetic phenotypes in somatic cells only.

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  • (PMID = 27960846.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Lee S, Ryoo H, Bae S, Song H, Kim M, Lee K, Lee W, Park K, Kim J, Baek J: Fixed dose rate infusion of gemcitabine and UFT combination chemotherapy in patients with advanced biliary cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e15581

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fixed dose rate infusion of gemcitabine and UFT combination chemotherapy in patients with advanced biliary cancer.
  • Gemcitabine and UFT combination chemotherapy showed promising results in advanced pancreatic cancer(APC) and fixed dose- rate(FDR) infusion(10mg/m<sup>2</sup>/min) of gemcitabine is more effective than 30min-infusion in APC patients.
  • Partial response was 24.2% and disease control rate was 51.5%.
  • The estimated median time to progression(TTP) was 87 days(95% CI 51-123).
  • Median overall survival was 243 days(95% CI 114-372).
  • Polymorphism of XRCC1 was related to TTP(TTP of wild, heterozygous variant and homozygous variant type was 162, 71 and 25 days, respectively. p=0.0039).
  • QOL as a secondary endpoint was not analyzed at this time.

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  • (PMID = 27962362.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Marzese DM, Gago FE, Vargas-Roig LM, Roqué M: Methylation profile of human breast cancer: A possible biomarker for the detection of circulating tumor cells. J Clin Oncol; 2009 May 20;27(15_suppl):11112

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The identification of circulating tumor cells (CTCs) in the blood of cancer patients, based on their aberrant methylation profile, appears as a potential tool for early detection and provides therefore the promise of a non-invasive and affordable cancer detection test.
  • The more frequently aberrant methylated genes were: rassf1A promoter (62.5%), esr1 (54.17%), apc (54.17%) and rassf1A exon 1 (50%).
  • This method allowed the detection of CTCs in the peripheral blood of a cancer patient by their aberrant rassf1A methylation.
  • CONCLUSIONS: The identification of the methylation profile of the tumor by MS-MLPA allowed to establish the metastasis origin of invaded axillary lymph nodes and to detect CTCs in peripheral blood of a cancer patient.

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  • (PMID = 27963494.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Capella G, Castellsague E, Rennert G, Gruber S: APC allele-specific expression in carriers of Ashkenazi Jewish mutation I1307K. J Clin Oncol; 2009 May 20;27(15_suppl):e22181

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] APC allele-specific expression in carriers of Ashkenazi Jewish mutation I1307K.
  • : e22181 Background: I1307K is a missense APC variant with incomplete penetrance that has been found in 6% of Jewish Ashkenazi population and confers a two-fold increased risk to develop multiple adenomas and colorectal tumours.
  • It remains unknown whether the presence of this mutation modifies APC expression.
  • CONCLUSIONS: I1307K variant is not associated with allelic specific expression at the germline level.
  • I1307K overexpression is not selected for during tumor progression.

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  • (PMID = 27963596.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Del Giglio A, Pinto JF, Fonseca FA, Marsicano SR, Delgado PO, Coelho PG, Sant'Anna AL, Maeda P: Chemotherapy induces microssatelite instability (MIS) in plasma free DNA (pfDNA), peripheral blood mononuclear fraction (PBMNF) cells, and urine free DNA (ufDNA) of breast cancer (BC) patients as well as in normal PBMNF cells in vitro in the absence of amifostine (A). J Clin Oncol; 2009 May 20;27(15_suppl):e11505

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e11505 Background: We have previously shown that alkylating agent based chemotherapy regimens (AQT) could induce MIS in the PBMNF of BC patients in parallel to a decrease in the expression of the protein hMSH2 in these cells (Fonseca et al., 2005, Breast Cancer Res, 7, R28-32).
  • Blood (pfDNA and PBMNNF) and urine (ufDNA) were evaluated at time 0,3 and 6 months with 6 MIS markers (BAT40,BAT26, MR2,TP53 PCR15.1, APC and ALU).
  • Interestingly, fpDNA levels increased significantly in patients with measurable disease who responded to therapy (47.4 ± 13.34 vs 14.37± 5.32; p = 0.021).
  • CONCLUSIONS: We conclude that Chemotherapy as well as Fulvestran can induce MIS in normal and malignant cells and that in vitro these effects could be reproduced by treatment with M and prevented in normal cells by A.

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  • (PMID = 27964585.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Servarayan CM, Chandramohan A, Datta D, Manickavasagam K: p53 and its influence in adenocarcinoma stomach. J Clin Oncol; 2009 May 20;27(15_suppl):e15685

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Various pathogenesis have been given for the adenocarcinoma, like mutation in the E-catherin gene, amplification of COX-2, HGF/ SF, VEGF; deletion of FHIT, APC, p53 but none have provided a definite target for treatment.
  • 52.63 % of the non-mucinous type of gastric adenocarcinoma showed positive p53 immunoreactivity.

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  • (PMID = 27962795.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Ch'ang H, Hwang T, Wang H, Chang M, Tien Y, Chen J, Hsieh R, Lin P, Shan Y, Cheng A, Chen L: A phase II study of gemcitabine-based chemoradiotherapy (CCRT) after triplet induction chemotherapy (ICT) for locally advanced pancreatic cancer (LAPC): A Taiwan Cooperative Oncology Group (TCOG) study. J Clin Oncol; 2009 May 20;27(15_suppl):e15562

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recently, we showed that triplet chemotherapy consisting of gemcitabine 800 mg/m<sup>2</sup> (10 mg/m<sup>2</sup>/min) followed by oxaliplatin 85 mg/m<sup>2</sup> and 48-hour infusion of 5-FU/LV 3,000 and 150 mg/m<sup>2</sup> Q 2 weeks, the GOFL regimen, is feasible and active for pts with APC.
  • Patients who did not experience disease progression (PD) after 6 cycles of GOFL would had CCRT consisting of weekly gemcitabine 400mg/m<sup>2</sup> plus 50.4Gy/28 fractions of radiation 4-6 weeks later.
  • After CCRT, pts were re-evaluated for surgical intervention and those with unresectable disease would continue GOFL until PD, unacceptable toxicity, patient's refusal or death.
  • Among the 34 (68%) with objective response or stable disease after 6 cycles of ICT, 27 (54%) who completed the assigned multimodality treatment are categorized as CCRT group; whiles 7 (14%) who either declined CCRT (in 5) or still on ICT (in 2) are categorized as non-CCRT group.
  • The median PFS and OS for the ITT population were 9.1 and 14.5 months, respectively.

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  • (PMID = 27962329.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Salazar LG, Slota M, Wallace D, Higgins D, Coveler AL, Dang Y, Childs J, Bates N, Waisman J, Disis ML: A phase I study of a DNA plasmid based vaccine encoding the HER2/neu (HER2) intracellular domain (ICD) in subjects with HER2+ breast cancer. J Clin Oncol; 2009 May 20;27(15_suppl):3054

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of a DNA plasmid based vaccine encoding the HER2/neu (HER2) intracellular domain (ICD) in subjects with HER2+ breast cancer.
  • Vaccine-induced immunity against the HER2 ICD correlates with antitumor responses in animal models.
  • DNA-based vaccines offer a strategy to immunize against multiple tumor antigens and are able to elicit both CTL and T helper immune responses.
  • However, DNA vaccines have been poorly immunogenic due in part to inefficient APC transfection.
  • A phase I study was conducted to evaluate the safety and immunogenicity of a DNA-based vaccine encoding the HER2 ICD.
  • Vaccine site biopsies were analyzed for plasmid persistence via RT-PCR, 1 and 6 months after vaccination.
  • 13/21 (62%) subjects in Arm 1 developed T-cell immunity, defined as HER2-specific T cell precursors:PBMC, to the HER2 protein (median 1:5,972, range 1:717-1:3,000,000) and to p776, a HER2 pan DR binding epitope (median 1:3,150, range 1:543-1:108,696).

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  • (PMID = 27961998.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Hoimes CJ, Lamb L, Lok W, Elligers K, Carbone R, Keley K, Lansigan F, Liu SH, Cheng YC, Saif MW: Effect of PHY906 on capecitabine (CAP)-induced diarrhea in patients with GI malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):e20595

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e20595 Background: 15.4% of pts with GI cancers treated with CAP alone at 1250mg/m<sup>2</sup> BID D1-14 q 3 wks (14/7) develop G3/4 diarrhea (Hoff et al. JCO, 2001).
  • METHODS: We prospectively evaluated 44 pts treated on a clinical study with CAP plus PHY906 for diarrhea (experimental arm) and compared to historical data by Hoff et al., CAP 14/7 alone arm (control arm).
  • Experimental arm consisted of pts with refractory solid tumors in phase I and gemcitabine-refractory advanced pancreatic cancer (APC) in phase II.
  • Ph II treated pts with APC at 1500 mg/m<sup>2</sup> and PHY906 800mg BID D1-4.
  • Phase I pts had GI malignancies; 15 (63%) had APC and 6 (25%) colorectal.
  • One pt with APC who received 3 cycles at the 1500mg/m<sup>2</sup> dose level was diarrhea-free until he was removed from the study; he continued on single-agent CAP at 1000mg/m<sup>2</sup> BID and developed G3 diarrhea.
  • As an underlying mechanism of CID may include cytokine activation, evalation of cytokines is ongoing.

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  • (PMID = 27961165.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Tang E, Kwong A, Wong C, Law F, Wong C, Ng E, Ma E, Ford JM: Novel de novo BRCA1 mutation in a woman with early onset breast cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e22143

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel de novo BRCA1 mutation in a woman with early onset breast cancer.
  • : e22143 Background: Germline mutations in BRCA1/2 account for a significant portion of hereditary breast/ovarian cancer.
  • Mutation carriers usually have a family history of breast/ovarian cancer or early onset disease.
  • Rarely, germline mutations are found only in the probands but not in any family members.
  • Such de novo mutations have been reported in diseases such as hemophilia A, thalassaemia and familial adenomatous polyposis.
  • De novo mutations in the BRCA1 or BRCA2 genes are rare and the few reported have been in BRCA2.
  • Here, we describe de novo as well as novel mutation of the BRCA1 gene in a breast cancer patient.
  • METHODS: Blood DNA samples from a 30 year old Chinese woman with breast cancer and no family history of cancer was tested for a BRCA1/2 mutation by full gene sequencing and Multiple Ligation-dependent Probe Amplification (MLPA).
  • MLPA revealed a large deletion of exons 1 to 12 of BRCA1 in the proband.
  • MLPA performed on 5 family members: proband's mother and father (who were 1<sup>st</sup> degree relative- cousins), stepmother (mother's biological sister), 2 sisters (1, same parents; 1, same father and stepmother) found no similar deletion.
  • CONCLUSIONS: We report a novel de novo BRCA1 deletion mutation encompassing exons 1 - 12 in a Chinese breast cancer patient of early onset with no family history.
  • Identification of this large deletion confirms the importance of pursuing rearrangement testing if full gene sequencing fails to detect a point mutation or short insertion deletion.
  • The mutation found in this study is de novo.

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  • (PMID = 27963527.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Morse M, Chapman R, Powderly J, Keler T, He L, Ramakrishna V, Vitale L, Clay T, Green J, Davis T: Phase I clinical results of an APC-targeted hCGβ vaccine (CDX-1307) with TLR agonists. J Clin Oncol; 2009 May 20;27(15_suppl):3006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I clinical results of an APC-targeted hCGβ vaccine (CDX-1307) with TLR agonists.
  • The CDX-1307 vaccine is composed of B11 fused with hCGβ, a tumor antigen correlated with advanced stage of disease and poor prognosis in a number of common epithelial cancers, but reported at variable rates of expression.
  • To date, a significant mixed response was seen in one patient with pancreatic cancer (id), while stable disease has been seen in 4 patients (2 with breast cancer = 25, 27 weeks and 2 with colorectal cancer = 9+ weeks).

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  • (PMID = 27962048.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Heald B, Moran R, Milas M, Burke C, Eng C: Familial adenomatous polyposis in a patient with unexplained mental retardation. Nat Clin Pract Neurol; 2007 Dec;3(12):694-700
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Familial adenomatous polyposis in a patient with unexplained mental retardation.
  • BACKGROUND: A 22-year-old woman was referred to a genomic medicine clinic for evaluation of suspected Prader-Willi syndrome (PWS) after normal DNA methylation studies on chromosome 15 were obtained.
  • DIAGNOSIS: Familial adenomatous polyposis with mental retardation, caused by an interstitial deletion of the long arm of chromosome 5 encompassing the APC (adenomatous polyposis coli) tumor suppressor locus.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Intellectual Disability / complications


39. Nojima M, Suzuki H, Toyota M, Watanabe Y, Maruyama R, Sasaki S, Sasaki Y, Mita H, Nishikawa N, Yamaguchi K, Hirata K, Itoh F, Tokino T, Mori M, Imai K, Shinomura Y: Frequent epigenetic inactivation of SFRP genes and constitutive activation of Wnt signaling in gastric cancer. Oncogene; 2007 Jul 12;26(32):4699-713
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent epigenetic inactivation of SFRP genes and constitutive activation of Wnt signaling in gastric cancer.
  • Activation of Wnt signaling has been implicated in gastric tumorigenesis, although mutations in APC (adenomatous polyposis coli), CTNNB1 (beta-catenin) and AXIN are seen much less frequently in gastric cancer (GC) than in colorectal cancer.
  • In the present study, we investigated the relationship between activation of Wnt signaling and changes in the expression of secreted frizzled-related protein (SFRP) family genes in GC.
  • [MeSH-major] Carcinoma / genetics. Epigenesis, Genetic. Proto-Oncogene Proteins / genetics. Stomach Neoplasms / genetics. Wnt Proteins / genetics

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
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  • (PMID = 17297461.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / TCF Transcription Factors; 0 / Wnt Proteins
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40. Trostel SY, Sackett DL, Fojo T: Oligomerization of p53 precedes its association with dynein and nuclear accumulation. Cell Cycle; 2006 Oct;5(19):2253-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Previous studies have identified several proteins that associate with microtubules and the dynein motor complex including p53, the glucocorticoid and the vitamin D receptors, and the APC (adenomatous polyposis coli) protein; but neither the residues important for this interaction nor the physical state of the proteins involved have been clarified.
  • This finding was confirmed and extended by examining a series of truncated p53 proteins that identified residues 336 to 348 as crucial for association with dynein and nuclear transport.
  • These studies suggest that mutations or modifications that affect p53 oligomerization not only interfere with DNA binding but also with its intracellular distribution.
  • They also highlight the importance of an intact microtubule network in the trafficking of crucial cellular proteins.
  • [MeSH-major] Cell Nucleus / metabolism. Dyneins / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Cell Line, Tumor. Cytosol / metabolism. DNA-Binding Proteins. Dimerization. Humans. Microtubules / metabolism. Multiprotein Complexes / metabolism. Point Mutation. Protein Binding. Protein Transport

