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1. 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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2. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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3. 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
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  • [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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4. 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
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  • [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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5. 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

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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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6. 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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7. 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
ZFIN. ZFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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8. 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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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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11. 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
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] 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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12. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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15. 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
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] [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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16. 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
Hazardous Substances Data Bank. AZACITIDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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17. 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
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] 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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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. 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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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. 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.
  • 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.

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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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23. 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.
  • 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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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. 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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28. 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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29. 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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30. 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%).

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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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31. 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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32. 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).
  • We incubated in vitro cultures of MCF- 7 cells and PBMNF cells with M at a dose of 0.7μg/ml for 30 minutes with and without A at 20% of the M dose and evaluated serially for 48 hours for MIS and hMH2 expression by immunohistochemistry.
  • 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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33. 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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34. 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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35. 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.
  • 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.
  • 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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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. 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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39. 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.
  • 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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40. 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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41. 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).
  • 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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42. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 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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43. 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
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] 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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44. Prall F, Weirich V, Ostwald C: Phenotypes of invasion in sporadic colorectal carcinomas related to aberrations of the adenomatous polyposis coli (APC ) gene. Histopathology; 2007 Feb;50(3):318-30
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  • [Title] Phenotypes of invasion in sporadic colorectal carcinomas related to aberrations of the adenomatous polyposis coli (APC ) gene.
  • AIMS: To determine whether the dissociation of tumour cells from neoplastic glands in colorectal carcinomas is caused by disruption of the wnt-signalling pathway and whether the adenomatous polyposis coli (APC) protein is implicated in this.
  • 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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45. 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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46. 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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  • [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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47. 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
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  • [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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48. 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
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  • [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


49. Guimarães AP, Rocha RM, da Cunha IW, Guimarães GC, Carvalho AL, de Camargo B, Lopes A, Squire JA, Soares FA: Prognostic impact of adenomatous polyposis coli gene expression in osteosarcoma of the extremities. Eur J Cancer; 2010 Dec;46(18):3307-15
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  • [Title] Prognostic impact of adenomatous polyposis coli gene expression in osteosarcoma of the extremities.
  • PURPOSE: To evaluate the impact of adjuvant chemotherapy on the outcome of osteosarcoma of the extremities, and to identify prognostic factors using the expression of adenomatous polyposis coli (APC), cadherin and β-catenin Wnt-signalling markers.
  • METHODS: The clinical, demographic, anatomic and pathological factors including a detailed analysis of the immunohistochemical expression of cadherin, β-catenin and APC were retrospectively examined in 97 patients with osteosarcoma of the extremities (metastatic and non-metastatic at diagnosis), treated with surgery and/or chemotherapy from 1985 to 2000.
  • RESULTS: APC immunoreactivity showed a statistically significant association with age and serum alkaline phosphatase levels (p = 0.025 and p = 0.038).
  • For overall survival, cadherin immunoreactivity and the interaction between APC expression and response to adjuvant chemotherapy were significant (p = 0.012 and p<0.001).
  • CONCLUSION: Lack of expression of cadherin was a significant variable to overall and disease-free survival.
  • Significantly, positive APC immunoreactivity and adjuvant chemotherapy were associated with a favourable treatment response.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Bone Neoplasms / genetics. Extremities. Genes, APC. Osteosarcoma / genetics

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20594821.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins
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50. Gounari F, Chang R, Cowan J, Guo Z, Dose M, Gounaris E, Khazaie K: Loss of adenomatous polyposis coli gene function disrupts thymic development. Nat Immunol; 2005 Aug;6(8):800-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of adenomatous polyposis coli gene function disrupts thymic development.
  • Loss of the adenomatous polyposis coli (APC) protein is a common initiating event in colon cancer.
  • Here we show that thymocyte-specific loss of APC deregulated beta-catenin signaling and suppressed Notch-dependent transcription.
  • Simultaneously, the loss of APC prolonged the mitotic metaphase-to-anaphase checkpoint and impaired chromosome segregation, blocking development beyond the double-negative 4 stage.
  • Thus, loss of APC in immature thymocytes has consequences distinct from those of deregulation of beta-catenin signaling and is essential for T cell differentiation.

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  • (PMID = 16025118.001).
  • [ISSN] 1529-2908
  • [Journal-full-title] Nature immunology
  • [ISO-abbreviation] Nat. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104547; United States / NCI NIH HHS / CA / R01 CA104547-01A1; United States / NIAID NIH HHS / AI / R01 AI059676-02; United States / NIAID NIH HHS / AI / R01 AI059676-01; United States / NIAID NIH HHS / AI / R01 AI059676
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Membrane Proteins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Notch; 0 / Trans-Activators; 0 / beta Catenin; EC 2.7.7.- / VDJ Recombinases
  • [Other-IDs] NLM/ NIHMS33757; NLM/ PMC4662936
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51. Gail R, Frank R, Wittinghofer A: Systematic peptide array-based delineation of the differential beta-catenin interaction with Tcf4, E-cadherin, and adenomatous polyposis coli. J Biol Chem; 2005 Feb 25;280(8):7107-17
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic peptide array-based delineation of the differential beta-catenin interaction with Tcf4, E-cadherin, and adenomatous polyposis coli.
  • Nuclear accumulation of the complex between beta-catenin and proteins of the T-cell factor (Tcf) family is a hallmark of many cancers.
  • Targeting this interaction for drug development is complicated by the fact that E-cadherin and adenomatous polyposis coli (APC) bind to overlapping sites on beta-catenin.
  • To identify selective beta-catenin binding hot spots of Tcf4, E-cadherin, and APC, array technology with peptides of up to 53 amino acids length was used.
  • We identified minimal binding motifs in the beta-catenin ligands and showed that most of the 15-mer and 20-mer repeats of APC did not interact, at least when non-phosphorylated, and defined a consensus binding motif also present in APC.
  • The method allowed us to locate a hydrophobic pocket that was relevant for the Tcf, but not the E-cadherin interaction, and would thus constitute an ideal drug target site.
  • [MeSH-major] Cadherins / metabolism. Cytoskeletal Proteins / metabolism. DNA-Binding Proteins / metabolism. Peptides / chemical synthesis. Protein Array Analysis. Trans-Activators / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Animals. Binding Sites. Combinatorial Chemistry Techniques. Drug Delivery Systems. Humans. Ligands. Mice. Models, Molecular. Protein Interaction Mapping / methods. TCF Transcription Factors. Transcription Factor 7-Like 2 Protein. beta Catenin

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  • (PMID = 15591320.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Cadherins; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Ligands; 0 / Peptides; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf7l2 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 2 Protein; 0 / Transcription Factors; 0 / beta Catenin
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52. Van der Auwera I, Van Laere SJ, Van den Bosch SM, Van den Eynden GG, Trinh BX, van Dam PA, Colpaert CG, van Engeland M, Van Marck EA, Vermeulen PB, Dirix LY: Aberrant methylation of the Adenomatous Polyposis Coli (APC) gene promoter is associated with the inflammatory breast cancer phenotype. Br J Cancer; 2008 Nov 18;99(10):1735-42
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  • [Title] Aberrant methylation of the Adenomatous Polyposis Coli (APC) gene promoter is associated with the inflammatory breast cancer phenotype.
  • Aberrant methylation of the adenomatous polyposis coli (APC) gene promoter occurs in about 40% of breast tumours and has been correlated with reduced APC protein levels.
  • To what extent epigenetic alterations of the APC gene may differ according to specific breast cancer phenotypes, remains to be elucidated.
  • Our aim was to explore the role of APC methylation in the inflammatory breast cancer (IBC) phenotype.
  • The status of APC gene promoter hypermethylation was investigated in DNA from normal breast tissues, IBC and non-IBC by both conventional and real-time quantitative methylation-specific PCR (MSP).
  • APC methylation levels were compared with APC mRNA and protein levels.
  • Hypermethylation of the APC gene promoter was present in 71% of IBC samples (n=21) and 43% of non-IBC samples (n=30) by conventional MSP (P=0.047).
  • The APC gene also showed an increased frequency of high methylation levels in IBC (in 74% of cases, n=19) vs non-IBC (in 46% of cases, n=35) using a qMSP assay (P=0.048).
  • We observed no significant association between APC methylation levels by qMSP and APC mRNA or protein expression levels.
  • In conclusion, for the first time, we report the association of aberrant methylation of the APC gene promoter with the IBC phenotype, which might be of biological and clinical importance.
  • [MeSH-major] Breast Neoplasms / genetics. DNA Methylation. Genes, APC


53. Li Q, Ishikawa TO, Oshima M, Taketo MM: The threshold level of adenomatous polyposis coli protein for mouse intestinal tumorigenesis. Cancer Res; 2005 Oct 1;65(19):8622-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The threshold level of adenomatous polyposis coli protein for mouse intestinal tumorigenesis.
  • The adenomatous polyposis coli (APC) gene, whose mutations are responsible for familial adenomatous polyposis, is a major negative controller of the Wnt/beta-catenin pathway.
  • To investigate the dose-dependent effects of APC protein in suppressing intestinal tumorigenesis, we constructed mutant mice carrying hypomorphic Apc alleles Apc(neoR) and Apc(neoF) whose expression levels were reduced to 20% and 10% of the wild type, respectively.
  • Although both hypomorphic heterozygotes developed intestinal polyps, tumor multiplicities were much lower than that in Apc(Delta716) mice, heterozygotes of an Apc null allele.
  • Like in Apc(Delta716) mice, loss of the wild-type Apc allele was confirmed for all polyps examined in the Apc(neoR) and Apc(neoF) mice.
  • In the embryonic stem cells homozygous for these hypomorphic Apc alleles, the level of the APC protein was inversely correlated with both the beta-catenin accumulation and beta-catenin/T-cell factor transcriptional activity.
  • These results suggest that the reduced APC protein level increases intestinal polyp multiplicity through quantitative stimulation of the beta-catenin/T-cell factor transcription.
  • We further estimated the threshold of APC protein level that forms one polyp per mouse as approximately 15% of the wild type.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Genes, APC. Intestinal Neoplasms / genetics
  • [MeSH-minor] Alleles. Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Female. Intestinal Polyps / genetics. Intestinal Polyps / metabolism. Intestinal Polyps / pathology. Loss of Heterozygosity. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. beta Catenin / metabolism

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  • (PMID = 16204028.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / beta Catenin
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54. Zhou XL, Giacobini M, Anderlid BM, Anckarsäter H, Omrani D, Gillberg C, Nordenskjöld M, Lindblom A: Association of adenomatous polyposis coli (APC) gene polymorphisms with autism spectrum disorder (ASD). Am J Med Genet B Neuropsychiatr Genet; 2007 Apr 5;144B(3):351-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of adenomatous polyposis coli (APC) gene polymorphisms with autism spectrum disorder (ASD).
  • We serendipitously identified a single nucleotide polymorphism (SNP), 8636C>A (rs1804197) in the 3'-untranslated region of the adenomatous polyposis coli (APC) gene to be associated with autism spectrum disorder (ASD).
  • In order to gain further evidence for the association between the APC locus and ASD, we genotyped four additional adjacent common SNPs (rs2229992, rs42427, rs459552, and rs465899) in the coding regions within the APC gene in a set of Swedish ASDs and controls.
  • One common haplotype TGAG was found to be associated with ASD after haplotype analysis using both Haploview v3.1.1 (P = 0.006) and COCAPHASE v2.403 (P = 0.030).
  • This result is the first to suggest that the genomic locus at APC is associated with ASD, and that the APC gene itself is a good predisposing candidate to be evaluated in future studies due to its important role in neuronal development and function.
  • [MeSH-major] Autistic Disorder / genetics. Genes, APC. Genetic Linkage. Polymorphism, Single Nucleotide