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  • (PMID = 16969106.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Multiprotein Complexes; 0 / Tumor Suppressor Protein p53; EC 3.6.4.2 / Dyneins
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41. Clarke AR: Studying the consequences of immediate loss of gene function in the intestine: APC. Biochem Soc Trans; 2005 Aug;33(Pt 4):665-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Studying the consequences of immediate loss of gene function in the intestine: APC.
  • The use of mouse models to study neoplasia is proving particularly powerful in dissecting the mechanisms underlying disease initiation and progression.
  • We have therefore adopted a strategy of using an inducible Cre-lox-based system to analyse the effects of loss of gene function, the use of which is reviewed here for the intestinal tumour suppressor APC (adenomatous polyposis coli).
  • Using this approach, we have conditionally and synchronously inactivated APC in virtually all the epithelial cells of the adult murine small intestine.
  • Deficiency in APC perturbs migration, alters the normal programme of differentiation and results in increased proliferation and apoptosis.
  • Microarray analysis reveals the transcriptome to be significantly altered; reflecting both gross phenotypic changes and changes in transcriptional activation.
  • These findings demonstrate that APC is indeed the critical determinant of cell fate in the intestinal epithelium, explaining its role as the cellular 'gatekeeper' in preventing neoplasia.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC
  • [MeSH-minor] Adenomatous Polyposis Coli Protein. Animals. Disease Models, Animal. Humans. Mice. Mutation

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  • (PMID = 16042569.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
  • [Number-of-references] 10
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42. Watanabe T, Noritake J, Kaibuchi K: Roles of IQGAP1 in cell polarization and migration. Novartis Found Symp; 2005;269:92-101; discussion 101-5, 223-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • +TIPs, including CLIP-170 and APC (adenomatous polyposis coli) are thought to function as capturing devices at specialized cortical regions.
  • Recently, we found that IQGAP1 directly binds to APC in addition to CLIP-170.
  • IQGAP1 and APC interdependently localize to leading edges in migrating cells.
  • IQGAP1 can link APC to actin filaments in vitro.
  • Thus, activation of Rac1 and Cdc42 in response to migration signals leads to recruitment of IQGAP1 and APC which, together with CLIP-170, form a complex that links the actin cytoskeleton and microtubule dynamics during cell polarization and migration.
  • [MeSH-major] Cell Movement / physiology. Cell Polarity / physiology. ras GTPase-Activating Proteins / metabolism
  • [MeSH-minor] Actins / metabolism. Adenomatous Polyposis Coli. Animals. Microtubule-Associated Proteins / metabolism. Microtubules / metabolism. Neoplasm Proteins / metabolism. cdc42 GTP-Binding Protein / metabolism. rac1 GTP-Binding Protein / metabolism. rho GTP-Binding Proteins / metabolism

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  • (PMID = 16355537.001).
  • [ISSN] 1528-2511
  • [Journal-full-title] Novartis Foundation symposium
  • [ISO-abbreviation] Novartis Found. Symp.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / IQ motif containing GTPase activating protein 1; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / ras GTPase-Activating Proteins; 148349-95-5 / cytoplasmic linker protein 170; EC 3.6.5.2 / cdc42 GTP-Binding Protein; EC 3.6.5.2 / rac1 GTP-Binding Protein; EC 3.6.5.2 / rho GTP-Binding Proteins
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43. Kuraguchi M, Ohene-Baah NY, Sonkin D, Bronson RT, Kucherlapati R: Genetic mechanisms in Apc-mediated mammary tumorigenesis. PLoS Genet; 2009 Feb;5(2):e1000367
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic mechanisms in Apc-mediated mammary tumorigenesis.
  • Many components of Wnt/beta-catenin signaling pathway also play critical roles in mammary tumor development, yet the role of the tumor suppressor gene APC (adenomatous polyposis coli) in breast oncongenesis is unclear.
  • To better understand the role of Apc in mammary tumorigenesis, we introduced conditional Apc mutations specifically into two different mammary epithelial populations using K14-cre and WAP-cre transgenic mice that express Cre-recombinase in mammary progenitor cells and lactating luminal cells, respectively.
  • Only the K14-cre-mediated Apc heterozygosity developed mammary adenocarcinomas demonstrating histological heterogeneity, suggesting the multilineage progenitor cell origin of these tumors.
  • These tumors harbored truncation mutation in a defined region in the remaining wild-type allele of Apc that would retain some down-regulating activity of beta-catenin signaling.
  • Expression profiles of acinar-type mammary tumors from K14-cre; Apc(CKO/+) mice showed luminal epithelial gene expression pattern, and clustering analysis demonstrated more correlation to MMTV-neu model than to MMTV-Wnt1.
  • In contrast, neither WAP-cre-induced Apc heterozygous nor homozygous mutations resulted in predisposition to mammary tumorigenesis, although WAP-cre-mediated Apc deficiency resulted in severe squamous metaplasia of mammary glands.
  • Collectively, our results suggest that not only the epithelial origin but also a certain Apc mutations are selected to achieve a specific level of beta-catenin signaling optimal for mammary tumor development and explain partially the colon- but not mammary-specific tumor development in patients that carry germline mutations in APC.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Mammary Neoplasms, Animal / genetics
  • [MeSH-minor] Animals. Female. Gene Expression Regulation, Neoplastic. Germ-Line Mutation. Integrases / genetics. Integrases / metabolism. Keratin-14 / genetics. Keratin-14 / metabolism. Mammary Glands, Animal / metabolism. Mice. Mice, Knockout. Mice, Transgenic. Milk Proteins / genetics. Milk Proteins / metabolism. Neoplasms / genetics. Signal Transduction. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 19197353.001).
  • [ISSN] 1553-7404
  • [Journal-full-title] PLoS genetics
  • [ISO-abbreviation] PLoS Genet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084301; United States / NCI NIH HHS / CA / CA-084301
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Keratin-14; 0 / Milk Proteins; 0 / beta Catenin; 0 / whey acidic proteins; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ PMC2629572
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44. Kuraguchi M, Wang XP, Bronson RT, Rothenberg R, Ohene-Baah NY, Lund JJ, Kucherlapati M, Maas RL, Kucherlapati R: Adenomatous polyposis coli (APC) is required for normal development of skin and thymus. PLoS Genet; 2006 Sep 15;2(9):e146
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  • [Title] Adenomatous polyposis coli (APC) is required for normal development of skin and thymus.
  • The tumor suppressor gene Apc (adenomatous polyposis coli) is a member of the Wnt signaling pathway that is involved in development and tumorigenesis.
  • Heterozygous knockout mice for Apc have a tumor predisposition phenotype and homozygosity leads to embryonic lethality.
  • To understand the role of Apc in development we generated a floxed allele.
  • Histological and immunochemical examinations revealed that K14-cre-mediated Apc loss resulted in aberrant growth in many ectodermally derived squamous epithelia, including hair follicles, teeth, and oral and corneal epithelia.
  • The aberrant growth of hair follicles and other appendages as well as the thymic abnormalities in K14-cre; Apc(CKO/CKO) mice suggest the Apc gene is crucial in embryonic cells to specify epithelial cell fates in organs that require epithelial-mesenchymal interactions for their development.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Skin / growth & development. Thymus Gland / growth & development
  • [MeSH-minor] Alleles. Animals. Embryo Loss. Embryo, Mammalian / abnormalities. Gene Expression Regulation. Genotype. Hair Follicle / cytology. Hair Follicle / pathology. Hedgehog Proteins / genetics. Humans. Keratins / genetics. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Nude. Molecular Sequence Data. Organ Specificity. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tooth / cytology. Tooth / pathology. beta Catenin / genetics

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  • (PMID = 17002498.001).
  • [ISSN] 1553-7404
  • [Journal-full-title] PLoS genetics
  • [ISO-abbreviation] PLoS Genet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ U13897; RefSeq/ NM/ 002230/ NM/ 004655/ NM/ 007462/ NM/ 007614/ NM/ 008412/ NM/ 008473/ NM/ 008476/ NM/ 008508/ NM/ 009170/ NM/ 010051/ NM/ 010703/ NM/ 012325/ NM/ 014970/ NM/ 015320/ NM/ 016958/ NM/ 027011/ NM/ 031170
  • [Grant] United States / NIEHS NIH HHS / ES / ES-11040; United States / NCI NIH HHS / CA / U01 CA084301; United States / NIDCR NIH HHS / DE / R37 DE011697; United States / NIDCR NIH HHS / DE / R01 DE011697; United States / NIDCR NIH HHS / DE / DE-16140; United States / NIDCR NIH HHS / DE / DE-11697; United States / NCI NIH HHS / CA / CA-084301; United States / NIEHS NIH HHS / ES / U01 ES011040; United States / NIDCR NIH HHS / DE / R01 DE016140
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Hedgehog Proteins; 0 / RNA, Messenger; 0 / Shh protein, mouse; 0 / beta Catenin; 68238-35-7 / Keratins
  • [Other-IDs] NLM/ PMC1564426
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45. Mihalatos M, Apessos A, Dauwerse H, Velissariou V, Psychias A, Koliopanos A, Petropoulos K, Triantafillidis JK, Danielidis I, Fountzilas G, Agnantis NJ, Nasioulas G: Rare mutations predisposing to familial adenomatous polyposis in Greek FAP patients. BMC Cancer; 2005;5:40
Genetic Alliance. consumer health - Familial Polyposis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare mutations predisposing to familial adenomatous polyposis in Greek FAP patients.
  • BACKGROUND: Familial Adenomatous Polyposis (FAP) is caused by germline mutations in the APC (Adenomatous Polyposis Coli) gene.
  • The vast majority of APC mutations are point mutations or small insertions/deletions which lead to truncated protein products.
  • Splicing mutations or gross genomic rearrangements are less common inactivating events of the APC gene.
  • METHODS: In the current study genomic DNA or RNA from ten unrelated FAP suspected patients was examined for germline mutations in the APC gene.
  • RESULTS: A 250 Kbp deletion in the APC gene starting from intron 5 and extending beyond exon 15 was identified in one patient.
  • A substitution of the +5 conserved nucleotide at the splice donor site of intron 9 in the APC gene was shown to produce frameshift and inefficient exon skipping in a second patient.
  • Four frameshift mutations (1577insT, 1973delAG, 3180delAAAA, 3212delA) and a nonsense mutation (C1690T) were identified in the rest of the patients.
  • CONCLUSION: Screening for APC mutations in FAP patients should include testing for splicing defects and gross genomic alterations.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Genetic Predisposition to Disease. Mutation
  • [MeSH-minor] Adult. Alternative Splicing. Chromatography, High Pressure Liquid. Codon, Nonsense. Exons. Family Health. Female. Frameshift Mutation. Gene Deletion. Gene Rearrangement. Genome. Germ-Line Mutation. Greece. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Pedigree. Phenotype. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA

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  • (PMID = 15833136.001).
  • [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 / Codon, Nonsense
  • [Other-IDs] NLM/ PMC1097718
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46. Berger FG, Kramer DL, Porter CW: Polyamine metabolism and tumorigenesis in the Apc(Min/+) mouse. Biochem Soc Trans; 2007 Apr;35(Pt 2):336-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polyamine metabolism and tumorigenesis in the Apc(Min/+) mouse.
  • While polyamine homoeostasis is clearly important in maintenance of normal cell function, the roles of these cations, as well as the enzymes that regulate their metabolism, in the neoplastic process are not clear.
  • In attempts to clarify the function of SSAT in tumour development, we have utilized the Apc(Min/+) mouse, which carries a mutant allele of the Apc (adenomatous polyposis coli) gene, rendering it susceptible to the formation of multiple adenomas in the small intestine and colon.
  • Using genetically engineered animals (i.e. transgenic and knockout mice), we have shown that SSAT acts as a tumour promoter in the Apc(Min/+) model.
  • Modulation of tumorigenesis is not associated with changes in tissue levels of either spermidine or spermine.
  • These findings, along with those made in other animal models of cancer, have prompted us to propose that metabolic flux through the polyamine biosynthetic and catabolic pathways, and the consequent changes in levels of various metabolites within the cell (i.e. the metabolome), is critical to tumour development.
  • [MeSH-major] Genes, APC. Intestinal Neoplasms / genetics. Polyamines / metabolism
  • [MeSH-minor] Acetyltransferases / genetics. Acetyltransferases / metabolism. Animals. Disease Models, Animal. Genetic Engineering. Mice. Mice, Mutant Strains. Ornithine Decarboxylase / metabolism

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  • (PMID = 17371273.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA222153; United States / NCI NIH HHS / CA / CA44013; United States / NCI NIH HHS / CA / CA76428; United States / NIDDK NIH HHS / DK / DK33886
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Polyamines; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.57 / diamine N-acetyltransferase; EC 4.1.1.17 / Ornithine Decarboxylase
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47. Zaoui K, Benseddik K, Daou P, Salaün D, Badache A: ErbB2 receptor controls microtubule capture by recruiting ACF7 to the plasma membrane of migrating cells. Proc Natl Acad Sci U S A; 2010 Oct 26;107(43):18517-22
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  • Memo-dependent inhibition of GSK3 allows the relocalization of APC (adenomatous polyposis coli) and cytoplasmic linker-associated protein 2 (CLASP2), known MT-associated proteins, to the plasma membrane and ruffles.
  • Peripheral microtubule extension also requires expression of the plus-end binding protein EB1 and its recently described interactor, the spectraplakin ACF7.
  • In fact, in migrating cells, ACF7 localizes to the plasma membrane and ruffles, in a Memo-, GSK3-, and APC-dependent manner.
  • This function of ACF7 does not require its recently described ATPase activity.
  • [MeSH-major] Cell Movement / physiology. Microfilament Proteins / metabolism. Microtubules / metabolism. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Adaptor Proteins, Signal Transducing / genetics. Adaptor Proteins, Signal Transducing / metabolism. Adenomatous Polyposis Coli Protein / antagonists & inhibitors. Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Tumor. Cell Membrane / metabolism. Female. Focal Adhesions / metabolism. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Glycogen Synthase Kinase 3 / metabolism. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Models, Biological. Nonheme Iron Proteins / antagonists & inhibitors. Nonheme Iron Proteins / genetics. Nonheme Iron Proteins / metabolism. RNA, Small Interfering / genetics. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Signal Transduction

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  • (PMID = 20937854.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [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 / CLASP2 protein, human; 0 / DIAPH1 protein, human; 0 / MACF1 protein, human; 0 / MEMO1 protein, human; 0 / Microfilament Proteins; 0 / Microtubule-Associated Proteins; 0 / Nonheme Iron Proteins; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2972954
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48. Näthke I: Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal regulation. Biochem Soc Trans; 2005 Aug;33(Pt 4):694-7
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  • [Title] Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal regulation.
  • A unique feature of colon cancer is that truncation mutations in the APC (adenomatous polyposis coli) gene are common to most tumours.
  • The high penetrance of APC mutations, especially in gut epithelium, supports the idea that APC may be involved in a number of the processes that govern the normal maintenance of this tissue: differentiation, migration, proliferation and apoptosis.
  • Indeed, APC is involved in the regulation of beta-catenin and it also is an important regulator of the cytoskeleton.
  • Thus mutations in APC lead to the accumulation of beta-catenin, which causes changes in differentiation, and they also produce changes in cytoskeletal organization, which results in altered cell migration and disrupted mitotic spindles.
  • The function of APC in cytoskeletal organization is related to its effect on microtubules and F-actin.
  • Depleting APC from cultured cells leads to changes in cytoskeletal organization.
  • In addition, N-terminal fragments of APC, like those commonly found in tumours, compromise cell migration in Dictyostelium and in early developing chicken embryos.
  • Consistent with the idea that such dominant effects are normally balanced by interactions within the full-length molecule, protein interactions of N-terminal fragments expressed in tumour cells can be altered by binding to C-terminal regions of APC commonly lost in tumours.
  • This review summarizes effects of APC on the cytoskeleton and discusses how these functions of APC may contribute to its role in cancer.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Colonic Neoplasms / pathology. Colorectal Neoplasms / genetics. Cytoskeleton / pathology. Mutation