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17221838.001).
  • [ISSN] 1552-4841
  • [Journal-full-title] American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics
  • [ISO-abbreviation] Am. J. Med. Genet. B Neuropsychiatr. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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55. 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
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  • [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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56. Togo T: Ca(2+) regulates the subcellular localization of adenomatous polyposis coli tumor suppressor protein. Biochem Biophys Res Commun; 2009 Oct 9;388(1):12-6
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  • [Title] Ca(2+) regulates the subcellular localization of adenomatous polyposis coli tumor suppressor protein.
  • Microtubule (MT) plus-end tracking proteins (+TIPs) are involved in the regulation of MT plus-end dynamics and stabilization.
  • In the present study, the behavior of adenomatous polyposis coli (APC) following an increase in [Ca(2+)](i) was observed using Xenopus A6 epithelial cell expressing GFP-tagged APC.
  • An increase in [Ca(2+)](i) by cell membrane disruption or by ionomycin treatment induced dissociation of APC without depolymerizing MTs.
  • Inhibition of a tyrosine kinase and GSK-3beta suppressed APC dissociation upon an increase in [Ca(2+)](i).
  • These results suggest that Ca(2+) stimulates redistribution of APC through a tyrosine kinase- and GSK-3beta-dependent pathway.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Calcium / metabolism
  • [MeSH-minor] Animals. Cell Membrane / metabolism. Cells, Cultured. Glycogen Synthase Kinase 3 / metabolism. Protein-Tyrosine Kinases / metabolism. Transfection. Xenopus

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  • (PMID = 19638276.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [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; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; SY7Q814VUP / Calcium
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57. Nagel R, le Sage C, Diosdado B, van der Waal M, Oude Vrielink JA, Bolijn A, Meijer GA, Agami R: Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer. Cancer Res; 2008 Jul 15;68(14):5795-802
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  • [Title] Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer.
  • Inactivation of the adenomatous polyposis coli (APC) gene is a major initiating event in colorectal tumorigenesis.
  • Most of the mutations in APC generate premature stop codons leading to truncated proteins that have lost beta-catenin binding sites.
  • APC-free beta-catenin stimulates the Wnt signaling pathway, leading to active transcription of target genes.
  • In the current study, we describe a novel mechanism for APC regulation.
  • We show that miR-135a&b target the 3' untranslated region of APC, suppress its expression, and induce downstream Wnt pathway activity.
  • Interestingly, we find a considerable up-regulation of miR-135a&b in colorectal adenomas and carcinomas, which significantly correlated with low APC mRNA levels.
  • This genetic interaction is also preserved in full-blown cancer cell lines expressing miR-135a&b, regardless of the mutational status of APC.
  • Thus, our results uncover a miRNA-mediated mechanism for the control of APC expression and Wnt pathway activity, and suggest its contribution to colorectal cancer pathogenesis.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / physiology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics
  • [MeSH-minor] 3' Untranslated Regions. Cell Line. Cell Line, Tumor. DNA Mutational Analysis. Gene Expression Profiling. HeLa Cells. Humans. Models, Biological. Promoter Regions, Genetic. Signal Transduction. Wnt Proteins / metabolism

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  • (PMID = 18632633.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / Adenomatous Polyposis Coli Protein; 0 / MicroRNAs; 0 / Wnt Proteins
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58. Toma M, Cimponeriu D, Pompilia A, Stavarachi M, Beluşică L, Radu I, Gavrilă L: Molecular analysis of mutations for the adenomatous polyposis coli (APC) gene in Romanian patients with colorectal cancer. J Med Life; 2008 Oct-Dec;1(4):423-8
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  • [Title] Molecular analysis of mutations for the adenomatous polyposis coli (APC) gene in Romanian patients with colorectal cancer.
  • Mutations in adenomatous polyposis coli (APC) gene have not been previously characterized among Romanian patients with colorectal cancer (CRC).
  • We initiate this study to detect the mutations in APC gene in blood and tumor samples collected from 16 patients (10 men and 6 women) and blood samples from 21 first and second degree relatives of the patients.
  • In the same time, we have searched for 5 bp deletions at codon 1061 of APC gene by PAGE and SSCP methods.
  • In one patient, was detected a deletion of exon 13th of APC gene both in DNA extracted from blood and tumor samples.
  • Multiple deletions (e.g. in exon 6, 12, and in 15L and 15W regions) in DNA extracted from the tumor sample were detected, but not in DNA probe obtained from blood cells.
  • Till now, no mutation affecting 1061 codon of APC gene was identified in the patients investigated in our study.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms / genetics. Genes, APC
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Adult. Aged. Female. Frameshift Mutation. Humans. Male. Middle Aged. Point Mutation. Romania / epidemiology

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  • (PMID = 20108522.001).
  • [ISSN] 1844-122X
  • [Journal-full-title] Journal of medicine and life
  • [ISO-abbreviation] J Med Life
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein
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59. Hall MJ, Liberman E, Dulkart O, Galazan L, Sagiv E, Shmueli E, Kazanov D, Hallak A, Moshkowitz M, Figer A, Kraus S, Inbar M, Neugut AI, Arber N: Risk of colorectal neoplasia associated with the adenomatous polyposis coli E1317Q variant. Ann Oncol; 2009 Sep;20(9):1517-21
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  • [Title] Risk of colorectal neoplasia associated with the adenomatous polyposis coli E1317Q variant.
  • BACKGROUND: Reports of the risk of colorectal neoplasia associated with a variant of the adenomatous polyposis coli (APC E1317Q) gene are conflicting.
  • MATERIALS AND METHODS: All study subjects were tested for the APC E1317Q variant at enrollment.
  • The crude and adjusted risks of neoplasia associated with the E1317Q variant were calculated.
  • E1317Q was more prevalent among cases: 15 of 458 (3.3%) cases were carriers compared with 11 of 1431 (0.8%) controls [odds ratio (OR) 4.4, 95% CI 2.0-9.6].
  • When stratified by neoplasia type, adenoma risk was significantly elevated in carriers (OR 4.1, 95% CI 1.8-9.4) but colorectal cancer risk was not (OR 2.1, 95% CI 0.8-5.3).
  • After adjustment, the E1317Q variant remained a significant predictor of colorectal adenoma (OR 4.6, 95% CI 2.0-10.8).
  • CONCLUSIONS: The APC E1317Q variant is associated with colorectal neoplasia, particularly colorectal adenomas, but further studies are still needed.

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  • (PMID = 19474113.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. 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
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60. Pan SY, Xie EF, Shu YQ, Gao L, Zhang LX, Chen D, Chen JB, Zhao WJ, Mu Y, Zhang JN: [Methylation quantification of adenomatous polyposis coli (APC) gene promoter in plasma of lung cancer patients]. Ai Zheng; 2009 Apr;28(4):384-9
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  • [Title] [Methylation quantification of adenomatous polyposis coli (APC) gene promoter in plasma of lung cancer patients].
  • BACKGROUND AND OBJECTIVE: The protein encoded by adenomatous polyposis coli (APC) gene participates in the signaling transduction pathway.
  • Substantial studies have revealed that hypermethylation of APC gene promoter is closely related to the pathogenesis and development of cancer.
  • This study was to develop a real-time quantitative methylation specific PCR (real-time QMSP) method, and detect the methylation of APC gene promoter in plasma of lung cancer patients.
  • METHODS: Genomic DNA with methylated APC gene promoter was extracted from the lung cancer cell line NCI-H460 using phenol-chloroform and quantified by spectrophotometric measurements.
  • The concentration of cell-free methylated APC gene promoter in the plasma samples was quantified by the external reference method with the standard curve constructed using simulated plasma.
  • Of 78 lung cancer patients, positive methylation of the APC gene promoter was detected in tumor tissues of 40 cases.
  • Among the 40 lung cancer patients, positive methylation of the APC gene promoter was found in the plasma of 19 patients (47.5%).
  • The concentrations of methylated APC promoter in the 19 lung cancer patients ranged from 1.67x10(2) to 6.78x10(3) copies/mL, with a median concentration of 1.67x10(3) copies/mL.
  • No positive methylation of the APC gene promoter was detected in the plasma of 38 lung cancer patients without APC gene methylation in tissues, 31 benign lung diseases and 23 healthy controls.
  • CONCLUSIONS: The newly developed real-time QMSP method allows the quantitative measurement of APC gene promoter methylation in plasma.
  • Hypermethylation of the APC gene promoter in plasma is a potential diagnostic marker for lung cancer diagnosis.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. DNA Methylation. Genes, APC. Lung Neoplasms / genetics. Promoter Regions, Genetic

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  • (PMID = 19622298.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / DNA, Neoplasm
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61. Cleary SP, Kim H, Croitoru ME, Redston M, Knight JA, Gallinger S, Gryfe R: Missense polymorphisms in the adenomatous polyposis coli gene and colorectal cancer risk. Dis Colon Rectum; 2008 Oct;51(10):1467-73; discussion 1473-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Missense polymorphisms in the adenomatous polyposis coli gene and colorectal cancer risk.
  • PURPOSE: Whereas truncating germline mutations of the adenomatous polyposis coli (APC) gene give rise to familial adenomatous polyposis, missense polymorphisms of APC may confer a weaker risk for colorectal cancer.
  • METHODS: We sequenced the entire open reading frame of the APC gene and tested for two common MYH mutations in a population-based series of patients with colorectal cancer and 5 to 99 adenomas.
  • Missense adenomatous polyposis coli alterations identified in this colorectal cancer multiple-polyp population were analyzed in a population-based series of patients with colorectal cancer and healthy control subjects.
  • RESULTS: Germline APC or mutY human homologue (MYH) alterations were identified in 16 of 39 colorectal cancer-multiple polyp patients.
  • Four missense APC gene alterations (S130G, E1317Q, D1822V, G2502S) were observed in 13 individuals and 3 additional patients carried presumed pathogenic (APC Y94X, biallelic MYH Y165C and heterozygous MYH G382D) mutations.
  • When independently assessed in 971 patients with colorectal cancer and 954 healthy control subjects, none of the identified missense APC alterations conferred a significantly increased risk for colorectal cancer, odds ratio (95 percent confidence intervals): S130G = 3.1 (0.29-32.25), E1317Q = 1.08 (0.59-2.74), G2502S = 1 (0.65-1.63), D1822V (heterozygous) = 0.79 (0.64-0.98), D1822V (homozygous) = 0.82 (0.63-1.27).
  • CONCLUSIONS: Germline missense APC alterations observed in 33 percent of patients with multiple colorectal neoplasms seemed to play a limited role in colorectal cancer risk when independently assessed by a population-based, case-control analysis.

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  • (PMID = 18612690.001).
  • [ISSN] 1530-0358
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA074783-06; United States / NCI NIH HHS / CA / CA074783-06; United States / NCI NIH HHS / CA / CA074783-07; United States / NCI NIH HHS / CA / U01 CA074783; United States / NCI NIH HHS / CA / U01 CA074783-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS139709; NLM/ PMC2768068
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62. 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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  • [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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63. Jaiswal AS, Balusu R, Armas ML, Kundu CN, Narayan S: Mechanism of adenomatous polyposis coli (APC)-mediated blockage of long-patch base excision repair. Biochemistry; 2006 Dec 26;45(51):15903-14
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  • [Title] Mechanism of adenomatous polyposis coli (APC)-mediated blockage of long-patch base excision repair.
  • Recently, we found an interaction between adenomatous polyposis coli (APC) and DNA polymerase beta (pol-beta) and showed that APC blocks strand-displacement synthesis of long-patch base excision repair (LP-BER) (Narayan, S., Jaiswal, A.
  • 280, 6942-6949); however, the mechanism is not clear.
  • Using an in vivo LP-BER assay system, we now show that the LP-BER is higher in APC-/- cells than in APC+/+ cells.
  • In addition to pol-beta, the pull-down experiments showed that the full-length APC also interacted with flap endonuclease 1 (Fen-1).
  • To further characterize the interaction of APC with pol-beta and Fen-1, we performed a domain-mapping of APC and found that both pol-beta and Fen-1 interact with a 138-amino acids peptide from the APC at the DRI-domain.
  • Our functional assays showed that APC blocks pol-beta-mediated 1-nucleotide (1-nt) as well as strand-displacement synthesis of reduced abasic, nicked-, or 1-nt gapped-DNA substrates.
  • Further studies demonstrated that APC blocks 5'-flap endonuclease as well as the 5'-3' exonuclease activity of Fen-1 resulting in the blockage of LP-BER.
  • From these results, we concluded that APC can have three different effects on the LP-BER pathway.
  • First, APC can block pol-beta-mediated 1-nt incorporation and strand-displacement synthesis.
  • Second, APC can block LP-BER by blocking the coordinated formation and removal of the strand-displaced flap.
  • Third, APC can block LP-BER by blocking hit-and-run synthesis.
  • These studies will have important implications for APC in DNA damage-induced carcinogenesis and chemoprevention.