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  • (PMID = 16042576.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
  • [Number-of-references] 33
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49. Clarke AR: Cancer genetics: mouse models of intestinal cancer. Biochem Soc Trans; 2007 Nov;35(Pt 5):1338-41
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  • [Title] Cancer genetics: mouse models of intestinal cancer.
  • 7, 519-531]. We have used these approaches to study tumorigenesis in the murine intestine.
  • Loss of function of the tumour-suppressor gene Apc (adenomatous polyposis coli) has been associated with the development of both human and murine neoplasia, principally those of the intestinal epithelium.
  • However, as Apc has been implicated in multiple cellular functions, the precise mechanisms underlying these associations remain somewhat unclear.
  • For Apc, these include failure in the differentiation programme, failure to migrate, aberrant proliferation and the aberrant induction of apoptosis.
  • Transcriptome analysis of this model has also identified potential new targets for therapeutic intervention, such as Sparc (secreted protein acidic and rich in cysteine), deficiency of which, we have now shown, suppresses adenoma formation.
  • Finally, we have been able to address how other genes modulate the consequences of Apc loss.
  • Thus we show that there is little effect following loss of cyclin D1, Tcf-1 and p53, but that there are marked differences following loss of either c-Myc or Mbd2.
  • The models therefore allow us to define the earliest events associated with carcinogenesis in the intestine.
  • [MeSH-major] Disease Models, Animal. Intestinal Neoplasms / genetics
  • [MeSH-minor] Animals. Epigenesis, Genetic. Genes, APC. Mice. Wnt Proteins / genetics. Wnt Proteins / metabolism

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  • (PMID = 17956346.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 9590
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Wnt Proteins
  • [Number-of-references] 32
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50. Aguilera O, Fraga MF, Ballestar E, Paz MF, Herranz M, Espada J, García JM, Muñoz A, Esteller M, González-Sancho JM: Epigenetic inactivation of the Wnt antagonist DICKKOPF-1 (DKK-1) gene in human colorectal cancer. Oncogene; 2006 Jul 6;25(29):4116-21
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  • Recently, CpG island promoter hypermethylation was shown to cause inactivation of two extracellular Wnt inhibitors in colon cancer: secreted frizzled-related proteins (sFRPs) and Wnt inhibitory factor-1 (WIF-1).
  • Here, we show for the first time that another extracellular Wnt inhibitor, the DICKKOPF-1 (DKK-1) gene, is transcriptionally silenced by CpG island promoter hypermethylation in colon cancer cell lines (n=9), whereas treatment with the DNA-demethylating agent 5-aza-2-deoxycytidine restored DKK-1 expression.
  • Restoration of DKK-1 function in non-expressing cells bearing a truncated APC (Adenomatous Polyposis Coli) gene had no effect on beta-catenin/T-cell factor-dependent transcription, but induced tumor suppressor-like features such as reduced colony formation density and tumor growth inhibition in nude mice.
  • Furthermore, while for both SFRP-1 and WIF-1 methylation-associated silencing occurred across the whole spectrum of colorectal tumorigenesis, DKK-1 promoter was selectively hypermethylated in advanced colorectal neoplasms (Duke's C and D tumors).
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / genetics. Epigenesis, Genetic. Genes, Tumor Suppressor. Intercellular Signaling Peptides and Proteins / genetics. Wnt Proteins / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Animals. Antimetabolites, Antineoplastic / pharmacology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Carrier Proteins / genetics. Carrier Proteins / secretion. Colon / metabolism. Colon / pathology. CpG Islands / genetics. DNA Methylation. Epithelium / metabolism. Epithelium / pathology. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Promoter Regions, Genetic / genetics. Repressor Proteins / genetics. Repressor Proteins / secretion. Signal Transduction / drug effects. Signal Transduction / genetics. Transplantation, Heterologous

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  • (PMID = 16491118.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Antimetabolites, Antineoplastic; 0 / Carrier Proteins; 0 / DKK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Repressor Proteins; 0 / WIF1 protein, human; 0 / Wnt Proteins; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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51. Hämmerlein A, Weiske J, Huber O: A second protein kinase CK1-mediated step negatively regulates Wnt signalling by disrupting the lymphocyte enhancer factor-1/beta-catenin complex. Cell Mol Life Sci; 2005 Mar;62(5):606-18
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  • [Title] A second protein kinase CK1-mediated step negatively regulates Wnt signalling by disrupting the lymphocyte enhancer factor-1/beta-catenin complex.
  • Deregulated activation of the canonical Wnt signalling pathway leads to stabilization of beta-catenin and is critically involved in carcinogenesis by an inappropriate induction of lymphocyte enhancer factor (LEF-1)/beta-catenin-dependent transcription of Wnt target genes.
  • Phosphorylation of the pathway components beta-catenin, Dishevelled, Axin and APC (adenomatous polyposis coli) by glycogen synthase kinase-3beta, CK1 and CK2 is of central importance in the regulation of the beta-catenin destruction complex.
  • Moreover, CK1-dependent phosphorylation in contrast to CK2 disrupts the association of beta-catenin and LEF-1 but does not impair DNA binding of LEF-1.
  • [MeSH-major] Casein Kinase I / physiology. Casein Kinase II / physiology. Cytoskeletal Proteins / metabolism. DNA-Binding Proteins / metabolism. Down-Regulation. Intercellular Signaling Peptides and Proteins / physiology. Trans-Activators / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Binding Sites. Cell Line, Tumor. DNA / metabolism. Genes, Reporter / genetics. Humans. Luciferases / analysis. Luciferases / genetics. Lymphoid Enhancer-Binding Factor 1. Phosphorylation. Protein Interaction Mapping. Protein Structure, Tertiary. Serine / metabolism. Signal Transduction. Transcription, Genetic / physiology. Wnt Proteins. beta Catenin

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  • (PMID = 15747065.001).
  • [ISSN] 1420-682X
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; 452VLY9402 / Serine; 9007-49-2 / DNA; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / Casein Kinase I; EC 2.7.11.1 / Casein Kinase II
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52. Tapia JC, Torres VA, Rodriguez DA, Leyton L, Quest AF: Casein kinase 2 (CK2) increases survivin expression via enhanced beta-catenin-T cell factor/lymphoid enhancer binding factor-dependent transcription. Proc Natl Acad Sci U S A; 2006 Oct 10;103(41):15079-84
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  • Increased expression of casein kinase 2 (CK2) is associated with hyperproliferation and suppression of apoptosis in cancer.
  • Mutations in the tumor suppressor APC (adenomatous polyposis coli) are frequent in colon cancer and often augment beta-catenin-T cell factor (Tcf)/lymphoid enhancer binding factor (Lef)-dependent transcription of genes such as c-myc and cyclin-D1.
  • TBB and 2-dimethylamino-4,5,6,7-tetrabromo-1H-benzimidazole significantly decreased proliferation and increased apoptosis of HT29(US) colon cancer cells.
  • RT-PCR and immunoblot analysis revealed that both inhibitors decreased survivin mRNA and protein levels in HT29(US) cells.
  • Similar effects were observed with TBB in human DLD-1 and SW-480 colorectal cells as well as ZR-75 breast cancer cells and HEK-293T embryonic kidney cells.

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  • (PMID = 17005722.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / FIC NIH HHS / TW / R03 TW006024; United States / FIC NIH HHS / TW / R03TW006024-03; United Kingdom / Wellcome Trust / / WT06491I/Z/01/Z
  • [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 / 4,5,6,7-tetrabromobenzotriazole; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / TCF Transcription Factors; 0 / Triazoles; 0 / beta Catenin; EC 2.7.11.1 / Casein Kinase II
  • [Other-IDs] NLM/ PMC1622780
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53. Svedlund J, Aurén M, Sundström M, Dralle H, Akerström G, Björklund P, Westin G: Aberrant WNT/β-catenin signaling in parathyroid carcinoma. Mol Cancer; 2010;9:294
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  • BACKGROUND: Parathyroid carcinoma (PC) is a very rare malignancy with a high tendency to recur locally, and recurrent disease is difficult to eradicate.
  • RESULTS: The APC (adenomatous polyposis coli) tumor suppressor gene was inactivated by DNA methylation in five analyzed PCs, as determined by RT-PCR, Western blotting, and quantitative bisulfite pyrosequencing analyses.
  • This was accompanied by accumulation of stabilized active nonphosphorylated β-catenin, strongly suggesting aberrant activation of the WNT/β-catenin signaling pathway in these tumors.
  • Treatment of a primary PC cell culture with the DNA hypomethylating agent 5-aza-2'-deoxycytidine (decitabine, Dacogen(r)) induced APC expression, reduced active nonphosphorylated β-catenin, inhibited cell growth, and caused apoptosis.
  • CONCLUSION: Aberrant WNT/β-catenin signaling by lost expression and DNA methylation of APC, and accumulation of active nonphosphorylated β-catenin was observed in the analyzed PCs.
  • [MeSH-major] Parathyroid Neoplasms / metabolism. Parathyroid Neoplasms / microbiology. Wnt Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / metabolism. Blotting, Western. DNA Methylation. Humans. Immunohistochemistry. In Vitro Techniques. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / genetics. Signal Transduction / physiology. Tumor Cells, Cultured

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  • (PMID = 21078161.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC2993678
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54. Whitfield JF: The calcium-sensing receptor--a driver of colon cell differentiation. Curr Pharm Biotechnol; 2009 Apr;10(3):311-6
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  • [Title] The calcium-sensing receptor--a driver of colon cell differentiation.
  • Dietary Ca(2+) reduces colon cell proliferation and carcinogenesis, but it becomes ineffective or even tumor-promoting during carcinogenesis.
  • It appears that Ca(2+) and the colon cell CaSR together brake the massive cell production in normal colon crypts.
  • The rapid proliferation of the transit-amplifying (TA) progeny of the colon stem cells at the bases of the crypts is driven by the "Wnt" signaling mechanism that stimulates proliferogenic genes and prevents apoptogenesis.
  • At this point the APC (adenomatous polyposis coli) protein appears and some of it enters the nucleus.
  • Cytoplasmic beta-catenin is prevented from returning to the nucleus by destruction in APCaxinGSK-3beta complexes or locked by the emerging E-cadherin into adherens junctions which link the cell to proliferatively shut-down functioning cells with APC-dependent cytoskeletons moving up and out of the crypt.
  • A common first step in colon carcinogenesis is the loss of functional APC which results in the retention of proliferogenic nuclear beta-cateninTcf-4.
  • [MeSH-major] Cell Differentiation / physiology. Colon / cytology. Receptors, Calcium-Sensing / physiology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Humans. Intestinal Mucosa / cytology. Intestinal Mucosa / drug effects. Neoplasms / pathology

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  • (PMID = 19355941.001).
  • [ISSN] 1873-4316
  • [Journal-full-title] Current pharmaceutical biotechnology
  • [ISO-abbreviation] Curr Pharm Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Calcium-Sensing
  • [Number-of-references] 81
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55. Gerner EW: Impact of dietary amino acids and polyamines on intestinal carcinogenesis and chemoprevention in mouse models. Biochem Soc Trans; 2007 Apr;35(Pt 2):322-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of dietary amino acids and polyamines on intestinal carcinogenesis and chemoprevention in mouse models.
  • Colon cancer in humans is influenced by both genetic and dietary risk factors.
  • The majority of colon cancers have somatic mutations in the APC (adenomatous polyposis coli) tumour-suppressor gene.
  • Dietary arginine enhances the risk of APC-dependent colon carcinogenesis in mouse models by a mechanism involving NOS2 (nitric oxide synthase 2), as elimination of NOS2 alleles suppresses this phenotype.
  • DFMO (difluoromethylornithine), a specific inhibitor of polyamine synthesis, also inhibits dietary arginine-induced colon carcinogenesis in C57BL/6J-Apc(Min)/J mice.
  • The primary consequence of dietary arginine is to increase the adenoma grade in these mice.
  • Either loss of NOS2 alleles or inhibition of polyamine synthesis suppresses the arginine-induced increase in adenoma grade.
  • In addition to promoting intestinal carcinogenesis, polyamines can also reduce the efficacy of certain intestinal cancer chemopreventive agents.
  • The NSAID (non-steroidal anti-inflammatory drug) sulindac is a potent inhibitor of intestinal carcinogenesis in the C57BL/6J-Apc(Min)/J mouse model and is used to treat humans with FAP (familial adenomatous polyposis).
  • Dietary putrescine reduces the ability of sulindac to suppress intestinal tumorigenesis in the mouse model.
  • These data suggest that reducing polyamine metabolism and dietary polyamine levels may enhance strategies for colon cancer chemoprevention.

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  • (PMID = 17371270.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA123065-02S1; United States / NCI NIH HHS / CA / P50 CA095060-07; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / R01 CA123065; United States / NCI NIH HHS / CA / R01 CA123065-02S1; United States / NCI NIH HHS / CA / CA095060-07
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 0 / Polyamines; ZQN1G5V6SR / Eflornithine
  • [Other-IDs] NLM/ NIHMS188389; NLM/ PMC2848482
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56. Souazé F, Viardot-Foucault V, Roullet N, Toy-Miou-Leong M, Gompel A, Bruyneel E, Comperat E, Faux MC, Mareel M, Rostène W, Fléjou JF, Gespach C, Forgez P: Neurotensin receptor 1 gene activation by the Tcf/beta-catenin pathway is an early event in human colonic adenomas. Carcinogenesis; 2006 Apr;27(4):708-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurotensin receptor 1 gene activation by the Tcf/beta-catenin pathway is an early event in human colonic adenomas.
  • Alterations in the Wnt/APC (adenomatous polyposis coli) signalling pathway, resulting in beta-catenin/T cell factor (Tcf)-dependent transcriptional gene activation, are frequently detected in familial and sporadic colon cancers.
  • Its proliferative and survival effects are mediated by a G-protein coupled receptor, the NT1 receptor.
  • NT1 receptor is not expressed in normal colon epithelial cells, but is over expressed in a number of cancer cells and tissues suggesting a link to the outgrowth of human colon cancer.
  • Our results demonstrate that the upregulation of NT1 receptor occurring in colon cancer is the result of Wnt/APC signalling pathway activation.
  • Consequently, we observed the activation of NT1 receptor gene by agents causing beta-catenin cytosolic accumulation, as well as a strong decline of endogenous receptor when wt-APC was restored.
  • At the cellular level, the re-establishment of wt-APC phenotype resulted in the impaired functionality of NT1 receptor, like the breakdown in NT-induced intracellular calcium mobilization and the loss of NT pro-invasive effect.
  • We corroborated the Wnt/APC signalling pathway on the NT1 receptor promoter activation with human colon carcinogenesis, and showed that NT1 receptor gene activation was perfectly correlated with nuclear or cytoplasmic beta-catenin localization while NT1 receptor was absent when beta-catenin was localized at the cell-cell junction in early adenomas of patients with familial adenomatous polyposis, hereditary non-polyposis colorectal cancer and loss of heterozygosity tumours.
  • In this report we establish a novel link in vitro between the Tcf/beta-catenin pathway and NT1 receptor promoter activation.
  • [MeSH-major] Adenoma / genetics. Colonic Neoplasms / genetics. Receptors, Neurotensin / biosynthesis. TCF Transcription Factors / physiology. beta Catenin / physiology
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / physiology. Cell Proliferation. Cell Survival. Cell Transformation, Neoplastic. Humans. Loss of Heterozygosity. Promoter Regions, Genetic. Signal Transduction. Up-Regulation. Wnt Proteins / physiology