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  • (PMID = 17176113.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] ENG
  • [Grant] 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 / CA097031-01A1; United States / NCI NIH HHS / CA / CA-100247-01; United States / NCI NIH HHS / CA / R01 CA097031; United States / NCI NIH HHS / CA / CA-097031-01; 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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.7.- / DNA Polymerase beta; EC 3.1.- / Exonucleases; EC 3.1.- / Flap Endonucleases; EC 3.1.11.- / FEN1 protein, human
  • [Other-IDs] NLM/ NIHMS61667; NLM/ PMC2528549
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64. Yazici N, Yalçin B, Soylemezoğlu F, Cila A, Akalan N, Koksal Y, Buyukpamukçu M: Intracranial desmoid tumor with familial adenomatous polyposis coli. Pediatr Neurosurg; 2008;44(2):140-3
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  • [Title] Intracranial desmoid tumor with familial adenomatous polyposis coli.
  • The association of desmoid tumors with familial adenomatous polyposis coli was reported previously, with the tumors involving trunk and extremities.
  • We report a 3.5-year-old girl with intracranial desmoid tumor with familial adenomatous polyposis coli.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Brain Neoplasms / pathology. Fibromatosis, Aggressive / pathology


65. Lee HN, Jeon GS, Kim DW, Cho IH, Cho SS: Expression of adenomatous polyposis coli protein in reactive astrocytes in hippocampus of kainic acid-induced rat. Neurochem Res; 2010 Jan;35(1):114-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of adenomatous polyposis coli protein in reactive astrocytes in hippocampus of kainic acid-induced rat.
  • The adenomatous polyposis coli gene (APC) was initially identified through its link to colon cancer.
  • It is associated with the regulation of cell cycle progression, survival, and differentiation of normal tissues.
  • Recent studies have demonstrated that APC is also expressed in the adult brain at high levels.
  • In this study, we evaluated the expression of APC and its association with beta-catenin signaling pathway, following the induction of an excitotoxic lesion by kainic acid (KA) injection, which cause pyramidal cell degeneration.
  • APC was predominantly present in oligodendrocytes in the normal brain, but was specifically associated with activated astrocytes in the KA-treated brain.
  • Our quantitative analysis revealed that APC significantly increased from 1 day post lesion (PI), reached peak values at 3 days PI, and decreased thereafter.
  • The phospho-GSK3beta levels also showed similar spatiotemporal patterns while beta-catenin expression was reduced at 1 and then increasingly returned to normal levels at 3, 7 days PI.
  • For the first time, our data demonstrate the injury-induced astrocytic changes in the levels of APC, GSK3beta, and beta-catenin in vivo, which may actively be participate in cell adhesion and in the signaling pathway regulating cell survivals during brain insults.
  • [MeSH-major] Astrocytes / metabolism. Genes, APC. Hippocampus / drug effects. Kainic Acid / toxicity

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  • (PMID = 19655246.001).
  • [ISSN] 1573-6903
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Excitatory Amino Acid Agonists; 0 / beta Catenin; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; SIV03811UC / Kainic Acid
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66. Sinnamon MJ, Carter KJ, Fingleton B, Matrisian LM: Matrix metalloproteinase-9 contributes to intestinal tumourigenesis in the adenomatous polyposis coli multiple intestinal neoplasia mouse. Int J Exp Pathol; 2008 Dec;89(6):466-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Matrix metalloproteinase-9 contributes to intestinal tumourigenesis in the adenomatous polyposis coli multiple intestinal neoplasia mouse.
  • We previously demonstrated that genetic ablation of MMP-7 reduced tumour multiplicity in multiple intestinal neoplasia (Min) mice possessing a genetic alteration in the adenomatous polyposis coli gene (APC).
  • These mice, commonly referred to as APC-Min mice, are a frequently used model of early intestinal tumourigenesis.
  • To examine further the role of MMPs in intestinal tumour development, we generated APC-Min mice genetically deficient in MMP-2, -9, -12 or -19.
  • Genetic ablation of MMP-2, -12 or -19 did not affect multiplicity or size of intestinal tumours when crossed into the APC-Min system.
  • Intestinal adenomas from MMP-9 deficient mice demonstrated a 50% decrease in proliferating cells compared with control tissues, with no difference in apoptosis.
  • These studies extend the potential targets for chemoprevention of intestinal adenomas to MMP-9 in addition to MMP-7 and exclude MMP-2,-12,-19 as attractive targets for intervention.

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  • (PMID = 19134056.001).
  • [ISSN] 1365-2613
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA060867-08; United States / NCI NIH HHS / CA / CA068485-03S10006; United States / NCI NIH HHS / CA / P30 CA068485-03S10006; United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / CA009592-19; United States / NCI NIH HHS / CA / T32 CA009592; United States / NCI NIH HHS / CA / CA060867-08; United States / NCI NIH HHS / CA / T32 CA009592-19; United States / NCI NIH HHS / CA / R01 CA060867
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.- / Matrix Metalloproteinases, Secreted; EC 3.4.24.- / matrix metalloproteinase 19; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.65 / Matrix Metalloproteinase 12
  • [Other-IDs] NLM/ NIHMS180077; NLM/ PMC2669608
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67. Cai SR, Zhang SZ, Zheng S: [Detection of adenomatous polyposis coli gene mutations in 31 familial adenomatous polyposis families by using denaturing high performance liquid chromatography]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Apr;25(2):164-7
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  • [Title] [Detection of adenomatous polyposis coli gene mutations in 31 familial adenomatous polyposis families by using denaturing high performance liquid chromatography].
  • OBJECTIVE: To analyze the adenomatous polyposis coli (APC) gene mutations in familial adenomatous polyposis (FAP) in Chinese.
  • METHODS: DNA was extracted from blood samples taken from 31 FAP families, and all exons of the APC gene were amplified with touch-down PCR.
  • APC gene mutations were screened by denaturing high performance liquid chromatography followed by sequencing if abnormal profile was detected.
  • RESULTS: Twelve categories of APC gene mutations were found in 15 FAP families (48.39%) including 4 novel mutations in coding region and 3 mutations in introns.
  • Most mutations were clustered in exon 15 of APC gene leading to frameshift and accounted for 86.67%.
  • CONCLUSION: The mutation rate of the APC gene in this group of Chinese FAP families was about 48.39%, and 4 novel mutations were detected.
  • Frameshift mutation was the major mutation type in Chinese FAP and mainly located in exon 15.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Chromatography, High Pressure Liquid / methods. Genes, APC / physiology

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  • (PMID = 18393237.001).
  • [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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68. Rial NS, Lazennec G, Prasad AR, Krouse RS, Lance P, Gerner EW: Regulation of deoxycholate induction of CXCL8 by the adenomatous polyposis coli gene in colorectal cancer. Int J Cancer; 2009 May 15;124(10):2270-80
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Regulation of deoxycholate induction of CXCL8 by the adenomatous polyposis coli gene in colorectal cancer.
  • Elevated deoxycholic acid (DCA), mutations in the adenomatous polyposis coli (APC) gene and chronic inflammation are associated with increased risk of colorectal cancer.
  • APC status was manipulated to determine whether DCA mediates inflammatory molecules in normal or initiated colonic mucosa.
  • DCA increased steady state mRNA and protein levels of CXCL8 in cells which do not express wild-type APC.
  • Steady-state CXCL8 mRNA and protein were suppressed when cells with conditional expression of wild-type APC were exposed to DCA.
  • Immunostaining did not detect CXCL8 in normal human colonic mucosa.
  • CXCL8 was expressed in adenomatous polyps and adenocarcinomas.
  • CXCL8 expression correlated with nuclear beta-catenin localization in epithelial cells of adenomas, but was associated with endothelial cells and neutrophils in the adenocarcinomas.
  • DCA-mediated CXCL8 promoter-reporter activity was elevated in a mutant APC background.
  • Wild-type APC suppressed this effect.
  • Mutation of activator protein-1 (AP-1) or nuclear factor kappa B (NF-kappaB) sites suppressed the activation of the CXCL8 promoter-reporter by DCA.
  • Chromatin immunoprecipitation revealed that AP-1 and NF-kappaB binding to the 5'-promoter of CXCL8 was induced by DCA.
  • Phenotypic assays determined that DCA-mediated invasion was blocked by antibody-directed against CXCL8 or wild-type APC.
  • These data suggest that DCA-mediated CXCL8 occurs in initiated colonic epithelium and neutralizing CXCL8 could reduce the invasive potential of tumors.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 19173296.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / P01 CA072008-08; United States / NCI NIH HHS / CA / CA95060; United States / NCI NIH HHS / CA / CA123065-02; United States / NCI NIH HHS / CA / R01 CA123065-02; United States / NCI NIH HHS / CA / P01 CA072008-01A10001; United States / NCI NIH HHS / CA / P50 CA095060-07; United States / NCI NIH HHS / CA / CA072008-01A10001; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / R01 CA123065; United States / NCI NIH HHS / CA / CA095060-08; United States / NCI NIH HHS / CA / CA023074; United States / NCI NIH HHS / CA / P01 CA072008; United States / NCI NIH HHS / CA / CA095060-07; United States / NCI NIH HHS / CA / P50 CA095060-08; United States / NCI NIH HHS / CA / 2P01 CA041108; United States / NCI NIH HHS / CA / 2P30CA023074
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / IL8 protein, human; 0 / Interleukin-8; 0 / RNA, Messenger; 005990WHZZ / Deoxycholic Acid
  • [Other-IDs] NLM/ NIHMS98402; NLM/ PMC2669776
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69. Gaspar C, Cardoso J, Franken P, Molenaar L, Morreau H, Möslein G, Sampson J, Boer JM, de Menezes RX, Fodde R: Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)-driven tumorigenesis. Am J Pathol; 2008 May;172(5):1363-80
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)-driven tumorigenesis.
  • The majority of sporadic colorectal cancers are triggered by mutations in the adenomatous polyposis coli (APC) tumor suppressor gene, leading to the constitutive activation of the Wnt/beta-catenin signaling pathway and formation of adenomas.
  • Despite this common genetic basis, colorectal cancers are very heterogeneous in their degree of differentiation, growth rate, and malignancy potential.
  • Here, we applied a cross-species comparison of expression profiles of intestinal polyps derived from hereditary colorectal cancer patients carrying APC germline mutations and from mice carrying a targeted inactivating mutation in the mouse homologue Apc.
  • This comparative approach resulted in the establishment of a conserved signature of 166 genes that were differentially expressed between adenomas and normal intestinal mucosa in both species.
  • Functional analyses of the conserved genes revealed a general increase in cell proliferation and the activation of the Wnt/beta-catenin signaling pathway.
  • Moreover, the conserved signature was able to resolve expression profiles from hereditary polyposis patients carrying APC germline mutations from those with bi-allelic inactivation of the MYH gene, supporting the usefulness of such comparisons to discriminate among patients with distinct genetic defects.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli Protein / metabolism. Cell Transformation, Neoplastic / metabolism. Colorectal Neoplasms / pathology. Intestinal Polyps / metabolism


70. Chung CS, Jiang Y, Cheng D, Birt DF: Impact of adenomatous polyposis coli (APC) tumor supressor gene in human colon cancer cell lines on cell cycle arrest by apigenin. Mol Carcinog; 2007 Sep;46(9):773-82
Hazardous Substances Data Bank. ZINC CHLORIDE .