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  • (PMID = 16299383.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Receptors, Neurotensin; 0 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; 0 / neurotensin type 1 receptor
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57. Leung WK, To KF, Man EP, Chan MW, Bai AH, Hui AJ, Chan FK, Sung JJ: Quantitative detection of promoter hypermethylation in multiple genes in the serum of patients with colorectal cancer. Am J Gastroenterol; 2005 Oct;100(10):2274-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative detection of promoter hypermethylation in multiple genes in the serum of patients with colorectal cancer.
  • OBJECTIVES: While promoter hypermethylation is a common molecular alteration of human colorectal cancer that could be detected in the bloodstream, we tested the feasibility of quantitative detection of aberrant DNA methylation in multiple genes in the serum samples of colorectal cancer patients.
  • The presence of methylated DNA in APC (adenomatous polyposis coli), hMLH1 (human MutL homolog 1), and HLTF (helicase-like transcription factor) was detected by quantitative methylation-specific PCR (MethyLight).
  • RESULTS: There was a significant difference in the concentration of methylated serum DNA between cancer patients and controls for HLTF (p= 0.015) and hMLH1 (p= 0.0001) genes, but not for APC gene (p= 0.21).
  • [MeSH-major] Colorectal Neoplasms / blood. DNA Methylation. DNA-Binding Proteins / blood. Genes, APC / physiology. Neoplasm Proteins / blood. Nuclear Proteins / blood. Promoter Regions, Genetic / physiology. Transcription Factors / blood
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Aged. Aged, 80 and over. Carrier Proteins. Feasibility Studies. Female. Glutathione S-Transferase pi. Glutathione Transferase / blood. Glutathione Transferase / genetics. Humans. Isoenzymes / blood. Isoenzymes / genetics. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity

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  • (PMID = 16181380.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / HLTF protein, human; 0 / Isoenzymes; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase
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58. Bliznashki I, Minev M, Mikhova A, Velev M: [A rare case of Gardner's syndrome complicated with rectal carcinoma]. Khirurgiia (Sofiia); 2007;(3):60-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A rare case of Gardner's syndrome complicated with rectal carcinoma].
  • Gardner's syndrome is a rare variant of the Familial Adenomatous Polyposis (FAP) in which affected individuals develop thousands of polyps within the gastrointestinal tract, with a 100 % risk of eventual malignant change.
  • Gardner's syndrome is an autosomal dominant disease, caused by mutations in APC ( adenomatous polyposis coli ) gene, which is located in chromosomal locus 5q21- q22.
  • They have investigated a family of 51 members with polyposis, some of them with multiple epidermoid cysts, fibromas and jaw osteomas.
  • Due to this high risk of malignancy the patients with Gardner's syndrome usually undergo surgical treatment by total or subtotal proctocolectomy.
  • We report a case with Gardner's syndrome - a 36 year-old male who has been operated on in Department of Surgery in Vth city clinical hospital in October 2003.
  • He had multiple adenomatous polyposis of colon, rectal cancer, osteomas of skull bones, subcutaneous fibromas and lipomas.
  • We discovered also by ultrasound examination a polyp of gall bladder.
  • His father has had also multiple polyposis with malignancy and metastatic lesions and he has died at age of 49 years.
  • [MeSH-major] Gardner Syndrome. Rectal Neoplasms
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / surgery. Adult. Cholecystectomy. Epidermal Cyst / diagnosis. Epidermal Cyst / genetics. Epidermal Cyst / surgery. Humans. Male. Osteoma / diagnosis. Osteoma / genetics. Osteoma / surgery. Proctocolectomy, Restorative

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  • (PMID = 18437113.001).
  • [ISSN] 0450-2167
  • [Journal-full-title] Khirurgii︠a︡
  • [ISO-abbreviation] Khirurgiia (Sofiia)
  • [Language] bul
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Bulgaria
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59. Narayan N, Massimi P, Banks L: CDK phosphorylation of the discs large tumour suppressor controls its localisation and stability. J Cell Sci; 2009 Jan 1;122(Pt 1):65-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CDK phosphorylation of the discs large tumour suppressor controls its localisation and stability.
  • The Discs Large (Dlg) protein is known to be involved in the regulation of cellular proliferation and polarity in a variety of tissues.
  • The human homologue DLG1 is thought to be a tumour suppressor, through formation of a complex with the APC (adenomatous polyposis coli) protein, causing negative regulation of the cell cycle.
  • An alternative oncogenic role has also been proposed, in which the PI3-kinase pathway is activated under the influence of the adenovirus E4 ORF1 protein.
  • In this study we show that phosphorylation is a major post-translational modification of the protein and it affects both location and function.
  • These phosphorylated sites together affect the nuclear localisation of the protein, and implicate the role of phosphorylation on Ser158 and Ser442 in its putative nuclear functions as a tumour suppressor.
  • In addition, the mutants at these sites demonstrate different half-lives as well as different susceptibilities to ubiquitylation, suggesting a role for these phosphorylation events in controlling DLG1 protein stability.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. CDC2 Protein Kinase / metabolism. Cyclin-Dependent Kinase 2 / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Cell Cycle / physiology. Cell Line. Cell Nucleus / metabolism. Humans. Molecular Sequence Data. Phosphorylation. Protein Stability. Sequence Alignment. Serine / metabolism

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  • (PMID = 19066288.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DLG1 protein, human; 0 / Membrane Proteins; 452VLY9402 / Serine; EC 2.7.11.22 / CDC2 Protein Kinase; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2
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60. Saif MW, Li J, Lamb L, Rosenberg A, Elligers K, Ruta S, Mezes M, Grant N, Liu SH, Chu E, Cheng Y: A phase II study of capecitabine (CAP) plus PHY906 in patients (pts) with advanced pancreatic cancer (APC). J Clin Oncol; 2009 May 20;27(15_suppl):e15508

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of capecitabine (CAP) plus PHY906 in patients (pts) with advanced pancreatic cancer (APC).
  • : e15508 Background: Gemcitabine (G) is regarded as the standard treatment for pts with APC.
  • Therefore, 1500mg/m<sup>2</sup> of CAP and PHY906 was further tested in a phase II study as second-line treatment in pts with APC.
  • METHODS: Pts with G-refractory APC with ECOG PS <2 were treated with CAP 1500mg/m<sup>2</sup> d1-7 with PHY906 800mg d1-4 q 2 wks.
  • There were 7 deaths on/within 30 days of study treatment, 6 related to PD and 1 had acute MI.
  • CONCLUSIONS: This is the first clinical study to evaluate a botanical formulation PHY906 with CAP in G-refractory APC pts.
  • CAP + PHY906 regimen appears a safe and feasible salvage therapy in APC and warrants further investigation.

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  • (PMID = 27962238.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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61. Wang Y, Coffey RJ, Osheroff N, Neufeld KL: Topoisomerase IIalpha binding domains of adenomatous polyposis coli influence cell cycle progression and aneuploidy. PLoS One; 2010 Apr 02;5(4):e9994
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topoisomerase IIalpha binding domains of adenomatous polyposis coli influence cell cycle progression and aneuploidy.
  • BACKGROUND: Truncating mutations in the tumor suppressor gene APC (Adenomatous Polyposis Coli) are thought to initiate the majority of colorectal cancers.
  • The 15- and 20-amino acid repeat regions of APC bind beta-catenin and have been widely studied for their role in the negative regulation of canonical Wnt signaling.
  • However, functions of APC in other important cellular processes, such as cell cycle control or aneuploidy, are only beginning to be studied.
  • Our previous investigation implicated the 15-amino acid repeat region of APC (M2-APC) in the regulation of the G2/M cell cycle transition through interaction with topoisomerase IIalpha (topo IIalpha).
  • METHODOLOGY/PRINCIPAL FINDINGS: We now demonstrate that the 20-amino acid repeat region of APC (M3-APC) also interacts with topo IIalpha in colonic epithelial cells.
  • Expression of M3-APC in cells with full-length endogenous APC causes cell accumulation in G2.
  • However, cells with a mutated topo IIalpha isoform and lacking topo IIbeta did not arrest, suggesting that the cellular consequence of M2- or M3-APC expression depends on functional topoisomerase II.
  • Both purified recombinant M2- and M3-APC significantly enhanced the activity of topo IIalpha.
  • Of note, although M3-APC can bind beta-catenin, the G2 arrest did not correlate with beta-catenin expression or activity, similar to what was seen with M2-APC.
  • More importantly, expression of either M2- or M3-APC also led to increased aneuploidy in cells with full-length endogenous APC but not in cells with truncated endogenous APC that includes the M2-APC region.
  • CONCLUSIONS/SIGNIFICANCE: Together, our data establish that the 20-amino acid repeat region of APC interacts with topo IIalpha to enhance its activity in vitro, and leads to G2 cell cycle accumulation and aneuploidy when expressed in cells containing full-length APC.
  • These findings provide an additional explanation for the aneuploidy associated with many colon cancers that possess truncated APC.

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  • (PMID = 20368985.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109220-05; United States / NCI NIH HHS / CA / R01 CA109220-03; United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA046413; United States / NCI NIH HHS / CA / P50 CA095103-09; None / None / / P50 CA095103-09; United States / NIGMS NIH HHS / GM / GM33944; United States / NCI NIH HHS / CA / R01 CA46413; United States / NCI NIH HHS / CA / R01 CA109220; United States / NCI NIH HHS / CA / CA046413-22; United States / NCI NIH HHS / CA / R01 CA109220-01; United States / NCI NIH HHS / CA / R01 CA109220-04; United States / NCI NIH HHS / CA / R01 CA10922; United States / NCI NIH HHS / CA / R01 CA046413-22; United States / NCI NIH HHS / CA / CA95103; United States / NIGMS NIH HHS / GM / R01 GM033944; United States / NCI NIH HHS / CA / R01 CA109220-02
  • [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 / Adenomatous Polyposis Coli Protein; 0 / Antigens, Neoplasm; 0 / Codon, Nonsense; 0 / DNA-Binding Proteins; 0 / beta Catenin; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC2848841
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62. Weijenberg MP, Lüchtenborg M, de Goeij AF, Brink M, van Muijen GN, de Bruïne AP, Goldbohm RA, van den Brandt PA: Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes. Cancer Causes Control; 2007 Oct;18(8):865-79
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes.
  • OBJECTIVE: To investigate baseline fat intake and the risk of colon and rectal tumors lacking MLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2) repair gene expression and harboring mutations in the APC (adenomatous polyposis coli) tumor suppressor gene and in the KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) oncogene.
  • METHODS: After 7.3 years of follow-up of the Netherlands Cohort Study (n = 120,852), adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) were computed, based on 401 colon and 130 rectal cancer patients.
  • RESULTS: Total, saturated and monounsaturated fat were not associated with the risk of colon or rectal cancer, or different molecular subgroups.
  • Linoleic acid, the most abundant polyunsaturated fatty acid in the diet, was associated with increased risk of colon tumors with only a KRAS mutation and no additional truncating APC mutation or lack of MLH1 expression (RR = 1.41, 95% CI 1.18-1.69 for one standard deviation (i.e., 7.5 g/day) increase in intake, p-trend over the quartiles of intake <0.001).
  • Linoleic acid intake was not associated with risk of colon tumors without any of the gene defects, or with tumors harboring aberrations in either MLH1 or APC.
  • CONCLUSION: Linoleic acid intake is associated with colon tumors with an aberrant KRAS gene, but an intact APC gene and MLH1 expression, suggesting a unique etiology of tumors with specific genetic aberrations.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Adenomatous Polyposis Coli Protein / genetics. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / genetics. Dietary Fats / administration & dosage. Genes, ras / genetics. Mutation / genetics. Nuclear Proteins / genetics

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  • (PMID = 17636402.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / Dietary Fats; 0 / MLH1 protein, human; 0 / Nuclear Proteins
  • [Other-IDs] NLM/ PMC2039842
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63. Neufeld KL: Nuclear APC. Adv Exp Med Biol; 2009;656:13-29
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear APC.
  • Mutational inactivation of the tumor suppressor gene APC (Adenomatous polyposis coli) is thought to be an initiating step in the progression of the vast majority ofcolorectal cancers.
  • Attempts to understand APC function have revealed more than a dozen binding partners as well as several subcellular localizations including at cell-cell junctions, associated with microtubules at the leading edge of migrating cells, at the apical membrane, in the cytoplasm and in the nucleus.
  • The present chapter focuses on APC localization and functions in the nucleus.
  • APC contains two classical nuclear localization signals, with a third domain that can enhance nuclear import.
  • Along with two sets of nuclear export signals, the nuclear localization signals enable the large APC protein to shuttle between the nucleus and cytoplasm.
  • Nuclear APC can oppose beta-catenin-mediated transcription.
  • This down-regulation of nuclear beta-catenin activity by APC most likely involves nuclear sequestration of beta-catenin from the transcription complex as well as interaction of APC with transcription corepressor CtBP.
  • Additional nuclear binding partners for APC include transcription factor activator protein AP-2alpha, nuclear export factor Crm1, protein tyrosine phosphatase PTP-BL and perhaps DNA itself.
  • Interaction of APC with polymerase beta and PCNA, suggests a role for APC in DNA repair.
  • The observation that increases in the cytoplasmic distribution of APC correlate with colon cancer progression suggests that disruption of these nuclear functions of APC plays an important role in cancer progression.
  • APC prevalence in the cytoplasm of quiescent cells points to a potential function for nuclear APC in control of cell proliferation.
  • Clear definition of APC's nuclear function(s) will expand the possibilities for early colorectal cancer diagnostics and therapeutics targeted to APC.

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  • (PMID = 19928349.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109220-05; United States / NCI NIH HHS / CA / R01 CA109220-03; United States / NCI NIH HHS / CA / R01 CA109220; United States / NCI NIH HHS / CA / R01 CA109220-01; United States / NCI NIH HHS / CA / R01 CA109220-04; United States / NCI NIH HHS / CA / R01 CA109220-02; United States / NCI NIH HHS / CA / R01CA109220-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Nuclear Export Signals; 0 / Nuclear Proteins; 0 / beta Catenin
  • [Number-of-references] 57
  • [Other-IDs] NLM/ NIHMS222396; NLM/ PMC3061301
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64. Groen EJ, Roos A, Muntinghe FL, Enting RH, de Vries J, Kleibeuker JH, Witjes MJ, Links TP, van Beek AP: Extra-intestinal manifestations of familial adenomatous polyposis. Ann Surg Oncol; 2008 Sep;15(9):2439-50
Genetic Alliance. consumer health - Familial Polyposis.