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  • [Title] Impact of adenomatous polyposis coli (APC) tumor supressor gene in human colon cancer cell lines on cell cycle arrest by apigenin.
  • This research assessed the importance of the adenomatous polyposis coli (APC) tumor suppressor mutation in the ability of apigenin to induce cell cycle arrest using HT29-APC cells, which contain inducible wild-type APC under the metallothionein promoter.
  • Treatment with apigenin (0, 20, 40, 60, and 80 microM) for 48 h resulted in reduction in the cell number (P < 0.05) concurrent with flow cytometry results showing a dose-dependent accumulation of cells in the G2/M phase in both HT29-APC and HT29-GAL cells without ZnCl(2) treatment.
  • Flow cytometric analysis showed an increase (P < 0.05) in the percentage of cells in G2/M when HT29-APC cells were treated with 80 microM apigenin for 120 h.
  • This increase was not present in HT29-APC cells when treated with both 80 microM apigenin and 100 microM ZnCl(2) for 120 h.
  • Western blot analysis verified the induction of APC protein expression in ZnCl(2)-treated HT29-APC cells but not in ZnCl(2)-treated HT29-GAL cells.
  • Apigenin plus ZnCl(2) treatment increased the expression of APC protein in HT29-APC cells by 50 fold above expression observed with ZnCl(2) alone.
  • Upon induction of the APC gene with ZnCl(2) in HT29-APC cells, the percentage of apoptotic cells increased significantly (P < 0.05) after 120-h treatment.
  • Additionally, apigenin treatment (80 microM) further increased the percentage of apopototic HT29-APC following ZnCl(2) treatment to induce wild-type APC expression.
  • These results suggest that APC dysfunction may be critical for apigenin to induce cell cycle arrest in human colon cancer cell lines and furthermore, apigenin enhances APC expression and apoptosis in cells with wild-type APC.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Apigenin / pharmacology. Cell Cycle / drug effects. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17620292.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [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 / Chlorides; 0 / Zinc Compounds; 7V515PI7F6 / Apigenin; 86Q357L16B / zinc chloride
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71. Kita K, Wittmann T, Näthke IS, Waterman-Storer CM: Adenomatous polyposis coli on microtubule plus ends in cell extensions can promote microtubule net growth with or without EB1. Mol Biol Cell; 2006 May;17(5):2331-45
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] Adenomatous polyposis coli on microtubule plus ends in cell extensions can promote microtubule net growth with or without EB1.
  • In interphase cells, the adenomatous polyposis coli (APC) protein accumulates on a small subset of microtubules (MTs) in cell protrusions, suggesting that APC may regulate the dynamics of these MTs.
  • We comicroinjected a nonperturbing fluorescently labeled monoclonal antibody and labeled tubulin to simultaneously visualize dynamics of endogenous APC and MTs in living cells.
  • MTs decorated with APC spent more time growing and had a decreased catastrophe frequency compared with non-APC-decorated MTs.
  • Endogenous APC associated briefly with shortening MTs.
  • To determine the relationship between APC and its binding partner EB1, we monitored EB1-green fluorescent protein and endogenous APC concomitantly in living cells.
  • Only a small fraction of EB1 colocalized with APC at any one time.
  • APC-deficient cells and EB1 small interfering RNA showed that EB1 and APC localized at MT ends independently.
  • Depletion of EB1 did not change the growth-stabilizing effects of APC on MT plus ends.
  • In addition, APC remained bound to MTs stabilized with low nocodazole, whereas EB1 did not.
  • Thus, we demonstrate that the association of endogenous APC with MT ends correlates directly with their increased growth stability, that this can occur independently of its association with EB1, and that APC and EB1 can associate with MT plus ends by distinct mechanisms.

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  • (PMID = 16525027.001).
  • [ISSN] 1059-1524
  • [Journal-full-title] Molecular biology of the cell
  • [ISO-abbreviation] Mol. Biol. Cell
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM061804; United States / NIGMS NIH HHS / GM / GM-61804
  • [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 / Antibodies, Monoclonal; 0 / Microtubule-Associated Proteins
  • [Other-IDs] NLM/ PMC1446093
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72. Brocardo M, Lei Y, Tighe A, Taylor SS, Mok MT, Henderson BR: Mitochondrial targeting of adenomatous polyposis coli protein is stimulated by truncating cancer mutations: regulation of Bcl-2 and implications for cell survival. J Biol Chem; 2008 Feb 29;283(9):5950-9
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] Mitochondrial targeting of adenomatous polyposis coli protein is stimulated by truncating cancer mutations: regulation of Bcl-2 and implications for cell survival.
  • The adenomatous polyposis coli (APC) protein tumor suppressor is mutated in the majority of colon cancers.
  • Most APC gene mutations cause deletion of the C terminus and disrupt APC regulation of beta-catenin turnover, microtubule dynamics, and chromosome segregation.
  • Truncated APC mutant peptides may also gain unique properties, not exhibited by wild-type APC, which contribute to tumor cell survival and proliferation.
  • Here we report a differential subcellular localization pattern for wild-type and mutant APC.
  • A pool of APC truncation mutants was detected at mitochondria by cellular fractionation and confocal microscopy.
  • In contrast, wild-type APC located poorly at mitochondria.
  • Similar results were observed for endogenous and stably induced forms of APC, with the shortest N-terminal mutant peptides (N750, N853, N1309, N1337) displaying the strongest mitochondrial staining.
  • The knock down of mutant APC(N1337) in SW480 tumor cells caused an increase in apoptosis and mitochondrial membrane permeability, and this correlated with reduced Bcl-2 protein levels in mitochondrial fractions.
  • Interestingly, the silencing of APC did not alter expression of beta-catenin or the apoptotic regulatory factors Bax, Bcl-xL, or survivin.
  • APC formed a complex with Bcl-2 in mitochondrial fractions, and this may contribute to the APC-dependent regulation of Bcl-2.
  • We propose that a subset of cancer mutations induce APC mitochondrial localization and that APC regulation of Bcl-2 at mitochondria may contribute to tumor cell survival.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Cell Proliferation. Colonic Neoplasms / metabolism. Mitochondria / metabolism. bcl-2-Associated X Protein / metabolism. bcl-X Protein / metabolism
  • [MeSH-minor] Amino Acid Sequence / genetics. Cell Line, Tumor. Cell Survival / genetics. Chromosome Segregation / genetics. Humans. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Microtubules / genetics. Microtubules / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Sequence Deletion / genetics. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 18160396.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 0 / beta Catenin
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73. Kaieda S, Matsui C, Mimori-Kiyosue Y, Ikegami T: Structural basis of the recognition of the SAMP motif of adenomatous polyposis coli by the Src-homology 3 domain. Biochemistry; 2010 Jun 29;49(25):5143-53
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  • [Title] Structural basis of the recognition of the SAMP motif of adenomatous polyposis coli by the Src-homology 3 domain.
  • Src-homology 3 (SH3) domains play critical roles in interaction networks of proteins by recognizing a proline-rich sequence motif, PxxP.
  • The SH3 domain of DDEF1 associates with the SAMP motifs of the adenomatous polyposis coli (APC) tumor suppressor.
  • The SAMP motifs are indispensable for the normal function of APC in tumor suppression.
  • Here we present the structural basis of the interaction between the DDEF1-SH3 domain and the APC-SAMP motifs.
  • We determined the solution structures of the DDEF1-SH3 domain both in a free state and in a complex with APC-SAMP.
  • As the affinity of the interaction was not sufficiently high for the determination of the complex structure in solution by conventional methods, we utilized a fusion protein of the DDEF1-SH3 domain and APC-SAMP.
  • The structures revealed that the SAMP motif adopts a class II polyproline type II helix even though it does not contain the PxxP motif and that a characteristically large hydrophobic pocket of the SH3 domain confers high selectivity to the interaction.
  • Furthermore, investigation into the backbone dynamics of the free and bound systems by NMR spin relaxation experiments demonstrated that the DDEF1-SH3 domain exhibits high flexibility at the peptide recognition site in the absence of the ligand and that most residues of the APC-SAMP motif display extensive local motions even in the stable complex.
  • [MeSH-major] Amino Acid Motifs. Genes, APC. src Homology Domains
  • [MeSH-minor] Amino Acid Sequence. Models, Molecular. Molecular Sequence Data. Nuclear Magnetic Resonance, Biomolecular. Protein Conformation. Sequence Homology, Amino Acid

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  • (PMID = 20509626.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 2RQT/ 2RQU
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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74. Eisinger AL, Nadauld LD, Shelton DN, Peterson PW, Phelps RA, Chidester S, Stafforini DM, Prescott SM, Jones DA: The adenomatous polyposis coli tumor suppressor gene regulates expression of cyclooxygenase-2 by a mechanism that involves retinoic acid. J Biol Chem; 2006 Jul 21;281(29):20474-82
ZFIN. ZFIN .

  • [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 gene regulates expression of cyclooxygenase-2 by a mechanism that involves retinoic acid.
  • Mutations in the adenomatous polyposis coli (APC) gene result in uncontrolled proliferation of intestinal epithelial cells and are associated with the earliest stages of colorectal carcinogenesis.
  • Cyclooxygenase-2 (COX-2) is elevated in human colorectal cancers and plays an important role in colorectal tumorigenesis; however, the mechanisms by which APC mutations result in increased COX-2 expression remain unclear.
  • We utilized APC mutant zebrafish and human cancer cells to investigate how APC modulates COX-2 expression.
  • We report that COX-2 is up-regulated in APC mutant zebrafish because of a deficiency in retinoic acid biosynthesis.
  • Treatment of both APC mutant zebrafish and human carcinoma cell lines with retinoic acid significantly reduces COX-2 expression.
  • APC mutant zebrafish express higher levels of C/EBP-beta than wild-type animals, and retinoic acid supplementation reduces C/EBP-beta expression to basal levels.
  • Both morpholino knockdown of C/EBP-beta in APC mutant zebrafish and silencing of C/EBP-beta using small interfering RNA in HT29 colon cancer cells robustly decrease COX-2 expression.
  • Our findings support a sequence of events in which mutations in APC result in impaired retinoic acid biosynthesis, elevated levels of C/EBP-beta, up-regulation of COX-2, increased prostaglandin E(2) accumulation, and activation of Wnt target genes.
  • [MeSH-minor] Alternative Splicing. Animals. Base Sequence. Cell Line. Cell Line, Tumor. DNA Primers. Dinoprostone / metabolism. Gene Expression Regulation, Enzymologic. Genes, APC. Humans. Morpholines. RNA, Messenger / genetics. Wnt Proteins / genetics. Zebrafish. beta Catenin / physiology

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  • (PMID = 16699180.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Morpholines; 0 / RNA, Messenger; 0 / Wnt Proteins; 0 / beta Catenin; 5688UTC01R / Tretinoin; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
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75. Potier M, Tran TA, Chantome A, Girault A, Joulin V, Bougnoux P, Vandier C, Pierre F: Altered SK3/KCa2.3-mediated migration in adenomatous polyposis coli (Apc) mutated mouse colon epithelial cells. Biochem Biophys Res Commun; 2010 Jun 18;397(1):42-7
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  • [Title] Altered SK3/KCa2.3-mediated migration in adenomatous polyposis coli (Apc) mutated mouse colon epithelial cells.
  • Lost of adenomatous polyposis coli gene (Apc) disturbs the migration of intestinal epithelial cells but the mechanisms have not been fully characterized.
  • Since we have demonstrated that SK3/KCa2.3 channel promotes cancer cell migration, we hypothesized that Apc mutation may affect SK3/KCa2.3 channel-mediated colon epithelial cell motility.
  • We report evidence that SK3/KCa2.3 channel promotes colon epithelial cells motility.
  • Following Apc mutation SK3/KCa2.3 expression is largely reduced leading to a suppression of the SK3/KCa2.3 channel mediated-cell migration.
  • Our findings reveal a previously unknown function of the SK3/KCa2.3 channel in epithelial colonic cells, and suggest that Apc is a powerful regulator SK3/KCa2.3 channel.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Cell Movement. Colon / metabolism
  • [MeSH-minor] Animals. Cell Line. Intestinal Mucosa / cytology. Intestinal Mucosa / metabolism. Mice. Mice, Mutant Strains. Small-Conductance Calcium-Activated Potassium Channels

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20519134.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [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 / Kcnn3 protein, mouse; 0 / Small-Conductance Calcium-Activated Potassium Channels
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76. Yokota Y, Kim WY, Chen Y, Wang X, Stanco A, Komuro Y, Snider W, Anton ES: The adenomatous polyposis coli protein is an essential regulator of radial glial polarity and construction of the cerebral cortex. Neuron; 2009 Jan 15;61(1):42-56
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  • [Title] The adenomatous polyposis coli protein is an essential regulator of radial glial polarity and construction of the cerebral cortex.
  • Using conditional gene targeting in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential function in the maintenance of polarized radial glial scaffold during brain development.
  • In the absence of APC, radial glial cells lose their polarity and responsiveness to the extracellular polarity maintenance cues, such as neuregulin-1.
  • Elimination of APC further leads to marked instability of the radial glial microtubule cytoskeleton.
  • The resultant changes in radial glial function and loss of APC in radial glial progeny lead to defective generation and migration of cortical neurons, severely disrupted cortical layer formation, and aberrant axonal tract development.
  • Thus, APC is an essential regulator of radial glial polarity and is critical for the construction of cerebral cortex in mammals.