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  • [Title] Extra-intestinal manifestations of familial adenomatous polyposis.
  • Familial adenomatous polyposis (FAP) is an autosomal dominantly inherited disorder, which results from a germ line mutation in the APC (adenomatous polyposis coli) gene.
  • FAP is characterized by the formation of hundreds to thousands of colorectal adenomatous polyps.
  • Although the development of colorectal cancer stands out as the most prevalent complication, FAP is a multisystem disorder of growth.
  • This means, it is comparable to other diseases such as the MEN syndromes, Von Hippel-Lindau disease and neurofibromatosis.
  • Therefore, a specialized multidisciplinary approach to optimize health care-common for other disorders-is not usually taken for FAP patients.
  • Thus, clinicians that care for and counsel members of high-risk families should have familiarity with all the extra-intestinal manifestations of this syndrome.
  • FAP-related complications, for which medical attention is essential, are not rare and their estimated lifetime risk presumably exceeds 30%.
  • We present a clinical overview of extra-intestinal manifestations, including management and treatment options for the FAP syndrome.
  • Furthermore, we provide recommendations for surveillance of FAP complications based on available literature.
  • [MeSH-major] Adenomatous Polyposis Coli / diagnosis. Neoplasms / diagnosis
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Germ-Line Mutation. Humans

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  • [CommentIn] Ann Surg Oncol. 2009 May;16(5):1446-8; author reply 1449-50 [19266242.001]
  • (PMID = 18612695.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
  • [Number-of-references] 111
  • [Other-IDs] NLM/ PMC2518080
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65. Modica S, Morgano A, Salvatore L, Petruzzelli M, Vanier MT, Valanzano R, Esposito DL, Palasciano G, Duluc I, Freund JN, Mariani-Costantini R, Moschetta A: Expression and localisation of insulin receptor substrate 2 in normal intestine and colorectal tumours. Regulation by intestine-specific transcription factor CDX2. Gut; 2009 Sep;58(9):1250-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and localisation of insulin receptor substrate 2 in normal intestine and colorectal tumours. Regulation by intestine-specific transcription factor CDX2.
  • BACKGROUND AND AIMS: Self-renewal and differentiation of intestinal epithelium is a tightly regulated process, whose perturbations are implicated in human colorectal tumourigenesis.
  • The insulin/insulin-like growth factor (IGF) signalling pathway may play an important role in intestinal epithelium homeostasis.
  • METHODS: Using complementary in vitro and in vivo human and murine models, expression (mRNA and protein levels), localisation (immunohistochemistry) and regulation of IRS2 were investigated in the normal intestine and colorectal tumours.
  • RESULTS: Significant IRS2 expression was detected in the intestine, with specific protein localisation in the villus region of the ileum and in the surface epithelium of the colon.
  • In human HT29 and Caco2 cells, IRS2 mRNA levels increased with spontaneous and induced differentiation, together with CDX2 (caudal-related homeobox protein 2), P21 and KLF4 (Krüppel-like factor 4).
  • Adenoviral infection with human CDX2 induced IRS2 expression in APC- (adenomatous polyposis coli) and beta-catenin-mutated cells.
  • On the other hand, IRS2 downregulation was observed in differentiated enterocytes after adenoviral infection with short hairpin CDX2 (shCDX2), in the intestine of CDX2 heterozygous mice and in colorectal tumours of Apc(Min/+) and patients with familial adenomatous polyposis (FAP).
  • IRS2 reporters were functionally activated via CDX2 and blocked via a dominant-negative CDX2 protein.
  • CONCLUSIONS: Combining gain- and loss-of-function approaches, an intriguing scenario is presented whereby IRS2 is significantly expressed in the apical intestinal compartment and is directly controlled by CDX2 in normal intestine and tumours.
  • [MeSH-major] Colorectal Neoplasms / chemistry. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Insulin Receptor Substrate Proteins / genetics. Intestinal Mucosa / chemistry. Multiple Endocrine Neoplasia / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Line, Tumor. Colon. HT29 Cells. Humans. Ileum. Immunohistochemistry. Insulin-Like Growth Factor I / metabolism. Male. Mice. Promoter Regions, Genetic. Protein Binding. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Gut. 2009 Sep;58(9):1179-80 [19671549.001]
  • (PMID = 19221108.001).
  • [ISSN] 1468-3288
  • [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
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / IRS2 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / RNA, Messenger; 67763-96-6 / Insulin-Like Growth Factor I
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66. Salahshor S, Goncalves J, Chetty R, Gallinger S, Woodgett JR: Differential gene expression profile reveals deregulation of pregnancy specific beta1 glycoprotein 9 early during colorectal carcinogenesis. BMC Cancer; 2005;5:66
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: APC (Adenomatous polyposis coli) plays an important role in the pathogenesis of both familial and sporadic colorectal cancer.
  • Patients carrying germline APC mutations develop multiple colonic adenomas at younger age and higher frequency than non-carrier cases which indicates that silencing of one APC allele may be sufficient to initiate the transformation process.
  • METHODS: To elucidate the biological dysregulation underlying adenoma formation we examined global gene expression profiles of adenomas and corresponding normal mucosa from an FAP patient.
  • Further analysis of sporadic and familial colorectal cancer confirmed that PSG9 is ectopically upregulated in vivo by cancer cells.
  • In total, deregulation of PSG9 mRNA was detected in 78% (14/18) of FAP adenomas and 75% (45/60) of sporadic colorectal cancer cases tested.
  • CONCLUSION: Detection of PSG9 expression in adenomas, and at higher levels in FAP cases, indicates that germline APC mutations and defects in Wnt signalling modulate PSG9 expression.
  • Since PSG9 is not found in the non-pregnant adult except in association with cancer, and it appears to be an early molecular event associated with colorectal cancer monitoring of its expression may be useful as a biomarker for the early detection of this disease.
  • [MeSH-major] Biomarkers, Tumor. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Genes, APC. Mutation. Pregnancy-Specific beta 1-Glycoproteins / biosynthesis
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Alleles. Blotting, Northern. Blotting, Western. Carcinoembryonic Antigen / metabolism. Cell Line, Tumor. Down-Regulation. Gene Expression Profiling. Gene Silencing. Genes, Reporter. Humans. Immunohistochemistry. In Situ Hybridization. Models, Genetic. Mucous Membrane / pathology. Oligonucleotide Array Sequence Analysis. Placenta / metabolism. Protein Isoforms. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Trophoblasts / metabolism. Up-Regulation. Wnt Proteins / metabolism

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  • (PMID = 15982419.001).
  • [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 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen; 0 / Pregnancy-Specific beta 1-Glycoproteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC1184062
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67. Whitfield JF: Calcium, calcium-sensing receptor and colon cancer. Cancer Lett; 2009 Mar 8;275(1):9-16
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calcium, calcium-sensing receptor and colon cancer.
  • There is much evidence that dietary Ca(2+) loading reduces colon cell proliferation and carcinogenesis in humans and rodents, but during carcinogenesis it becomes ineffective or even tumor-promoting.
  • We are beginning to see how Ca(2+) balances the continuous massive cell production in colon crypts by driving the terminal differentiation and eventually the apoptosis of the cells mainly on the mucosal surface, and how this Ca(2+) control is lost during colon carcinogenesis.
  • The rapid proliferation of the transit-amplifying (TA) progeny of the colon stem cells is driven by the so-called "Wnt" signaling mechanism, which involves the stimulation of proliferogenic genes such as those for c-Myc and cyclin D1 and the silencing of the gene for the cell cycle-stopping p21(Cip1/WAF1) protein by nuclear beta-catenin*Tcf-4 complexes.
  • TA cells avoid mitotic damage and premature apoptosis by expressing the protein survivin.
  • It appears that TA cell cycling stops and terminal differentiation starts when the cells reach a higher level in the crypt where there is enough lumenal Ca(2+) to stimulate the expression and activation of CaSRs (Ca(2+)-sensing receptors), the signals from which stimulate the expression of E-cadherin.
  • Along with this, the APC (adenomatous polyposis coli) protein appears and some of it enters the nucleus.
  • There it makes the TA cells susceptible to the eventual apoptotic balancing by stopping survivin expression and the beta-catenin*Tcf-4 complex from driving further cell cycling by releasing beta-catenin from the nucleus, and delivering it to cytoplasmic APC*axin*GSK-3beta complexes for ultimate proteasomal destruction.
  • Cytoplasmic beta-catenin is then prevented from returning to the nucleus by either being intercepted and destroyed by APC*axin*GSK-3beta complexes or locked by the emerging E-cadherin into membrane adherens junctions which tie the cell into the sheet of proliferatively shut-down cells with APC-dependent cytoskeletons moving to the mouth of the crypt and onto the flat mucosal surface.
  • A common first step in sporadic colon carcinogenesis is the loss of functional APC which disorients upwardly directed migration and causes the retention of nuclear beta-catenin and proliferogenic beta-catenin*Tcf-4 complexes as well as genomic instability.
  • [MeSH-minor] Animals. Apoptosis. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Nucleus / metabolism. Cell Proliferation. Cyclin D1 / metabolism. Cytoplasm / metabolism. DNA-Binding Proteins / metabolism. Glycogen Synthase Kinase 3 / metabolism. Humans. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Transcription Factors / metabolism. beta Catenin / metabolism

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  • (PMID = 18725175.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / DNA-Binding Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, Calcium-Sensing; 0 / TCF4 protein, human; 0 / Transcription Factors; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; SY7Q814VUP / Calcium
  • [Number-of-references] 80
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68. Chen J, Röcken C, Lofton-Day C, Schulz HU, Müller O, Kutzner N, Malfertheiner P, Ebert MP: Molecular analysis of APC promoter methylation and protein expression in colorectal cancer metastasis. Carcinogenesis; 2005 Jan;26(1):37-43
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular analysis of APC promoter methylation and protein expression in colorectal cancer metastasis.
  • APC (adenomatous polyposis coli) promoter methylation has been linked to the early development of colorectal cancers.
  • However, the role of APC methylation and its effect on protein expression in colon cancer metastasis is largely unknown.
  • In this study, we investigated APC promoter methylation by Methylight analysis and analysed the APC protein levels by immunohistochemistry and western blot analysis in 24 liver metastasis and 39 primary colorectal cancers.
  • Promoter methylation of the APC gene was found to be a frequent event in liver metastasis (10/24) and significantly more frequent compared with primary colorectal cancer (7/39, P = 0.047).
  • APC methylation was not found in 14 matched normal colon tissues.
  • APC protein was detected in the cytoplasm of primary and metastatic cancer cells and non-tumorous colon epithelium.
  • By western blot analysis, APC protein levels were found to be decreased in primary tumour tissues compared with the normal colon mucosa.
  • In contrast, APC protein levels were not decreased in the cancer cells that had metastasized to the liver.
  • APC protein levels were independent of the presence of APC promoter methylation or gene mutations.
  • In summary, APC promoter methylation is a frequent epigenetic alteration in colorectal cancer metastasis.
  • However, we observed no significant association between APC promoter methylation or gene mutation and APC protein expression in colorectal metastasis.
  • Therefore, metastatic cancer cells seem to harbour a heterogenous genetic and epigenetic background, in which cancer cells may exhibit APC promoter methylation that is independent of APC expression.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. DNA Methylation. Genes, APC / physiology. Neoplasm Metastasis / genetics

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  • (PMID = 15375009.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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69. Song YH, Zhang CJ: [Effect of Hydralazine on demethylation status and expression of APC gene, proliferation and apoptosis of human cervical cancer cell lines]. Zhonghua Bing Li Xue Za Zhi; 2007 Sep;36(9):614-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of Hydralazine on demethylation status and expression of APC gene, proliferation and apoptosis of human cervical cancer cell lines].
  • OBJECTIVE: To investigate the correlation between methylation status and gene expression of APC (adenomatous polyposis coli) gene in HeLa, CaSki and SiHa cell lines of cervical carcinoma, and explore the effect of hydralazine on the transcription regulation of the 5'CpG island demethylation of APC gene and the proliferation and apoptosis of the cell lines.
  • METHODS: Methylation status and the expression of APC gene were analyzed using methylated specific PCR, RT-PCR and FQ-PCR methods.
  • The expression of beta-catenin protein which correlates closely with APC was detected by SP method after treatment with Hydralazine.
  • (1) APC gene was methylated or hemimethylated respectively in HeLa and CaSki cell lines, at the same time, APC gene was not methylated in SiHa cell. (2) After having been treated by 40 micromol/L Hydralazine for 72 hours, growth inhibitory ratios of HeLa, CaSki and SiHa cell lines were (52.12 +/- 3.78)%, (44.31 +/- 2.59)% and (47.73 +/- 4.73)% respectively, on the contrary, normal cell HECV's growth inhibitory ratio was only (27.18 +/- 0.79)%.
  • APC gene in HeLa and CaSki cell lines which were treated by 40 micromol/L Hydralazine for 72 hours was demethylated and expressed positively, the expression of APC mRNA in HeLa, CaSki and SiHa cell lines increased to 10.35, 11.40 and 0.73 times respectively. (3) Hydralazine, when used at the concentration of 40 micromol/L for 72 hours, induced S phase and G2/M phase arrest and apoptosis in HeLa and CaSki cells. beta-catenin protein can be expressed in cell membrane after treatment with Hydralazine.
  • CONCLUSION: APC gene methylation plays an important role in the carcinogenesis of cervical cells and can re-express after the treatment with Hydralazine which also could inhibit the growth of the cervical cancer cells.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Apoptosis / drug effects. Cell Proliferation / drug effects. Genes, APC. Hydralazine / pharmacology. Uterine Cervical Neoplasms

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  • (PMID = 18070451.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / beta Catenin; 26NAK24LS8 / Hydralazine
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70. Scheel SK, Porzner M, Pfeiffer S, Ormanns S, Kirchner T, Jung A: Mutations in the WTX-gene are found in some high-grade microsatellite instable (MSI-H) colorectal cancers. BMC Cancer; 2010;10:413
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  • Whereas in CIN CRCs APC (Adenomatous Polyposis Coli) is affected in most cases, high grade MSI (MSI-H) CRCs frequently display mutations in various genes, like the APC-, AXIN2- or CTNNBI (beta-CATENIN) gene itself.
  • METHODS: DNA was extracted from 632 formalin-fixed, paraffin-embedded metastatic CRCs (UICCIV) and analyzed for MSI-H by investigating the stability of the highly sensitive microsatellite markers BAT25 and BAT26 applying fluorescence capillary electrophoresis (FCE).
  • Then, in the MSI-H cases, well described mutational hot spot regions from the APC-, AXIN2- and CTNNBI genes were analyzed for genomic alterations by didesoxy-sequencing while the WTX T6-microsatellite was analyzed by fragment analysis.
  • Furthermore, the KRAS and the BRAF proto-oncogenes were analyzed for the most common activating mutations applying pyro-sequencing. mRNA expression of WTX from MSI-H and MSS cases and a panel of colorectal cancer cell lines was investigated using reverse transcription (RT-) PCR and FCE.
  • Only one case, a male patient, expressed the mutated WTX gene while being wild type for all other investigated genes.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / secondary. Frameshift Mutation / genetics. Gene Expression Regulation, Neoplastic. Microsatellite Instability. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adult. Aged. DNA, Neoplasm / genetics. Female. Genes, APC. Genotype. Humans. Male. Microsatellite Repeats. Middle Aged. Polymerase Chain Reaction. Prognosis. Proto-Oncogene Proteins B-raf / genetics. beta Catenin / genetics

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  • (PMID = 20696052.001).
  • [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 / AMER1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / DNA, Neoplasm; 0 / Tumor Suppressor Proteins; 0 / beta Catenin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  • [Other-IDs] NLM/ PMC2928794
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71. Voutsadakis IA: Pathogenesis of colorectal carcinoma and therapeutic implications: the roles of the ubiquitin-proteasome system and Cox-2. J Cell Mol Med; 2007 Mar-Apr;11(2):252-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pathways of the molecular pathogenesis of colorectal carcinoma have been extensively studied and molecular lesions during the development of the disease have been revealed.
  • High up in the list of colorectal cancer lesions are APC (adenomatous polyposis coli), K-ras, Smad4 (or DPC4-deleted in pancreatic cancer 4) and p53 genes.
  • The ubiquitin-proteasome system (UPS) is comprised of a multi-unit cellular protease system that regulates several dozens of cell proteins after their ligation with the protein ubiquitin.
  • Given that among these proteins are regulators of the cell cycle, apoptosis, angiogenesis, adhesion and cell signalling, this system plays a significant role in cell fate and carcinogenesis.
  • UPS inhibition has been found to be a pre-requisite for apoptosis and is already clinically exploited with the proteasome inhibitor bortezomib in multiple myeloma.
  • Inhibition of Cox-2 by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce colon polyp formation in genetically predisposed populations and in the general population.

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  • (PMID = 17488476.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Ubiquitin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 298
  • [Other-IDs] NLM/ PMC3822826
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72. Valanzano R, Ficari F, Curia MC, Aceto G, Veschi S, Cama A, Battista P, Tonelli F: Balance between endoscopic and genetic information in the choice of ileorectal anastomosis for familial adenomatous polyposis. J Surg Oncol; 2007 Jan 1;95(1):28-33
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  • [Title] Balance between endoscopic and genetic information in the choice of ileorectal anastomosis for familial adenomatous polyposis.
  • BACKGROUND AND OBJECTIVES: The number of rectal polyps and the site of mutations in the APC (Adenomatous polyposis coli) gene have been used to guide the surgical management in patients with familial adenomatous polyposis (FAP).
  • The aim of this study is to assess the utility of the APC mutation screening compared to the degree of the rectal polyposis in surgical decision making.
  • APC gene was screened for mutations by heteroduplex analysis, single strand conformation polymorphism, in vitro synthesized protein (IVSP), and DNA sequencing.
  • Patients negative for APC mutations were tested for MYH mutations.
  • RESULTS: On the basis of preoperative polyp rectal count we categorized patients as follows: Group I, 5 or fewer adenomas; Group II, 6-9 adenomas; Group III, 10 or more adenomas.
  • Carpeting polyposis of the rectal stump developed in three patients with APC mutation at codon 1309 and two of them needed later proctectomy.
  • Diffuse rectal polyposis was observed in one patient with mutation at exon 9 who had 10 small polyps at time of surgery.
  • Mutation at the 5'-end of APC (codons 144-232), mutation of MYH and unknown APC or MYH mutation were correlated with a low number of polyps both at presentation and follow-up.
  • Identification of specific germ-line APC or MYH mutation can address the choice of surgical treatment.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / surgery. Genes, APC. Germ-Line Mutation. Proctoscopy

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  • (PMID = 17192888.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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73. Al-Sukhni E, Ridgway PF, O'Connor B, McLeod RS, Swallow CJ: Extent of resection for curable colorectal cancer in young patients: A 27-year experience at a tertiary care centre. J Clin Oncol; 2009 May 20;27(15_suppl):e15059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Some familial GI cancer experts have recommended that younger patients with curable CRC undergo definitive subtotal colectomy at initial presentation.
  • Type of resection was classified as complete (total/subtotal colectomy, proctocolectomy) or segmental.
  • The young patients had significantly higher rates of identifiable risk factors for CRC (IBD, FAP/HNPCC, family history of cancer) and were significantly more likely to undergo complete resection (23.38% vs 6.01%, OR 4.78).
  • Factors contributing to complete resection were site of disease (colon), IBD, and family history of CRC (Table).
  • Four patients (2.6%) who underwent segmental resection developed metachronous disease at a median of 66.38 months post resection.
  • Factors predictive of a complete resection included IBD, family history of CRC, and colonic primary site.
  • Overall survival was not influenced by extent of resection.

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  • (PMID = 27964525.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Kinoshita T, Uesaka K, Shimizu Y, Sakamoto H, Kimura W, Sunada S, Sunada S, Imaizumi T, Ozawa I, Okamoto A, Oda T: Effects of adjuvant intra-operative radiation therapy after curative resection in pancreatic cancer patients : Results of a randomized study by 11 institutions in Japan. J Clin Oncol; 2009 May 20;27(15_suppl):4622

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  • [Title] Effects of adjuvant intra-operative radiation therapy after curative resection in pancreatic cancer patients : Results of a randomized study by 11 institutions in Japan.
  • : 4622 Background: To evaluate the benefits of adjuvant intra-operative radiation therapy after curative resection in advanced pancreatic cancer (APC) patients, a multi-center phase III trial was conducted by 11 participating institutions in Japan.
  • METHODS: Eligibility included pts with potentially resectable APC (duct cell origin) by image diagnosis.
  • Patients were randomized in a 1:1 ratio to adjuvant IORT or surgery alone less than a week before surgery.
  • The radiation field included the tumor bed and in most cases included the celiac axis, superior mesenteric artery, and the portal vein.

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  • (PMID = 27964217.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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75. Jaiswal AS, Balusu R, Narayan S: Involvement of adenomatous polyposis coli in colorectal tumorigenesis. Front Biosci; 2005;10:1118-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Involvement of adenomatous polyposis coli in colorectal tumorigenesis.
  • Mutation in the adenomatous polyposis coli (APC) gene is considered to be one of the earliest events in the colon cancer development.
  • The familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC) are the most commonly inherited colorectal cancers.
  • FAP and HNPCC develop due to mutations in APC and DNA mismatch repair (MMR) genes, respectively.
  • APC is known to regulate the levels of beta-catenin, an important mediator of cell-cell adhesion and transcriptional regulator.
  • Mutations in APC gene are also linked with chromosomal instability in colon cancer cells.
  • The role of APC is also implicated in cell migration, cell-cell adhesion, cell cycle control, and apoptosis.
  • This article summarizes the structure-function studies and the role of APC mutations in colon cancer development.
  • [MeSH-major] Adenomatous Polyposis Coli / physiopathology. Adenomatous Polyposis Coli Protein / physiology. Colorectal Neoplasms / etiology

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  • (PMID = 15769611.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-097031; United States / NCI NIH HHS / CA / CA-100247
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / beta Catenin
  • [Number-of-references] 174
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76. De Rosa M, Galatola M, Borriello S, Duraturo F, Masone S, Izzo P: Implication of adenomatous polyposis coli and MUTYH mutations in familial colorectal polyposis. Dis Colon Rectum; 2009 Feb;52(2):268-74
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  • [Title] Implication of adenomatous polyposis coli and MUTYH mutations in familial colorectal polyposis.
  • PURPOSE: Familial adenomatous polyposis is an autosomal dominantly inherited syndrome characterized by hundreds or thousands of colorectal polyps and a high risk of colorectal cancer at a young age.
  • Truncating germline mutations in the adenomatous polyposis coli gene are detected in approximately 80 percent of patients with classical familial adenomatous polyposis and in approximately 10 percent of the attenuated familial adenomatous polyposis patients.
  • METHODS: We investigated the adenomatous polyposis coli and MUTYH genes mutations in a well-characterized series of 25 unrelated Italian patients with familial adenomatous polyposis.
  • RESULTS: We characterized the specific adenomatous polyposis coli gene mutation in 10 probands, and identified eight truncating mutations (4 novel and 4 known mutations) and two splicing mutations.
  • Moreover, 11 MUTYH gene mutations have been identified in 7 patients without a dominant family history of polyposis.
  • CONCLUSIONS: This study enlarges the genotype-phenotype correlations of familial adenomatous polyposis and suggests that messenger alterations could be responsible for a subset of familial adenomatous polyposis cases without germ-line adenomatous polyposis coli or MUTYH gene mutations.
  • It also confirms that genotype-phenotype correlations in MUTYH-associated polyposis are very complex.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. DNA Glycosylases / genetics. Mutation
  • [MeSH-minor] Adolescent. Genes, APC. Genotype. Humans. Male. Middle Aged. Sequence Analysis, DNA

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  • (PMID = 19279422.001).
  • [ISSN] 1530-0358
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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77. Kumamoto H, Ooya K: Immunohistochemical detection of beta-catenin and adenomatous polyposis coli in ameloblastomas. J Oral Pathol Med; 2005 Aug;34(7):401-6
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  • [Title] Immunohistochemical detection of beta-catenin and adenomatous polyposis coli in ameloblastomas.
  • BACKGROUND: To clarify the roles of the Wnt signaling pathway in oncogenesis and cytodifferentiation of odontogenic tumors, expression of beta-catenin and adenomatous polyposis coli (APC) was analyzed in ameloblastomas as well as in tooth germs.
  • METHODS: Tissue specimens of 10 tooth germs, 40 benign ameloblastomas, and five malignant ameloblastomas were examined immunohistochemically with the use of antibodies against beta-catenin and APC.
  • Nuclear beta-catenin expression was recognized in nine of 40 ameloblastomas and two of five malignant ameloblastomas, but not in tooth germs.
  • APC was evidently expressed in odontogenic epithelial cells neighboring the basement membrane in tooth germs and ameloblastomas, and the reactivity was significantly lower in benign and malignant ameloblastomas than in tooth germs.
  • Follicular ameloblastomas and acanthomatous ameloblastomas tended to show high nuclear beta-catenin expression and low APC reactivity, as compared with other ameloblastoma variants.
  • CONCLUSION: Expression of beta-catenin and APC in tooth germs and ameloblastomas suggests that aberration of the Wnt signaling pathway might play a role in oncogenesis and cytodifferentiation of odontogenic epithelium via deregulation of cell proliferation.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / analysis. Ameloblastoma / chemistry. Cytoskeletal Proteins / analysis. Jaw Neoplasms / chemistry. Trans-Activators / analysis

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  • (PMID = 16011608.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin
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78. Kouzmenko AP, Takeyama K, Kawasaki Y, Akiyama T, Kato S: Truncation mutations abolish chromatin-associated activities of adenomatous polyposis coli. Oncogene; 2008 Aug 21;27(36):4888-99
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  • [Title] Truncation mutations abolish chromatin-associated activities of adenomatous polyposis coli.
  • The adenomatous polyposis coli (APC) is a tumor suppressor whose loss of function leads to colon cancer.
  • APC shuttles between the nucleus and cytoplasm, however its role in the nucleus remains elusive.
  • We have found that nuclear APC specifically associates with transcriptionally active chromatin through structural elements located downstream to the region of frequent truncation mutations found in colorectal tumors.
  • We show that a recombinant APC fragment comprising such elements associates in vivo with euchromatin and preferentially binds in vitro to acetylated histone H3.
  • Induction of DNA double-strand breaks (DSB) stimulates accumulation of APC at the damaged DNA chromatin marked by histone H2AX and S139-phosphorylated histone H2AX.
  • A nuclear complex containing the DNA-dependent protein kinase catalytic subunit (DNAPKcs) and APC associates with chromatin in response to DNA DSB.
  • APC knockdown with siRNA decreased the rate of DNA DSB-induced S139 histone H2AX phosphorylation in cells expressing endogenous full-length APC, but not in colon cancer cells with its truncation mutants, whereas ectopic APC expression stimulated the H2AX phosphorylation regardless of the type of endogenous APC.
  • Our data suggest that APC involves in the DSB DNA repair and that truncation mutations impair chromatin-associated functions of APC.
  • [MeSH-major] Adenomatous Polyposis Coli / physiopathology. Chromatin / metabolism. Mutation
  • [MeSH-minor] Binding Sites. Cell Line. DNA Damage. DNA Repair. Genes, APC. Histone Acetyltransferases / metabolism. Humans. Transcriptional Activation

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  • (PMID = 18454178.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromatin; EC 2.3.1.48 / Histone Acetyltransferases
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79. Hanson CA, Miller JR: Non-traditional roles for the Adenomatous Polyposis Coli (APC) tumor suppressor protein. Gene; 2005 Nov 21;361:1-12
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  • [Title] Non-traditional roles for the Adenomatous Polyposis Coli (APC) tumor suppressor protein.
  • The Adenomatous Polyposis Coli (APC) tumor suppressor is a multifunctional protein that is mutated in a majority of colon cancers.
  • The role of APC as an antagonist of the Wnt signaling pathway is well known and it is widely accepted that inappropriate activation of this pathway through loss of APC function contributes to the progression of colon cancers.
  • However, a body of evidence is growing to support the idea that APC plays non-traditional functions outside of the Wnt pathway with roles in cell migration, adhesion, chromosome segregation, spindle assembly, apoptosis, and neuronal differentiation.
  • This review highlights the research into alternate functions for APC beyond its role in Wnt signaling and discusses the possible contributions for these non-traditional functions of APC in tumor formation.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / physiology
  • [MeSH-minor] Animals. Apoptosis / physiology. Cell Adhesion / physiology. Cell Cycle / physiology. Cell Movement / physiology. Humans. Microtubules / metabolism. Protein Binding. Spindle Apparatus / physiology. beta Catenin / metabolism

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  • (PMID = 16185824.001).
  • [ISSN] 0378-1119
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / beta Catenin
  • [Number-of-references] 106
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80. Nielsen M, Weiss MM, Vasen HF, Hes FJ: [From gene to disease; MutYH-associated polyposis coli (MAP)]. Ned Tijdschr Geneeskd; 2005 Dec 31;149(53):2970-2
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  • [Title] [From gene to disease; MutYH-associated polyposis coli (MAP)].
  • [Transliterated title] Van gen naar ziekte; MutYH-geassocieerde polyposis coli (MAP).
  • MutYH-associated polyposis coli (MAP) is an autosomal recessive inherited form of polyposis and colorectal carcinoma associated with germline mutations in the MutYH gene on chromosome I.
  • The MutYH protein is a base excision repair glycosylase which is involved in the repair of damage caused by the oxidation ofa guanine leading to 8-oxo-7,8-dihydroguanine.
  • If the MutYH protein is dysfunctional, G:C --> T:A mutations in the APC-gene give rise to polyposis and in 50-60% of cases also colorectal carcinoma.
  • MutYH polyposis differs from familial adenomatous polyposis coli in its mode of transmission, later age of onset, a less florid form of polyposis, and fewer extra colonic manifestations.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Chromosomes, Human, Pair 1. Colorectal Neoplasms / genetics. DNA Glycosylases / genetics. Germ-Line Mutation

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  • (PMID = 16425850.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
  • [Number-of-references] 14
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81. Brocardo M, Henderson BR: Detection of cytoplasmic and nuclear localization of adenomatous polyposis coli (APC) protein in cells. Methods Mol Biol; 2008;468:77-89
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  • [Title] Detection of cytoplasmic and nuclear localization of adenomatous polyposis coli (APC) protein in cells.
  • The adenomatous polyposis coli (APC) tumour suppressor gene is mutated in the majority of colon cancers.
  • APC is a multi-domain protein whose distribution at different subcellular locations correlates with unique cellular processes.
  • Our laboratory has focused on the link between APC subcellular location and function, and has characterized pathways for the trafficking of APC both into and out of the nucleus.
  • Antibody specificity is an important factor in the determination of APC localization, and in this chapter we outline a strategy for the unambiguous detection of APC using a combination of biochemical and cell biology approaches.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Cell Nucleus / metabolism. Cytoplasm / metabolism. Subcellular Fractions / metabolism