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  • (PMID = 19146812.001).
  • [ISSN] 1097-4199
  • [Journal-full-title] Neuron
  • [ISO-abbreviation] Neuron
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS050968; United States / NIMH NIH HHS / MH / MH63660; United States / NIMH NIH HHS / MH / R01 MH060929-11; United States / NIMH NIH HHS / MH / R01 MH060929-10; United States / NIMH NIH HHS / MH / MH060929-10; United States / NINDS NIH HHS / NS / P30 NS045892; United States / NINDS NIH HHS / NS / NS050968; United States / NIMH NIH HHS / MH / R01 MH060929; United States / NIMH NIH HHS / MH / MH060929-11; United States / NIMH NIH HHS / MH / R01 MH063660; United States / NINDS NIH HHS / NS / NS045892
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Neuregulin-1; 0 / beta Catenin
  • [Other-IDs] NLM/ NIHMS92407; NLM/ PMC2804250
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77. Gerner EW, Ignatenko NA, Lance P, Hurley LH: A comprehensive strategy to combat colon cancer targeting the adenomatous polyposis coli tumor suppressor gene. Ann N Y Acad Sci; 2005 Nov;1059:97-105
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  • [Title] A comprehensive strategy to combat colon cancer targeting the adenomatous polyposis coli tumor suppressor gene.
  • Somatic cells in the majority of colorectal polyps and cancers contain mutations/deletions in the adenomatous polyposis coli (APC) tumor suppressor gene.
  • APC is involved in normal intestinal development and acts to influence a variety of cellular processes.
  • Loss of APC function leads to intestinal neoplasia in both mice and humans.
  • APC influences expression of specific genes, including the c-Myc oncogene, which functions as a transcriptional activator.
  • Loss of APC function leads to alterations in c-Myc-regulated genes including ornithine decarboxylase (ODC), the first enzyme in polyamine synthesis.
  • A single nucleotide polymorphism (SNP) in the ODC promoter affecting c-Myc-dependent expression has been associated with risk of colorectal and other cancers.
  • Pharmaceuticals that target structural features of the c-Myc promoter, and suppress expression of c-Myc and other genes regulated by similar promoter elements, are being developed as potential colorectal cancer chemotherapies.
  • APC and APC-dependent genes, such as c-Myc and ODC, may be useful as genetic markers of risk and as targets for chemoprevention and therapy for colorectal cancer.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Colonic Neoplasms / drug therapy. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Aspirin / pharmacology. Base Sequence. Eflornithine / pharmacology. Humans. Models, Biological. Molecular Sequence Data. Neoplasms / metabolism. Polymorphism, Single Nucleotide. Proto-Oncogene Proteins c-myc / metabolism

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  • (PMID = 16382048.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins c-myc; R16CO5Y76E / Aspirin; ZQN1G5V6SR / Eflornithine
  • [Number-of-references] 29
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78. Hebbar S, Guillotte AM, Mesngon MT, Zhou Q, Wynshaw-Boris A, Smith DS: Genetic enhancement of the Lis1+/- phenotype by a heterozygous mutation in the adenomatous polyposis coli gene. Dev Neurosci; 2008;30(1-3):157-70
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  • [Title] Genetic enhancement of the Lis1+/- phenotype by a heterozygous mutation in the adenomatous polyposis coli gene.
  • Hemizygous Lis1 mutations cause type 1 lissencephaly, a neuronal migration disorder in humans.
  • Because dynactin, a dynein regulator, interacts with end-binding protein 1 (EB1) and beta-catenin, two known binding partners of the adenomatous polyposis coli (APC) protein, we looked for a genetic interaction between Lis1 and APC.
  • Mice with a heterozygous truncating mutation in APC (Min mutation) do not exhibit neuronal migration defects or develop hydrocephalus.
  • However, the presence of the APC mutation increases the migration deficit and the incidence of hydrocephalus in Lis1+/- animals.
  • Lis1 and dynein distribution is altered in cells derived from Min mice, and both Lis1 and dynein interact with the C terminus of APC in vitro.
  • Together, our findings point to a previously unknown interaction between APC and Lis1 during mammalian brain development.
  • [MeSH-major] 1-Alkyl-2-acetylglycerophosphocholine Esterase / genetics. Adenomatous Polyposis Coli Protein / genetics. Genetic Predisposition to Disease / genetics. Hydrocephalus / genetics. Lissencephaly / genetics. Microtubule-Associated Proteins / genetics. Mutation / genetics
  • [MeSH-minor] Animals. Animals, Newborn. Brain / abnormalities. Brain / cytology. Brain / metabolism. Cell Movement / genetics. Cells, Cultured. Disease Models, Animal. Dyneins / genetics. Dyneins / metabolism. Female. Gene Expression Regulation, Developmental / genetics. Heterozygote. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Phenotype. Protein Structure, Tertiary / genetics

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
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  • (PMID = 18075263.001).
  • [ISSN] 1421-9859
  • [Journal-full-title] Developmental neuroscience
  • [ISO-abbreviation] Dev. Neurosci.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR017698; United States / NCRR NIH HHS / RR / P20 RR017698-08
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Microtubule-Associated Proteins; EC 3.1.1.47 / 1-Alkyl-2-acetylglycerophosphocholine Esterase; EC 3.1.1.47 / Pafah1b1 protein, mouse; EC 3.6.4.2 / Dyneins
  • [Other-IDs] NLM/ NIHMS287373; NLM/ PMC3097246
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79. Peng H, Zhong XY, Liu KP, Li SM: Expression and significance of adenomatous polyposis coli, beta-catenin, E-cadherin and cyclin D1 in esophageal squamous cell carcinoma assessed by tissue microarray. Ai Zheng; 2009 Jan;28(1):38-41
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  • [Title] Expression and significance of adenomatous polyposis coli, beta-catenin, E-cadherin and cyclin D1 in esophageal squamous cell carcinoma assessed by tissue microarray.
  • This study was to investigate the roles of four proteins in the Wnt pathway in tumorigenesis of ESCC, and their significances in the early diagnosis of ESCC.
  • METHODS: The expression of adenomatous polyposis coli (APC), beta-catenin, E-cadherin and cyclinD1 was detected by immunohistochemistry using tissue microarrays consisting of 199 specimens of ESCC, 164 specimens of normal mucosa, 34 specimens of basal cell hyperplasia and 30 specimens of dysplasia adjacent to cancer tissues.
  • RESULTS: The positive rates of APC and E-cadherin in ESCC were lower than those in the normal group (69.6% vs. 98.0%, p < 0.01; 19.6% vs. 96.3%, p < 0.01).
  • In accordance with the following order, normal epithelia --> basal cell hyperplasia --> dysplasia --> ESCC, hypoexpression of APC proteins occurred in ESCC, abnormalities of beta-catenin and E-cadherin started to appear in dysplasia, and overexpression of Cyclin D1 emerged from basal cell hyperplasia.
  • From well to poorly differentiated ESCC, the expression of APC, E-cadherin and cyclin D1 were gradually reduced, while beta-catenin was increased.
  • The expression of beta-catenin was not correlated with APC (r = -0.10, p > 0.05), was negatively correlated with E-cadherin (r = -0.31,p < 0.01) and positively correlated with cyclin D1(r = 0.49, p < 0.01).
  • CONCLUSION: APC, E-cadherin, beta-catenin and cyclin D1 may play important roles in tumorigenesis of ESCC.
  • Therefore, detection of E-cadherin, beta-catenin and cyclin D1 proteins may be helpful for the early diagnosis of ESCC.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / analysis. Cadherins / analysis. Carcinoma, Squamous Cell / chemistry. Cyclin D1 / analysis. Esophageal Neoplasms / chemistry. Tissue Array Analysis / methods. beta Catenin / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Genes, APC. Humans. Male. Middle Aged. Signal Transduction. Wnt Proteins / physiology


80. de Ferro SM, Suspiro A, Fidalgo P, Lage P, Rodrigues P, Fragoso S, Vitoriano I, Baltazar C, Albuquerque C, Bettencourt A, Leitão CN: Aggressive phenotype of MYH-associated polyposis with jejunal cancer and intra-abdominal desmoid tumor: report of a case. Dis Colon Rectum; 2009 Apr;52(4):742-5
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  • [Title] Aggressive phenotype of MYH-associated polyposis with jejunal cancer and intra-abdominal desmoid tumor: report of a case.
  • MYH-associated polyposis is an inherited autosomal recessive disease, linked to biallelic germline MYH mutations, which predisposes to the development of multiple colorectal adenomas and cancer.
  • The colonic and extracolonic phenotype of this syndrome is very heterogeneous.
  • We report the case of a young male patient with an aggressive MYH-associated polyposis phenotype.
  • At aged 35 years, Spigelman Stage IV duodenal adenomatosis was detected.
  • When he was 39 years old, he developed three synchronous jejunal adenocarcinomas and a mesenteric desmoid tumor.
  • Based on this report, we believe that screening of the entire small bowel should be recommended in MYH-associated polyposis patients, especially in those with duodenal adenomas.
  • Similar to patients with familial adenomatous polyposis, desmoid tumors also may be part of the clinical spectrum of MYH-associated polyposis and may prove to be a significant clinical problem in patients submitted to prophylactic colectomy.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms / genetics. Fibromatosis, Aggressive / genetics. Jejunal Neoplasms / genetics. Neoplasms, Multiple Primary / genetics. Peritoneal Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenoma / genetics. Adult. DNA Glycosylases / genetics. Duodenal Neoplasms / genetics. Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Intestinal Neoplasms / genetics. Intestinal Obstruction / etiology. Liver Neoplasms / secondary. Male. Mesentery. Mutation. Phenotype. Syndrome

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  • (PMID = 19404084.001).
  • [ISSN] 1530-0358
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases
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81. Bortlik M, Vitkova I, Papezova M, Kohoutova M, Novotny A, Adamec S, Chalupna P, Lukas M: Deficiency of Adenomatous Polyposis Coli protein in sporadic colorectal adenomas and its associations with clinical phenotype and histology. World J Gastroenterol; 2006 Jun 28;12(24):3901-5
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  • [Title] Deficiency of Adenomatous Polyposis Coli protein in sporadic colorectal adenomas and its associations with clinical phenotype and histology.
  • AIM: To evaluate the frequency of the loss of the Adenomatous Polyposis Coli (APC) protein and to compare the APC status with the characteristics of colorectal adenomas.
  • METHODS: Immunohistochemical analysis of the APC protein was performed on 118 adenomas and the results were compared with parameters of malignant potential, location of adenomas, macroscopic appearance and age of the patients.
  • RESULTS: A complete loss of the APC protein was found in 28 (24%) adenomas, while 90 (76%) were APC positive.
  • The mean size of adenomas was 13.5 +/- 14.2 mm (95% CI 10.5-16.5) in APC-positive, and 13.8 +/- 15.5 mm (95% CI 7.8-19.8) in APC-negative adenomas (P = 0.364).
  • Statistical analysis revealed no difference between APC-positive and negative adenomas as to the histological type (P = 0.327) and grade of dysplasia (P = 0.494).
  • We found that even advanced adenomas did not differ in their APC status from the non-advanced tumors (P = 0.414).
  • Finally, no difference was found when the location (P = 0.157), macroscopic appearance (P = 0.571) and age of patients (P = 0.438) were analysed and compared between both APC positive and negative adenomas.
  • CONCLUSION: Most adenomas expressed full-length APC protein, suggesting that protein expression is not a reliable marker for assessment of APC gene mutation.
  • Complete loss of APC protein did not influence morphology, location, or appearance of adenomas, nor was it affected by the patient's age.
  • [MeSH-major] Adenoma / genetics. Adenoma / pathology. Adenomatous Polyposis Coli Protein / genetics. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology

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  • (PMID = 16804979.001).
  • [ISSN] 1007-9327
  • [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 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC4087942
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82. Jiang RZ, Zhu EX, Liu TJ: [Expression of beta-catenin and adenomatous polyposis coli protein and correlation between them in the development of mouse tooth germ]. Hua Xi Kou Qiang Yi Xue Za Zhi; 2009 Aug;27(4):370-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of beta-catenin and adenomatous polyposis coli protein and correlation between them in the development of mouse tooth germ].
  • OBJECTIVE: To examine the distributions of beta-catenin and adenomatous polyposis coli (APC) protein in the tooth germ, and obtain the messages of function of the two factors and the relationship between them.
  • METHODS: Mice were selected and cohabited with the ratio of female mice to male ones being 2:1, and Embryo day 0.5 was confirmed based on the finding of vaginal plug.
  • The distributions of beta-catenin and APC protein in the Embryos on day 13.5, 14.5, 15.5, 16.5, 17.5 were examined in the paraffin-embedded sections by immunohistochemistry methods.
  • During the bud stage, strong positive expression of APC protein was found in the oral epithelium and the dental lamina, but the expression displayed a down-regulation tendency.
  • There was negative correlation between beta-catenin and APC protein (P<0.01).
  • [MeSH-major] Adenomatous Polyposis Coli Protein. beta Catenin
  • [MeSH-minor] Animals. Cytoskeletal Proteins. Female. Immunohistochemistry. Male. Mice. Tooth Germ

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  • (PMID = 19769251.001).
  • [ISSN] 1000-1182
  • [Journal-full-title] Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology
  • [ISO-abbreviation] Hua Xi Kou Qiang Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cytoskeletal Proteins; 0 / beta Catenin
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83. Zhang WM, Gao Y: [Roles of Wnt-1, beta-catenin and adenomatous polyposis coli in the differentiation and proliferation of oral squamous cell carcinoma]. Zhonghua Kou Qiang Yi Xue Za Zhi; 2005 Nov;40(6):491-4
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  • [Title] [Roles of Wnt-1, beta-catenin and adenomatous polyposis coli in the differentiation and proliferation of oral squamous cell carcinoma].
  • OBJECTIVE: To investigate the expressions of Wnt-1, beta-catenin and adenomatous polyposis coli (APC) in oral squamous cell carcinoma (OSCC).
  • METHODS: Surgical specimens from 66 OSCC patients were examined for Wnt-1, beta-catenin, APC and MIB-1 expressions by immunohistochemical staining.
  • RESULTS: Among all the 37 cases of well differentiated OSCCs, there were 30, 25 and 31 cases of high expressions of Wnt-1, APC and beta-catenin, respectively, 7, 12 and 6 cases of low expressions.
  • Among all the 29 cases of moderate and poor differentiated OSCCs, there were 6, 9 and 11 cases of high expressions of Wnt-1, APC and beta-catenin respectively, 23, 20 and 18 cases of low expressions.
  • Among all the 66 cases of OSCCs, there were 32 cases of high expressions of MIB-1 and 34 cases of low expressions.
  • Expressions of Wnt-1, beta-catenin and APC showed significant difference in different differentiation of OSCC.
  • CONCLUSIONS: Wnt-1, beta-catenin and APC expressions were related to the differentiation of OSCC.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Carcinoma, Squamous Cell / metabolism. Cell Differentiation. Cell Proliferation. Mouth Neoplasms / metabolism. Wnt1 Protein / metabolism. beta Catenin / metabolism

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  • (PMID = 16329837.001).
  • [ISSN] 1002-0098
  • [Journal-full-title] Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology
  • [ISO-abbreviation] Zhonghua Kou Qiang Yi 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 / Wnt1 Protein; 0 / beta Catenin
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84. Senda T, Iizuka-Kogo A, Onouchi T, Shimomura A: Adenomatous polyposis coli (APC) plays multiple roles in the intestinal and colorectal epithelia. Med Mol Morphol; 2007 Jun;40(2):68-81
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  • [Title] Adenomatous polyposis coli (APC) plays multiple roles in the intestinal and colorectal epithelia.
  • The adenomatous polyposis coli (APC) gene is mutated in familial adenomatous polyposis and in most sporadic colorectal tumors.
  • During both embryonic and postnatal periods, APC is widely expressed in a variety of tissues, including the brain and gastrointestinal tract.
  • The APC gene product (APC) is a large multidomain protein consisting of 2843 amino acids.
  • APC downregulates the Wnt signaling pathway through its binding to beta-catenin and Axin.
  • Most mutated APC proteins in colorectal tumors lack the beta-catenin-binding regions and fail to inhibit Wnt signaling, leading to the overproliferation of tumor cells.
  • Several mouse models (APC580D, APCDelta716, APC1309, APCMin, APC1638T) have been established to investigate carcinogenesis caused by APC mutations.
  • APC also binds to APC-stimulated guanine nucleotide exchange factor, the kinesin superfamily-associated protein 3, IQGAP1, microtubules, EB1, and discs large (DLG).
  • APC has both nuclear localization signals and nuclear export signals in its molecule, suggesting its occasional nuclear localization and export of beta-catenin from the nucleus.
  • APC is highly expressed in the intestinal and colorectal epithelia and may be involved in homeostasis of the enterocyte renewal phenomena, in which proliferation, migration, differentiation, and apoptosis are highly regulated both temporally and spatially.
  • Through the many binding proteins mentioned, APC can exert multiple functions involved in epithelial homeostasis.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Colon / physiopathology. Colorectal Neoplasms / physiopathology. Repressor Proteins / metabolism
  • [MeSH-minor] Animals. Binding Sites / genetics. Epithelium / physiology. Epithelium / physiopathology. Gene Expression Regulation, Neoplastic. Genes, APC. Humans. Mice. Mice, Knockout. Microtubules / metabolism. Mutation / genetics. Protein Binding / genetics. Rats. Signal Transduction


85. Kroboth K, Newton IP, Kita K, Dikovskaya D, Zumbrunn J, Waterman-Storer CM, Näthke IS: Lack of adenomatous polyposis coli protein correlates with a decrease in cell migration and overall changes in microtubule stability. Mol Biol Cell; 2007 Mar;18(3):910-8
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  • [Title] Lack of adenomatous polyposis coli protein correlates with a decrease in cell migration and overall changes in microtubule stability.
  • Most sporadic colorectal tumors carry truncation mutations in the adenomatous polyposis coli (APC) gene.
  • The APC protein is involved in many processes that govern gut tissue.
  • In addition to its involvement in the regulation of beta-catenin, APC is a cytoskeletal regulator with direct and indirect effects on microtubules.
  • Cancer-related truncation mutations lack direct and indirect binding sites for microtubules in APC, suggesting that loss of this function contributes to defects in APC-mutant cells.
  • In this study, we show that loss of APC results in disappearance of cellular protrusions and decreased cell migration.
  • Consistent with the ability of APC to affect cell shape, the overexpression of APC in cells can induce cellular protrusions.
  • These data demonstrate that cell migration and microtubule stability are linked to APC status, thereby revealing a weakness in APC-deficient cells with potential therapeutic implications.


86. Kastritis E, Murray S, Kyriakou F, Horti M, Tamvakis N, Kavantzas N, Patsouris ES, Noni A, Legaki S, Dimopoulos MA, Bamias A: Somatic mutations of adenomatous polyposis coli gene and nuclear b-catenin accumulation have prognostic significance in invasive urothelial carcinomas: evidence for Wnt pathway implication. Int J Cancer; 2009 Jan 1;124(1):103-8
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  • [Title] Somatic mutations of adenomatous polyposis coli gene and nuclear b-catenin accumulation have prognostic significance in invasive urothelial carcinomas: evidence for Wnt pathway implication.
  • Wnt pathway signaling is crucial in many cancers and data indicate crosstalk with other key cancer pathways, however in urothelial carcinogenesis it has not been extensively studied.
  • We searched for mutations in adenomatous polyposis coli (APC), a key regulator of the pathway, and studied b-catenin expression and interactions with the expression of other markers of apoptosis, angiogenesis, and proliferation in patients with invasive urothelial cancer.
  • The mutation cluster region of APC was directly sequenced in 70 patients with muscle invasive disease who were treated with surgery and adjuvant chemotherapy.
  • Patients having either APC missense mutations or b-catenin nuclear accumulation had less frequent COX-2 overexpression (24% vs. 76%, p = 0.043) and more frequent lymph node involvement (75% vs. 38%, p = 0.023).
  • Patients with either APC mutations or b-catenin accumulation had shorter disease-free interval (13.4 vs. 28 months, p = 0.07), whereas in multivariate analysis they had shorter disease-specific survival (60.5 vs. 20.6 months, p = 0.048).
  • Somatic APC missense mutations are not rare in advanced urothelial neoplasms.
  • Either APC mutations and/or aberrant expression of b-catenin are associated with worse outcome.
  • Further study of the role of the Wnt pathway, potential crosstalk with other pathways and potential candidate therapeutic targets in urothelial cancer is needed.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Carcinoma / genetics. Cell Nucleus / metabolism. Mutation. Urinary Bladder Neoplasms / genetics. Urothelium / pathology. Wnt Proteins / metabolism. beta Catenin / biosynthesis

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  • (PMID = 18844223.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents; 0 / Wnt Proteins; 0 / beta Catenin; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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87. Wong NC, Novakovic B, Weinrich B, Dewi C, Andronikos R, Sibson M, Macrae F, Morley R, Pertile MD, Craig JM, Saffery R: Methylation of the adenomatous polyposis coli (APC) gene in human placenta and hypermethylation in choriocarcinoma cells. Cancer Lett; 2008 Sep 8;268(1):56-62
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  • [Title] Methylation of the adenomatous polyposis coli (APC) gene in human placenta and hypermethylation in choriocarcinoma cells.
  • Methylation of the human APC gene promoter is associated with several different types of cancers and has also been documented in some pre-cancerous tissues.
  • We have examined the methylation of APC gene promoters in human placenta and choriocarcinoma cells.
  • This revealed a general hypomethylation of the APC-1b promoter and a pattern with monoallelic methylation of the APC-1a promoter in full term placental tissue.
  • Increased methylation of this promoter was observed in all choriocarcinoma-derived trophoblast cell lines, suggesting a trophoblastic origin of placental APC methylation and implicating APC hypermethylation in the development of this group of gestational tumours.
  • Our demonstration of placental methylation of the APC-1a promoter represents the first observation of monoallelic methylation of this gene in early development, and provides further support for a role of canonical Wnt signalling in placental trophoblast invasiveness.
  • [MeSH-major] Choriocarcinoma / genetics. DNA Methylation. Genes, APC. Placenta / metabolism