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  • (PMID = 19099247.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [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
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82. Faux MC, Coates JL, Catimel B, Cody S, Clayton AH, Layton MJ, Burgess AW: Recruitment of adenomatous polyposis coli and beta-catenin to axin-puncta. Oncogene; 2008 Oct 2;27(44):5808-20
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  • [Title] Recruitment of adenomatous polyposis coli and beta-catenin to axin-puncta.
  • The adenomatous polyposis coli (APC) tumour suppressor is a multifunctional protein involved in the regulation of Wnt signalling and cytoskeletal dynamics.
  • Little is known about how APC controls these disparate functions.
  • In this study, we have used APC- and axin-fluorescent fusion proteins to examine the interactions between these proteins and show that the functionally distinct populations of APC are also spatially separate.
  • Axin-RFP recruits beta-catenin destruction complex proteins, including APC, beta-catenin, glycogen synthase kinase-3-beta (GSK3-beta) and casein kinase-1-alpha (CK1-alpha).
  • Recruitment into axin-RFP puncta sequesters APC from clusters at cell extensions and this prevents its microtubule-associated functions.
  • The interaction between APC-GFP and axin-RFP within the cytoplasmic puncta is direct and dramatically alters the dynamic properties of APC-GFP.
  • However, recruitment of APC to axin puncta is not absolutely required for beta-catenin degradation.
  • An axinDeltaDIX mutant did not form puncta, but still mediated recruitment of destruction complex proteins and phosphorylation of beta-catenin.
  • We conclude that there are distinct pools of APC and that the formation of axin puncta, rather than the axin/APC complex, is essential for beta-catenin destruction.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Repressor Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Animals. Axin Protein. Cell Line. Cytoplasm / metabolism. Cytoplasm / ultrastructure. Dogs. Fluorescence Resonance Energy Transfer. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Mice. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism

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  • (PMID = 18591934.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Axin Protein; 0 / Recombinant Fusion Proteins; 0 / Repressor Proteins; 0 / beta Catenin; 147336-22-9 / Green Fluorescent Proteins
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83. Wang TT, Chen SQ, Zhang XM: [Germline mutation of adenomatous polyposis coli gene in Chinese patients with familial adenomatous polyposis]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Apr;25(2):199-202
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Germline mutation of adenomatous polyposis coli gene in Chinese patients with familial adenomatous polyposis].
  • OBJECTIVE: To explore the characteristics of adenomatous polyposis coli (APC) gene germline mutations in Chinese patients with familial adenomatous polyposis (FAP).
  • METHODS: Eighteen members from nine FAP pedigrees were studied by using multiplex ligation-dependent probe amplification(MLPA) to detect large fragment deletion of APC gene.
  • Then, PCR were performed to amplify all exons of APC gene for mutation screening by denaturing high performance liquid chromatography (DHPLC).
  • They were c.3184_3187 del CAAA in pedigree 2, c.5432C to T in pedigree 4 and c.3925_3929 del AAAAG in pedigree 9 respectively.
  • CONCLUSION: APC gene germline mutations can cause the development of FAP.
  • The FAP patients without APC gene germline mutations could be caused by other mechanisms.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC / physiology
  • [MeSH-minor] Adult. Chromatography, High Pressure Liquid. Female. Genetic Predisposition to Disease / genetics. Germ-Line Mutation. Humans. Male. Middle Aged. Pedigree

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  • (PMID = 18393246.001).
  • [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
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84. Kohler EM, Derungs A, Daum G, Behrens J, Schneikert J: Functional definition of the mutation cluster region of adenomatous polyposis coli in colorectal tumours. Hum Mol Genet; 2008 Jul 1;17(13):1978-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional definition of the mutation cluster region of adenomatous polyposis coli in colorectal tumours.
  • The mutation cluster region (MCR) of adenomatous polyposis coli (APC) is located within the central part of the open reading frame, overlapping with the region encoding the 20 amino acid repeats (20R) that are beta-catenin-binding sites.
  • Each mutation in the MCR leads to the synthesis of a truncated APC product expressed in a colorectal tumour.
  • The MCR extends from the 3' border of the first 20R coding region to approximately the middle of the third 20R coding region, reflecting both positive and negative selections of the N- and C-terminal halves of the APC protein in colon cancer cells, respectively.
  • In contrast, the second 20R escapes selection and can be either included or excluded from the truncated APC products found in colon cancer cells.
  • To specify the functional outcome of the selection of the mutations, we investigated the beta-catenin binding capacity of the first three 20R in N-terminal APC fragments.
  • Similarly, we also show that the tumour-associated truncations abolish the interaction of beta-catenin with the third 20R.
  • Thus, our data provide a functional definition of the MCR: the APC fragments typical of colon cancer are selected for the presence of a single functional 20R, the first one, and are therefore equivalent relative to beta-catenin binding.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / chemistry. Adenomatous Polyposis Coli Protein / metabolism. Colonic Neoplasms / genetics. Sequence Deletion. beta Catenin / metabolism
  • [MeSH-minor] Amino Acid Sequence. Bacterial Proteins / genetics. Bacterial Proteins / metabolism. Cell Line, Tumor. Humans. Luminescent Proteins / genetics. Luminescent Proteins / metabolism. Multigene Family. Protein Binding. Recombinant Fusion Proteins / chemistry. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Repetitive Sequences, Amino Acid

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  • (PMID = 18387968.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Bacterial Proteins; 0 / Luminescent Proteins; 0 / Recombinant Fusion Proteins; 0 / beta Catenin; 0 / yellow fluorescent protein, Bacteria
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85. Yang Y, Takeuchi S, Tsukasaki K, Yamada Y, Hata T, Mori N, Fukushima A, Seo H, Koeffler HP, Taguchi H: Methylation analysis of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma. Leuk Res; 2005 Jan;29(1):47-51
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  • [Title] Methylation analysis of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma.
  • We investigated methylation status of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma (ATL).
  • APC methylation was found in 15 of 31 (48%) primary samples, and 2 of 4 (50%) ATL cell lines.
  • Methylation of the APC gene occurred more frequently in acute ATL (12/21) (57%) than chronic ATL (1/8) (13%) (P = 0.03).
  • APC was not expressed in the APC-methylated ATL cell line ST1.
  • Demethylation with 5-azacytidine treatment restored APC expression in the ST1 cell line.
  • Our data show that hypermethylation of the APC gene is involved in the pathogenesis of ATL.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. DNA Methylation. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Azacitidine / pharmacology. Cell Line, Tumor. CpG Islands / genetics. Disease Progression. Humans. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Leuk Res. 2005 May;29(5):475-6 [15755498.001]
  • (PMID = 15541474.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; M801H13NRU / Azacitidine
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86. Wachsmannova-Matelova L, Stevurkova V, Adamcikova Z, Holec V, Zajac V: Polymorphisms in the adenomatous polyposis coli gene in Slovak families suspected of FAP. Neuro Endocrinol Lett; 2009;30 Suppl 1:25-8
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  • [Title] Polymorphisms in the adenomatous polyposis coli gene in Slovak families suspected of FAP.
  • OBJECTIVES: Polymorphism in the adenomatous polyposis coli (APC) gene was analyzed in 33 families suspected of familial adenomatous polyposis (FAP) without identified APC gene mutation.
  • Screening of 104 members of mentioned families for polymorphism in the APC gene, was performed using single strand conformation polymorphism (SSCP) and DNA sequencing.
  • CONCLUSION: The most frequently detected polymorphism D1822V is potentially associated with the risk of colorectal cancer.
  • Three detected polymorphisms - Y486Y, T1493T and S1756S - also seem to be associated with colon cancer risk.
  • All these polymorphisms may be used as markers for diagnosis of colorectal cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Polymorphism, Genetic
  • [MeSH-minor] Cohort Studies. Exons. Family. Genetic Predisposition to Disease. Humans. Mutation. Polymorphism, Single-Stranded Conformational. Sequence Analysis, DNA. Slovakia

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  • (PMID = 20027139.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
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87. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • METHODS AND RESULTS: In a series of 99 clinically sporadic colorectal carcinomas, APC exon 15 mutations, loss of heterozygosity (LOH) and promoter methylation were found in 49, 20 and 23 cases, respectively.
  • Singly, these APC aberrations were not associated with the degree of tumour cell dissociation, but dissociation was higher for the cases with combined APC mutation and LOH.
  • Immunohistochemical beta-catenin translocation to the nucleus correlated with APC aberrations.
  • Tumour growth pattern (expansive/infiltrative/diffuse) and tumour stroma (desmoplastic common-type versus keloid-like) showed a statistically significant association with tumour cell dissociation and with beta-catenin translocation.
  • Of other molecular alterations tested (p53 mutation; LOH at 17p13, 18q, 9p21; CpG island methylator phenotype), only the highly microsatellite unstable status (n = 11) was negatively associated.
  • CONCLUSIONS: In colorectal carcinomas, wnt dysregulation relates to APC aberrations, but wnt dysregulation and APC aberrations are not strictly required for tumour cell dissociation, and additional and/or alternative factors must play a role.
  • [MeSH-major] Adenocarcinoma, Mucinous / genetics. Colorectal Neoplasms / genetics. Genes, APC. Loss of Heterozygosity / genetics. Mutation
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cadherins / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Female. Humans. Male. Microsatellite Instability. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Phenotype. Translocation, Genetic. Wnt Proteins / genetics. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 17257127.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Wnt Proteins; 0 / beta Catenin
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88. Kato N, Shibuya H, Fukase M, Tamura G, Motoyama T: Involvement of adenomatous polyposis coli (APC) gene in testicular yolk sac tumor of infants. Hum Pathol; 2006 Jan;37(1):48-53
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  • [Title] Involvement of adenomatous polyposis coli (APC) gene in testicular yolk sac tumor of infants.
  • On the other hand, recent epigenetic studies suggest the involvement of some tumor suppressor genes, including the adenomatous polyposis coli (APC) gene.
  • In the present study, we examined 10 infantile pure YSTs for mutation, allelic loss, promoter methylation, and protein expression status of the APC gene to evaluate whether the APC gene plays a significant role in the pathogenesis of infantile YSTs.
  • Loss of heterozygosity at 5q21, where the APC gene is localized, was detected in at least 3 (30%) of the 9 YSTs examined.
  • Immunohistochemically, 8 infantile YSTs did not express the APC protein, whereas 2 YSTs without showing APC methylation, as well as germ cells of normal infantile testes, expressed this protein in the cytoplasm.
  • These data indicate that inactivation of the APC gene, by allelic loss and/or promoter methylation, is related to the occurrence of infantile YSTs.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Endodermal Sinus Tumor / genetics. Genes, APC. Loss of Heterozygosity. Testicular Neoplasms / genetics

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  • (PMID = 16360415.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. 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
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89. Aceto G, Curia MC, Veschi S, De Lellis L, Mammarella S, Catalano T, Stuppia L, Palka G, Valanzano R, Tonelli F, Casale V, Stigliano V, Cetta F, Battista P, Mariani-Costantini R, Cama A: Mutations of APC and MYH in unrelated Italian patients with adenomatous polyposis coli. Hum Mutat; 2005 Oct;26(4):394
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  • [Title] Mutations of APC and MYH in unrelated Italian patients with adenomatous polyposis coli.
  • The analysis of APC and MYH mutations in adenomatous polyposis coli patients should provide clues about the genetic heterogeneity of the syndrome in human populations.
  • The entire coding region and intron-exon borders of the APC and MYH genes were analyzed in 60 unrelated Italian adenomatous polyposis coli patients.
  • APC analysis revealed 26 point mutations leading to premature termination, one missense variant and one deletion spanning the entire coding region in 32 unrelated patients.
  • Novel truncating point mutations included c.1176_1177insT (p.His393_PhefsX396), c.1354_1355del (p.Val452_SerfsX458), c.2684C>A (p.Ser895X), c.2711_2712del (p.Arg904_LysfsX910), c.2758_2759del (p.Asp920_CysfsX922), c.4192_4193del (p.Ser1398_SerfsX1407), c.4717G>T (p.Glu1573X) and a novel cryptic APC exon 6 splice site.
  • MYH analysis revealed nine different germline variants in nine patients, of whom five were homozygotes or compound heterozygotes.
  • The mutations included 4 novel MYH missense variants (c.692G>A, p.Arg231His; c.778C>T, p.Arg260Trp; c.1121T>C, p.Leu374Pro; and c.1234C>T, p.Arg412Cys) affecting conserved amino acid residues in the ENDO3c or NUDIX domains of the protein and one novel synonymous change (c.672C>T, p.Asn224Asn).
  • Genotype-phenotype correlations were found in carriers of APC mutations but not in carriers of biallelic MYH mutations, except for a negative correlation with low number of polyps.
  • A distinctive characteristic of patients negative for APC and MYH mutations was a significantly (p<0.0001) older age at diagnosis compared to patients with APC mutations.
  • Moreover, the proportion of cases with an attenuated polyposis phenotype was higher (p = 0.0008) among patients negative for APC and MYH mutations than among carriers of APC or biallelic MYH mutations.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. DNA Glycosylases / genetics. Genes, APC. Mutation
  • [MeSH-minor] Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Genetic Variation. Genotype. Humans. Italy. Phenotype

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16134147.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] eng
  • [Databank-accession-numbers] OMIM/ 175100/ 604933/ 608456
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
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90. Takacs CM, Baird JR, Hughes EG, Kent SS, Benchabane H, Paik R, Ahmed Y: Dual positive and negative regulation of wingless signaling by adenomatous polyposis coli. Science; 2008 Jan 18;319(5861):333-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dual positive and negative regulation of wingless signaling by adenomatous polyposis coli.
  • The majority of colorectal carcinomas contain truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor, a negative regulator of Wnt/Wingless signaling.
  • Here, we demonstrate that Drosophila Apc homologs also have an activating role in both physiological and ectopic Wingless signaling.
  • The Apc amino terminus is important for its activating function, whereas the beta-catenin binding sites are dispensable.
  • Apc likely promotes Wingless transduction through down-regulation of Axin, a negative regulator of Wingless signaling.
  • Given the evolutionary conservation of APC in Wnt signal transduction, an activating role may also be present in vertebrates with relevance to development and cancer.