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  • (PMID = 18485586.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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88. Ki H, Oh M, Chung SW, Kim K: Beta-catenin can bind directly to CRM1 independently of adenomatous polyposis coli, which affects its nuclear localization and LEF-1/beta-catenin-dependent gene expression. Cell Biol Int; 2008 Apr;32(4):394-400
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  • [Title] Beta-catenin can bind directly to CRM1 independently of adenomatous polyposis coli, which affects its nuclear localization and LEF-1/beta-catenin-dependent gene expression.
  • However, the precise mechanism for the nuclear export of beta-catenin is not completely understood.
  • We found that beta-catenin can bind directly to CRM1 through its central armadillo (ARM) repeats region, independently of the adenomatous polyposis coli (APC) protein.
  • CRM1 competed with E-cadherin and LEF-1 for binding to beta-catenin. beta-catenin could interact directly with APC through its essential sequences between amino acids 342 and 350.
  • The site-directed beta-catenin mutant (NES2(-)), which could interact with CRM1, but not with APC, still retained its ability to export from the nucleus and its transactivational activity.
  • This suggests that CRM1 can function as an efficient nuclear exporter for beta-catenin independently of APC.
  • [MeSH-minor] Active Transport, Cell Nucleus. Adenomatous Polyposis Coli Protein / metabolism. Amino Acid Sequence. Animals. Binding, Competitive. Cadherins / metabolism. Mice. Models, Biological. Molecular Sequence Data. NIH 3T3 Cells. Nuclear Export Signals. Protein Binding. Repetitive Sequences, Amino Acid

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  • (PMID = 18262809.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [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 / Cadherins; 0 / Karyopherins; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Nuclear Export Signals; 0 / Receptors, Cytoplasmic and Nuclear; 0 / beta Catenin; 0 / exportin 1 protein
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89. Koester MP, Müller O, Pollerberg GE: Adenomatous polyposis coli is differentially distributed in growth cones and modulates their steering. J Neurosci; 2007 Nov 14;27(46):12590-600
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  • [Title] Adenomatous polyposis coli is differentially distributed in growth cones and modulates their steering.
  • Axonal steering reactions depend on the transformation of environmental information into internal, directed structures, which is achieved by differential modulation of the growth cone cytoskeleton; key elements are the microtubules, which are regulated in their dynamics by microtubule-associated proteins (MAPs).
  • We investigated a potential role of the MAP adenomatous polyposis coli (APC) for growing axons, employing embryonic visual system as a model system.
  • APC is concentrated in the distalmost (i.e., growing) region of retinal ganglion cell axons in vivo and in vitro.
  • Within the growth cone, APC is enriched in the central domain; it only partially colocalizes with microtubules.
  • When axons are induced to turn toward a cell or away from a substrate border, APC is present in the protruding and absent from the collapsing growth cone regions, thus indicating the future growth direction of the axon.
  • To assess the functional role of the differential distribution of APC in navigating growth cones, the protein was inactivated via micro-scale chromophore-assisted laser inactivation in one half of the growth cone.
  • If the N-terminal APC region (crucial for its oligomerization) is locally inactivated, the treated growth cone side collapses and the axon turns away.
  • In contrast, if the 20 aa repeats in the middle region of APC (which can negatively regulate its microtubule association) are inactivated, protrusions are formed and the growth cone turns toward.
  • Our data thus demonstrate a crucial role of APC for axon steering attributable to its multifunctional domain structure and differential distribution in the growth cone.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Cell Differentiation / physiology. Central Nervous System / embryology. Central Nervous System / metabolism. Growth Cones / metabolism
  • [MeSH-minor] Animals. Body Patterning / physiology. Body Patterning / radiation effects. Cell Communication / physiology. Chick Embryo. Chickens. Humans. Lasers. Microtubules / metabolism. Microtubules / ultrastructure. Protein Structure, Tertiary / physiology. Protein Structure, Tertiary / radiation effects. Retinal Ganglion Cells / cytology. Retinal Ganglion Cells / metabolism. Retinal Ganglion Cells / radiation effects. Visual Pathways / cytology. Visual Pathways / embryology. Visual Pathways / metabolism

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  • (PMID = 18003838.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [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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90. Takizawa S, Nagasaka K, Nakagawa S, Yano T, Nakagawa K, Yasugi T, Takeuchi T, Kanda T, Huibregtse JM, Akiyama T, Taketani Y: Human scribble, a novel tumor suppressor identified as a target of high-risk HPV E6 for ubiquitin-mediated degradation, interacts with adenomatous polyposis coli. Genes Cells; 2006 Apr;11(4):453-64
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  • [Title] Human scribble, a novel tumor suppressor identified as a target of high-risk HPV E6 for ubiquitin-mediated degradation, interacts with adenomatous polyposis coli.
  • Recently, we have identified human scribble (hScrib), human homolog of the Drosophila tumor suppressor Scribble, as a substrate of human papillomavirus E6 oncoproteins for ubiquitin-mediated degradation dependent on ubiquitin-protein ligase E6AP.
  • Human Scribble, classified as a LAP protein containing leucine-rich repeats and PDZ domains, interacts with E6 through its PDZ domains and C-terminal PDZ domain-binding motif of E6 protein.
  • Interaction between human Discs Large (hDlg), which is a substrate of E6 for the ubiquitin-mediated degradation, and adenomatous polyposis coli (APC) has been shown.
  • Here, we investigated whether hScrib and APC interact with each other in vitro and in vivo.
  • Interaction between hScrib and APC is mediated by the PDZ domains 1 and 4 of hScrib and C-terminal PDZ domain-binding motif of APC.
  • Human Scribble co-localized with APC at the synaptic sites of hippocampal neuron and at the tip of membrane protrusion in the epithelial cell line.
  • Interference of the interaction between hScrib and APC caused disruption of adherens junction.
  • Knockdown of hScrib expression by RNAi disrupts localization of APC at the adherens junction.
  • These data suggest that hScrib may participate in the hDlg-APC complex through its PDZ domains and regulate cell cycle and neural function by associating with APC.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Membrane Proteins / metabolism. Oncogene Proteins, Viral / genetics. Tumor Suppressor Proteins / metabolism. Ubiquitin / metabolism. Ubiquitin-Protein Ligases / metabolism


91. Ramburan A, Oladiran F, Smith C, Hadley GP, Govender D: Microsatellite analysis of the adenomatous polyposis coli (APC) gene and immunoexpression of beta catenin in nephroblastoma: a study including 83 cases treated with preoperative chemotherapy. J Clin Pathol; 2005 Jan;58(1):44-50
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  • [Title] Microsatellite analysis of the adenomatous polyposis coli (APC) gene and immunoexpression of beta catenin in nephroblastoma: a study including 83 cases treated with preoperative chemotherapy.
  • AIMS: To determine whether microsatellite mutations of the adenomatous polyposis coli (APC) gene have pathological or prognostic significance in nephroblastomas and to correlate APC alterations with beta catenin immunoexpression.
  • Polymerase chain reaction using four APC microsatellite markers-D5S210, D5S299, D5S82, and D5S346-was performed and the products analysed.
  • Although there was a significant correlation between the results for individual markers and the clinicopathological data, the overall results do not support a prognostic role for APC in nephroblastoma.
  • CONCLUSION: Microsatellite analysis of APC and immunoexpression of beta catenin did not provide significant pathological or prognostic information in this cohort of nephroblastomas.
  • [MeSH-major] Cytoskeletal Proteins / metabolism. Genes, APC. Kidney Neoplasms / genetics. Microsatellite Repeats / genetics. Trans-Activators / metabolism. Wilms Tumor / genetics

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  • (PMID = 15623481.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC1770552
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92. Balusu R, Jaiswal AS, Armas ML, Kundu CN, Bloom LB, Narayan S: Structure/function analysis of the interaction of adenomatous polyposis coli with DNA polymerase beta and its implications for base excision repair. Biochemistry; 2007 Dec 11;46(49):13961-74
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  • [Title] Structure/function analysis of the interaction of adenomatous polyposis coli with DNA polymerase beta and its implications for base excision repair.
  • Mutations in the adenomatous polyposis coli (APC) gene are associated with an early onset of colorectal carcinogenesis.
  • Previously, we described a novel role for the APC polypeptide in base excision repair (BER).
  • We have shown that APC interacts with DNA polymerase beta (Pol-beta) and flap endonuclease 1 (Fen-1) and blocks Pol-beta-directed strand-displacement synthesis.
  • In this study, we have mapped the APC interaction site in Pol-beta and have found that Thr79, Lys81, and Arg83 of Pol-beta were critical for its interaction with APC.
  • The Pol-beta protein (T79A/K81A/R83A) blocked strand-displacement DNA synthesis in which tetrahydrofuran was used as DNA substrate.
  • We further showed that the APC-mediated blockage of LP-BER was due to inhibition of Fen-1 activity.
  • Analysis of the APC-mediated blockage of SN-BER indicated that the interaction of APC with Pol-beta blocked SN-BER activity by inhibiting Pol-beta-directed deoxyribose phosphate lyase activity.
  • Collectively, our findings indicate that APC blocked both Pol-beta-directed SN- and LP-BER pathways and increased sensitivity of cells to alkylation induced DNA damage.

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  • (PMID = 17999539.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [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 / 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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; AT5C31J09G / Methyl Methanesulfonate; EC 2.7.7.- / 5'-deoxyribose phosphate lyase; EC 2.7.7.- / DNA Polymerase beta; EC 4.6.- / Phosphorus-Oxygen Lyases
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93. Leite JS, Isidro G, Martins M, Regateiro F, Albuquerque O, Amaro P, Romãozinho JM, Boavida G, Castro-Sousa F: Is prophylactic colectomy indicated in patients with MYH-associated polyposis? Colorectal Dis; 2005 Jul;7(4):327-31
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  • [Title] Is prophylactic colectomy indicated in patients with MYH-associated polyposis?
  • OBJECTIVES: The MYH gene has recently been associated with multiple colorectal tumours.
  • It participates in the DNA base-excision-repair, avoiding mutations in other genes, namely the APC and Ki-ras.
  • Recently, biallelic MYH mutations have been described in patients with attenuated polyposis and in 7.5% with classic polyposis and no detectable APC mutation.
  • The aim of this study was to analyse the incidence of germ-line MYH mutations in selected Portuguese families recorded in a hereditary tumour registry and to evaluate the risk of colorectal cancer in this syndrome.
  • PATIENTS AND METHODS: Nineteen APC mutation negative patients, 13 presenting attenuated polyposis and 6 with classic familial adenomatous polyposis (> 100 adenomas), were screened for germline biallelic MYH mutations.
  • RESULTS: Biallelic germline mutations in MYH were identified in 9 of the attenuated polyposis and in one of the classic polyposis patients.
  • The mean age at the clinical diagnosis was 50.6 years (from 35 to 69 years); six were men and four women.
  • Five patients belonged to families with affected siblings; three showed evidence for vertical transmission and two had no evidence for familial transmission of the disease.
  • Eight patients had associated malignant degeneration: three T3N+, four T3N0 and one T1N+.
  • CONCLUSION: A large frequency of biallelic MYH mutations (69%) was found in APC mutation negative patients belonging to families with attenuated polyposis; the highest percentage was observed in families presenting evidence for horizontal transmission of the disease.
  • The high percentage of degeneration found in these patients suggests that colonoscopy with polypectomies is not sufficient and prophylactic colectomy is recommended.
  • The identification of MYH associated polyposis is important to evaluate the level of risk, particularly for the siblings.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / surgery. Colorectal Neoplasms / prevention & control. Myosin Heavy Chains / genetics
  • [MeSH-minor] Adult. Aged. Colectomy. Female. Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Male. Middle Aged. Portugal. Risk