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  • (PMID = 18202290.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA105038; United States / NCI NIH HHS / CA / KO8CA078532; United States / NCI NIH HHS / CA / R01CA105038
  • [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 / APC protein, Drosophila; 0 / APC1 (adenomatous polyposis coli) protein, Drosophila; 0 / APC2 protein, Drosophila; 0 / Adaptor Proteins, Signal Transducing; 0 / Armadillo Domain Proteins; 0 / Axin Protein; 0 / Cytoskeletal Proteins; 0 / Drosophila Proteins; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Wnt1 Protein; 0 / armadillo protein, Drosophila; 0 / axin protein, Drosophila; 0 / wg protein, Drosophila
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91. Nadauld LD, Chidester S, Shelton DN, Rai K, Broadbent T, Sandoval IT, Peterson PW, Manos EJ, Ireland CM, Yost HJ, Jones DA: Dual roles for adenomatous polyposis coli in regulating retinoic acid biosynthesis and Wnt during ocular development. Proc Natl Acad Sci U S A; 2006 Sep 5;103(36):13409-14
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  • [Title] Dual roles for adenomatous polyposis coli in regulating retinoic acid biosynthesis and Wnt during ocular development.
  • Congenital hypertrophy/hyperplasia of the retinal pigmented epithelium is an ocular lesion found in patients harboring mutations in the adenomatous polyposis coli (APC) tumor suppressor gene.
  • We report that Apc-deficient zebrafish display developmental abnormalities of both the lens and retina.
  • Injection of dominant-negative Lef reduced Wnt signaling in the lens but did not rescue retinal differentiation defects.
  • In contrast, treatment of apc mutants with all-trans retinoic acid rescued retinal differentiation defects but had no apparent effect on the lens.
  • We identified Rdh5 as a retina-specific retinol dehydrogenase controlled by APC.
  • Morpholino knockdown of Rdh5 phenocopied the apc mutant retinal differentiation defects and was rescued by treatment with exogenous all-trans retinoic acid.
  • Microarray analyses of apc mutants and Rdh5 morphants revealed a profound overlap in the transcriptional profile of these embryos.
  • These findings support a model wherein Apc serves a dual role in regulating Wnt and retinoic acid signaling within the eye and suggest retinoic acid deficiency as an explanation for APC mutation-associated retinal defects such as congenital hypertrophy/hyperplasia of the retinal pigmented epithelium.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Eye / embryology. Tretinoin / metabolism. Wnt Proteins / metabolism. Zebrafish / embryology

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  • (PMID = 16938888.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ000308
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116468
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Oligonucleotides, Antisense; 0 / Wnt Proteins; 5688UTC01R / Tretinoin
  • [Other-IDs] NLM/ PMC1569177
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92. Wong HL, Peters U, Hayes RB, Huang WY, Schatzkin A, Bresalier RS, Velie EM, Brody LC: Polymorphisms in the adenomatous polyposis coli (APC) gene and advanced colorectal adenoma risk. Eur J Cancer; 2010 Sep;46(13):2457-66
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  • [Title] Polymorphisms in the adenomatous polyposis coli (APC) gene and advanced colorectal adenoma risk.
  • While germline mutations in the adenomatous polyposis coli (APC) gene cause the hereditary colon cancer syndrome (familial adenomatous polyposis (FAP)), the role of common germline APC variants in sporadic adenomatous polyposis remains unclear.
  • We studied the association of eight APC single nucleotide polymorphisms (SNPs), possibly associated with functional consequences, and previously identified gene-environment (dietary fat intake and hormone replacement therapy (HRT) use) interactions, in relation to advanced colorectal adenoma in 758 cases and 767 sex- and race-matched controls, randomly selected from the screening arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.
  • Cases had at least one verified advanced adenoma of the distal colon; controls, a negative sigmoidoscopy.
  • We did not observe an association between genotypes for any of the eight APC SNPs and advanced distal adenoma risk (P(global gene-based)=0.92).
  • Frequencies of identified common haplotypes did not differ between cases and controls (P(global haplotype test)=0.97).
  • However, the risk for advanced distal adenoma was threefold higher for one rare haplotype (cases: 2.7%; controls: 1.6%) (odds ratio (OR)=3.27; 95% confidence interval (CI)=1.08-9.88).
  • The genetic association between D1822V and advanced distal adenoma was confined to persons consuming a high-fat diet (P(interaction)=0.03).
  • Similar interactions were not observed with HRT use.
  • In our large, nested case-control study of advanced distal adenoma and clinically verified adenoma-free controls, we observed no association between specific APC SNPs and advanced adenoma.
  • Fat intake modified the APC D1822V-adenoma association, but further studies are warranted.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Germ-Line Mutation / genetics. Polymorphism, Single Nucleotide / genetics

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20510605.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HG000120-12
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dietary Fats
  • [Other-IDs] NLM/ NIHMS202303; NLM/ PMC2924917
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93. Penman GA, Leung L, Näthke IS: The adenomatous polyposis coli protein (APC) exists in two distinct soluble complexes with different functions. J Cell Sci; 2005 Oct 15;118(Pt 20):4741-50
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The adenomatous polyposis coli protein (APC) exists in two distinct soluble complexes with different functions.
  • Mutations resulting in the truncation of the adenomatous polyposis coli (APC) protein are common to most colonic tumours.
  • The APC protein has emerged as a multifunctional protein that contributes to cytoskeletal organisation and is involved in the regulation of beta-catenin.
  • Both, changes in transcription due to increases in beta-catenin, as well as defects in directed cell migration and cell division contribute to cancer when APC is mutated.
  • Little is known about how separate functions of APC are coordinated.
  • In this study, we identified two distinct soluble protein pools containing APC.
  • The second pool contained at least two different forms of APC: APC that was bound to partially assembled beta-catenin-targeting complexes and APC that could bind microtubules.
  • Similarly, tumour cells with truncated APC only contained the partially assembly beta-catenin-targeting complex.
  • We also found that highly elevated levels of beta-catenin in tumour cells containing wild-type APC correlated with a decrease in the ability of the endogenous APC protein to bind microtubules.
  • Additionally, APC lacking the direct microtubule binding site was more effective at downregulating beta-catenin.
  • Together, our data suggest that the interaction of APC with microtubules and the beta-catenin-targeting complex are mutually exclusive, and indicate that the distribution of endogenous APC between different pools is dynamic, which allows cells to distribute it as required.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / chemistry. Adenomatous Polyposis Coli Protein / metabolism
  • [MeSH-minor] Animals. Axin Protein. Cell Line. Centrifugation, Density Gradient. Enzyme Inhibitors / pharmacology. Glycogen Synthase Kinase 3 / analysis. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Glycogen Synthase Kinase 3 / metabolism. Humans. Macromolecular Substances / chemistry. Macromolecular Substances / metabolism. Microtubules / metabolism. Protein Binding. Repressor Proteins / metabolism. Solubility. beta Catenin / analysis

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  • (PMID = 16188939.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Axin Protein; 0 / Enzyme Inhibitors; 0 / Macromolecular Substances; 0 / Repressor Proteins; 0 / beta Catenin; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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94. Farías GG, Vallés AS, Colombres M, Godoy JA, Toledo EM, Lukas RJ, Barrantes FJ, Inestrosa NC: Wnt-7a induces presynaptic colocalization of alpha 7-nicotinic acetylcholine receptors and adenomatous polyposis coli in hippocampal neurons. J Neurosci; 2007 May 16;27(20):5313-25
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wnt-7a induces presynaptic colocalization of alpha 7-nicotinic acetylcholine receptors and adenomatous polyposis coli in hippocampal neurons.
  • We report here that Wnt-7a, a ligand active in the canonical Wnt signaling pathway, induces dissociation of the adenomatous polyposis coli (APC) protein from the beta-catenin cytoplasmic complex and the interaction of APC with alpha7-nAChRs in hippocampal neurons.
  • Interestingly, Wnt-7a induces the relocalization of APC to membranes, clustering of APC in neurites, and coclustering of APC with different, presynaptic protein markers.
  • Wnt-7a also increases the number and size of coclusters of alpha7-nAChRs and APC in presynaptic terminals.
  • Longer-term exposure to Wnt-7a increases nAChR alpha7 subunit levels in an APC-independent manner and increases clusters of alpha7-nAChRs in neurites via an APC-dependent process.
  • Together, these results demonstrate that stimulation through the canonical Wnt pathway regulates the presynaptic localization of APC and alpha7-nAChRs with APC serving as an intermediary in the alpha7-nAChR relocalization process.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Hippocampus / metabolism. Neurons / metabolism. Presynaptic Terminals / metabolism. Proto-Oncogene Proteins / physiology. Receptors, Nicotinic / metabolism. Wnt Proteins / physiology

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  • (PMID = 17507554.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA015389; United States / NINDS NIH HHS / NS / NS040417
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Chrna7 protein, human; 0 / Chrna7 protein, mouse; 0 / Chrna7 protein, rat; 0 / Proto-Oncogene Proteins; 0 / Receptors, Nicotinic; 0 / Wnt Proteins; 0 / Wnt7a protein, mouse; 0 / Wnt7a protein, rat; 0 / alpha7 Nicotinic Acetylcholine Receptor; 0 / beta Catenin
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95. Benchabane H, Ahmed Y: The adenomatous polyposis coli tumor suppressor and Wnt signaling in the regulation of apoptosis. Adv Exp Med Biol; 2009;656:75-84
Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The adenomatous polyposis coli tumor suppressor and Wnt signaling in the regulation of apoptosis.
  • The adenomatous polyposis coli (APC) tumor suppressor is an essential negative regulator in the evolutionarily conserved Wnt/Wingless (Wg) signal transduction pathway.
  • During normal development, Wnt signaling is required not only to induce cell proliferation and cell fate specification, but also to induce apoptotic cell death.
  • However in some malignant states triggered by APC loss, inappropriate activation of Wnt signaling promotes cell survival and inhibits cell death, indicating that the cellular response to APC loss and Wnt signaling is highly dependent on cell context.
  • This chapter summarizes our current understanding of the role of APC and Wnt signaling in the regulation of apoptosis, based upon studies from fly and mouse in vivo models, as well as cultured carcinoma cells.

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  • (PMID = 19928354.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105038-04; United States / NCI NIH HHS / CA / R01 CA105038; United States / NCI NIH HHS / CA / R01 CA105038-04; United States / NCI NIH HHS / CA / R01CA105038; United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Wnt Proteins
  • [Number-of-references] 71
  • [Other-IDs] NLM/ NIHMS279106; NLM/ PMC3066060
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96. Jaiswal AS, Narayan S: A novel function of adenomatous polyposis coli (APC) in regulating DNA repair. Cancer Lett; 2008 Nov 28;271(2):272-80
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel function of adenomatous polyposis coli (APC) in regulating DNA repair.
  • Prevailing literature suggests diversified cellular functions for the adenomatous polyposis coli (APC) gene.
  • Among them a recently discovered unique role of APC is in DNA repair.
  • The APC gene can modulate the base excision repair (BER) pathway through an interaction with DNA polymerase beta (Pol-beta) and flap endonuclease 1 (Fen-1).
  • Taken together with the transcriptional activation of APC gene by alkylating agents and modulation of BER activity, APC may play an important role in carcinogenesis and chemotherapy by determining whether cells with DNA damage survive or undergo apoptosis.

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  • (PMID = 18662849.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-100247; United States / NCI NIH HHS / CA / R01 CA100247-01; United States / NCI NIH HHS / CA / CA100247-01; United States / NCI NIH HHS / CA / R01 CA097031-01A1; United States / NCI NIH HHS / CA / CA-097031; United States / NCI NIH HHS / CA / CA097031-01A1; United States / NCI NIH HHS / CA / R01 CA097031; United States / NCI NIH HHS / CA / R01 CA100247
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Alkylating Agents; EC 2.7.7.- / DNA Polymerase beta; EC 3.1.- / Flap Endonucleases
  • [Number-of-references] 81
  • [Other-IDs] NLM/ NIHMS78341; NLM/ PMC2585005
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97. Kim IJ, Kim K, Kang HC, Jang SG, Park JG: DHPLC analysis of adenomatous polyposis coli (APC) mutations using ready-to-use APC plates: simple detection of multiple base pair deletion mutations. Genet Test; 2008 Jun;12(2):295-8
Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DHPLC analysis of adenomatous polyposis coli (APC) mutations using ready-to-use APC plates: simple detection of multiple base pair deletion mutations.
  • The adenomatous polyposis coli (APC), which is the susceptible gene for familial adenomatous polyposis (FAP) and sporadic colorectal cancer, spans 15 exons.
  • The open reading frame of APC is 8529 bp, which encodes 2843 amino acids.
  • Thus, we developed a novel APC ready-to-use plate for high-throughput mutational analysis by denaturing high performance liquid chromatography (DHPLC).
  • To prepare the ready-to-use APC plate, all 38 primer pairs and PCR mixtures were aliquoted into individual wells of a 96-well plate, and frozen at -20 degrees C until use.
  • We examined a total of 27 FAP patient samples with APC germline mutations (17 for multiple bp deletions, 1 for 1 bp deletion, 9 for nonsense mutations) and 50 APC-negative noncarriers.
  • All 17 multiple bp deletion mutations were detected during the initial 50 degrees C running analysis and thus ruled out for further analyses.
  • More than 50% of the APC germline mutations were multiple base pair deletions and efficiently selected by omitting time-consuming partial denaturing conditions.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli Protein / genetics. Base Pairing / genetics. Chromatography, High Pressure Liquid / methods. Gene Deletion. Mutation

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  • (PMID = 18554166.001).
  • [ISSN] 1090-6576
  • [Journal-full-title] Genetic testing
  • [ISO-abbreviation] Genet. Test.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
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98. Azzopardi D, Dallosso AR, Eliason K, Hendrickson BC, Jones N, Rawstorne E, Colley J, Moskvina V, Frye C, Sampson JR, Wenstrup R, Scholl T, Cheadle JP: Multiple rare nonsynonymous variants in the adenomatous polyposis coli gene predispose to colorectal adenomas. Cancer Res; 2008 Jan 15;68(2):358-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple rare nonsynonymous variants in the adenomatous polyposis coli gene predispose to colorectal adenomas.
  • It has been proposed that multiple rare variants in numerous genes collectively account for a substantial proportion of multifactorial inherited predisposition to a variety of diseases, including colorectal adenomas (CRA).
  • We have studied this hypothesis by sequencing the adenomatous polyposis coli (APC) gene in 691 unrelated North American patients with CRAs and 969 matched healthy controls.
  • Rare inherited nonsynonymous variants of APC were significantly overrepresented in patients who did not carry conventional pathogenic mutations in the APC or MutY homologue genes [non-familial adenomatous polyposis (FAP) non-MUTYH-associated polyposis (MAP) patients; 81 of 480, 16.9%] compared with patients with FAP or MAP (20 of 211, 9.5%, P = 0.0113), and this overrepresentation was highest in those non-FAP non-MAP patients with 11 to 99 CRAs (30 of 161, 18.6%, P = 0.0103).
  • Furthermore, significantly more non-FAP non-MAP patients carried rare nonsynonymous variants in the functionally important beta-catenin down-regulating domain compared with healthy controls (32 of 480 versus 37 of 969, P = 0.0166).
  • These data suggest that multiple rare nonsynonymous variants in APC play a significant role in predisposing to CRAs.
  • [MeSH-major] Adenoma / genetics. Adenomatous Polyposis Coli Protein / genetics. Colorectal Neoplasms / genetics. Genetic Predisposition to Disease. Polymorphism, Single Nucleotide
  • [MeSH-minor] Adult. Case-Control Studies. DNA Mutational Analysis. Down-Regulation. Female. Humans. Male. Middle Aged. Protein Structure, Tertiary. beta Catenin / metabolism

  • Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
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  • (PMID = 18199528.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G0301154
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / beta Catenin
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99. Liu Z, Yang L, Cui DX, Liu BL, Zhang XB, Ma WF, Zhang Q: [Methylation status and protein expression of adenomatous polyposis coli (APC) gene in breast cancer]. Ai Zheng; 2007 Jun;26(6):586-90
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Methylation status and protein expression of adenomatous polyposis coli (APC) gene in breast cancer].
  • BACKGROUND & OBJECTIVE: Protein expression product of adenomatous polyposis coli (APC) gene is an important component of Wnt signal transduction pathway.
  • APC gene inactivation leads to dysfunction of beta-catenin protein degradation, and then activates Tcf/Lef and causes abnormal transcription of oncogenes, such as c-myc, c-jun and cyclin D1, finally leads to carcinogenesis.
  • This study was to investigate the correlation of methylation status of APC gene promoter 1A to protein expression of APC gene in breast cancer, and analyze the correlation of aberrant methylation of APC gene to clinicopathologic features of breast cancer.
  • METHODS: Methylation status of APC gene promoter 1A in 76 specimens of breast cancer and corresponding adjacent tissues was detected by methylation-specific polymerase chain reaction; the expression of APC protein was detected by immunohistochemistry.
  • RESULTS: The methylation rate of APC gene promoter 1A was significantly higher in breast cancer than in pericancerous normal breast tissue (36.8% vs. 0, P < 0.05).
  • The positive rate of APC protein was significantly lower in breast cancer than in normal breast tissue (52.4% vs. 100%, P < 0.05).
  • The promoter methylation of APC gene was positively correlated to TNM stage (r=0.296, P < 0.05), but negatively correlated to the expression of APC protein (r=-0.368, P < 0.05).
  • CONCLUSION: Abnormal methylation of APC gene occurs in the progression of breast cancer, which is the main cause for the absence of APC protein expression, and the major mechanism of inactivation of APC gene.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. DNA Methylation. Genes, APC


100.