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  • (PMID = 15932553.001).
  • [ISSN] 1462-8910
  • [Journal-full-title] Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
  • [ISO-abbreviation] Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.6.4.1 / Myosin Heavy Chains
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94. Li Z, Näthke IS: Tumor-associated NH2-terminal fragments are the most stable part of the adenomatous polyposis coli protein and can be regulated by interactions with COOH-terminal domains. Cancer Res; 2005 Jun 15;65(12):5195-204
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  • [Title] Tumor-associated NH2-terminal fragments are the most stable part of the adenomatous polyposis coli protein and can be regulated by interactions with COOH-terminal domains.
  • Truncation mutations in the adenomatous polyposis coli (APC) gene are responsible for familial and sporadic colorectal cancer.
  • APC is a large, multifunctional protein involved in cell migration, proliferation, and differentiation.
  • Dominant effects that have been attributed to the NH2-terminal fragments of APC expressed in tumors may result from loss of functions due to lack of COOH-terminal regions or gain of functions due to fewer regulatory interactions.
  • Resolving this issue and determining how structural changes contribute to the multiple functions of the APC protein requires knowledge about the structural organization of the APC molecule.
  • We discovered that the NH2-terminal region of APC was most resistant to proteolytic degradation, whereas middle and COOH-terminal regions were significantly more sensitive.
  • Binding of APC to microtubules protected COOH-terminal regions of APC against proteolysis, consistent with the idea that this region of the molecule becomes ordered when bound to microtubules.
  • Furthermore, interactions between the NH2- and COOH-terminal domains of APC were identified in vitro and in vivo, suggesting that NH2-terminal fragments of APC may be regulated by interactions with COOH-terminal domains.
  • Indeed, expressing COOH-terminal APC fragments in tumor cells resulted in changes in the protein interactions of endogenous NH2-terminal fragments in these cells.
  • Thus, the dominant function of NH2-terminal APC fragments found in tumor cells could be explained by loss of this regulation in tumors where COOH-terminal domains are missing.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Peptide Fragments / metabolism
  • [MeSH-minor] Cell Line, Tumor. HeLa Cells. Humans. Immunoprecipitation. Microtubules / metabolism. Peptide Hydrolases / metabolism. Phosphorylation. Protein Conformation. Protein Structure, Tertiary

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  • (PMID = 15958564.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Peptide Fragments; EC 3.4.- / Peptide Hydrolases
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95. Moseley JB, Bartolini F, Okada K, Wen Y, Gundersen GG, Goode BL: Regulated binding of adenomatous polyposis coli protein to actin. J Biol Chem; 2007 Apr 27;282(17):12661-8
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  • [Title] Regulated binding of adenomatous polyposis coli protein to actin.
  • Adenomatous polyposis coli (APC) protein is a large tumor suppressor that is truncated in most colorectal cancers.
  • The carboxyl-terminal third of APC protein mediates direct interactions with microtubules and the microtubule plus-end tracking protein EB1.
  • In addition, APC has been localized to actin-rich regions of cells, but the mechanism and functional significance of this localization have remained unclear.
  • Here we show that purified carboxyl-terminal basic domain of human APC protein (APC-basic) bound directly to and bundled actin filaments and associated with actin stress fibers in microinjected cells.
  • Actin filaments and microtubules competed for binding to APC-basic, but APC-basic also could cross-link actin filaments and microtubules at specific concentrations, suggesting a possible role in cytoskeletal cross-talk.
  • APC interactions with actin in vitro were inhibited by its ligand EB1, and co-microinjection of EB1 prevented APC association with stress fibers.
  • Point mutations in EB1 that disrupted APC binding relieved the inhibition in vitro and restored APC localization to stress fibers in vivo, demonstrating that EB1-APC regulation is direct.
  • Because tumor formation and metastasis involve coordinated changes in the actin and microtubule cytoskeletons, this novel function for APC and its regulation by EB1 may have direct implications for understanding the molecular basis of tumor suppression.
  • [MeSH-major] Actin Cytoskeleton / chemistry. Adenomatous Polyposis Coli Protein / chemistry. Stress Fibers / chemistry
  • [MeSH-minor] Animals. Humans. Mice. NIH 3T3 Cells. Neoplasms / metabolism. Point Mutation. Protein Binding / genetics. Protein Structure, Tertiary / genetics

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  • (PMID = 17293347.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM062939; Italy / Telethon / / TI/ GFP03006; United States / NIGMS NIH HHS / GM / GM062939; United States / NIGMS NIH HHS / GM / GM63691
  • [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
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96. Catimel B, Nice EC, Kärrlander M, Ross J, Catimel J, Burgess AW, Faux M: Purification and characterization of a high specificity polyclonal antibody to the adenomatous polyposis coli tumour suppressor protein. Biomed Chromatogr; 2006 Jun-Jul;20(6-7):569-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Purification and characterization of a high specificity polyclonal antibody to the adenomatous polyposis coli tumour suppressor protein.
  • Recombinant proteins, commonly expressed in fusion with an affinity tag to facilitate purification, are often used as immunogens for polyclonal antibody production.
  • Careful immunopurification of the antibody product is often the key to obtaining a high-specificity polyclonal antibody against the protein domain of interest.
  • This study describes the purification and characterization of such an antibody directed against the adenomatous polyposis coli (APC) tumour suppressor.
  • This antibody was then characterized by immunoprecipitation, proteomic analyses and immunofluorescence staining and shown to be a valuable reagent for the study of APC biology.
  • Using this antibody we successfully isolated and identified APC, using MS/MS, from transfected cell lines.
  • A novel phosphorylation site on APC was identified at ser 1436.
  • Similar strategies involving multiple immuno-affinity steps coupled with surface plasmon resonance (SPR), immunoprecipitation proteomic and immunofluorescence analyses should be generally applicable for the purification and characterization of other polyclonal antibodies.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / immunology. Antibodies / isolation & purification

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  • [Copyright] Copyright 2006 John Wiley & Sons, Ltd.
  • (PMID = 16779787.001).
  • [ISSN] 0269-3879
  • [Journal-full-title] Biomedical chromatography : BMC
  • [ISO-abbreviation] Biomed. Chromatogr.
  • [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 / Antibodies
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97. Yang J, Zhang W, Evans PM, Chen X, He X, Liu C: Adenomatous polyposis coli (APC) differentially regulates beta-catenin phosphorylation and ubiquitination in colon cancer cells. J Biol Chem; 2006 Jun 30;281(26):17751-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenomatous polyposis coli (APC) differentially regulates beta-catenin phosphorylation and ubiquitination in colon cancer cells.
  • Most colorectal cancers have mutations of the adenomatous polyposis coli (APC) gene or the beta-catenin gene that stabilize beta-catenin and activate beta-catenin target genes, leading ultimately to cancer.
  • The molecular mechanisms of APC function in beta-catenin degradation are not completely known.
  • APC binds beta-catenin and is involved in the Axin complex, suggesting that APC regulates beta-catenin phosphorylation.
  • Some evidence also suggests that APC regulates beta-catenin nuclear export.
  • Here, we examine the effects of APC mutations on beta-catenin phosphorylation, ubiquitination, and degradation in the colon cancer cell lines SW480, DLD-1, and HT29, each of which contains a different APC truncation.
  • Although the current models suggest that beta-catenin phosphorylation should be inhibited by APC mutations, we detected significant beta-catenin phosphorylation in these cells.
  • However, beta-catenin ubiquitination and degradation were inhibited in SW480 but not in DLD-1 and HT29 cells.
  • The ubiquitination ofbeta-catenin in SW480 cells can be rescued by exogenous expression of APC.
  • The APC domains required for beta-catenin ubiquitination were analyzed.
  • Our results suggest that APC regulates beta-catenin phosphorylation and ubiquitination by distinct domains and by separate molecular mechanisms.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli Protein / metabolism. Colonic Neoplasms / metabolism. Ubiquitin / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Dinucleotide Repeats. HT29 Cells. Humans. Mutation. Phosphorylation. Protein Structure, Tertiary

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  • (PMID = 16798748.001).
  • [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 / CA 112007
  • [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 / Ubiquitin; 0 / beta Catenin
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98. Matsui C, Kaieda S, Ikegami T, Mimori-Kiyosue Y: Identification of a link between the SAMP repeats of adenomatous polyposis coli tumor suppressor and the Src homology 3 domain of DDEF. J Biol Chem; 2008 Nov 21;283(47):33006-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a link between the SAMP repeats of adenomatous polyposis coli tumor suppressor and the Src homology 3 domain of DDEF.
  • The adenomatous polyposis coli (APC) tumor suppressor protein is a multifunctional protein with a well characterized role in the Wnt signal transduction pathway and in cytoskeletal regulation.
  • The SAMP repeats region of APC, an Axin-binding site, is known to be important for tumor suppression and for the developmental function of APC.
  • We performed a yeast two-hybrid screening using the first SAMP motif-containing region of Xenopus APC as bait and obtained several SAMP binding candidates including DDEF2 (development and differentiation enhancing factor 2), which is an ADP-ribosylation factor (Arf) GTPase-activating protein (GAP (ArfGAP)) involved in the regulation of focal adhesions.
  • In vitro and in cells the Src homology 3 (SH3) domain of DDEF2 and its close homolog, DDEF1, are associated with the SAMP motif of APC competitively with Axin1.
  • When fluorescent protein-tagged APC and DDEF are expressed in Xenopus A6 cells, co-localization at microtubule ends is observed.
  • Overexpression and RNA interference experiments indicate that APC and DDEFs cooperatively regulate the distributions of microtubules and focal adhesions.
  • Our findings reveal that the SAMP motif of APC specifically binds to the SH3 domains of DDEFs, providing new insights into the functions of APC in cell migration.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / chemistry. Adenomatous Polyposis Coli Protein / chemistry. src Homology Domains / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Humans. Magnetic Resonance Spectroscopy. Mice. Molecular Sequence Data. Protein Conformation. Protein Structure, Tertiary. Rats. Recombinant Proteins / chemistry. Sequence Homology, Amino Acid. Xenopus laevis


99. Zhu M, Li JS, Tian D, Ma Y, Li NP, Wu RL: [Spatial-temporal distribution of glycogen synthase kinase 3beta and adenomatous polyposis coli protein are involved in the injury and repair of airway epithelial cells induced by scratching]. Sheng Li Xue Bao; 2007 Apr 25;59(2):197-203
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Spatial-temporal distribution of glycogen synthase kinase 3beta and adenomatous polyposis coli protein are involved in the injury and repair of airway epithelial cells induced by scratching].
  • To investigate the roles of glycogen synthase kinase 3beta (GSK3beta) and adenomatous polyposis coli (APC) protein in wound repair of airway epithelial cells (AECs), we established a wound model of airway epithelium in vitro.
  • (2) The localizations of APC protein was observed by using immunofluorescence technique;.
  • (3) Immunoprecipitation was used to investigate the relationship between APC protein and GSK3beta during the repair of 16HBE cells.
  • (2) Results of immunofluorescence study showed that APC protein clustered with tubulin in the region of the migrating leading cells 6 h after scratching, which was dissimilar with that in the cells 0 h after scratching;.
  • (3) GSK3beta and APC protein were immunoprecipitated and analysed on SDS-PAGE.
  • We found that GSK3beta and APC protein were precipitated, indicating that the two proteins existed in a complex.
  • After scratching, dissociation of the two proteins occurred.
  • Taken together, we conclude that scratching caused a decrease in phosphorylation of GSK3beta, and that reduced phosphorylation of GSK3beta promoted APC protein to bind to the plus ends of microtubules and stabilize the growing ends.
  • These observations suggest that APC protein and GSK3beta may synergistically play an important role in the repair of airway epithelium.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Bronchi / injuries. Epithelial Cells / pathology. Glycogen Synthase Kinase 3 / physiology. Wound Healing / physiology

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  • (PMID = 17437043.001).
  • [ISSN] 0371-0874
  • [Journal-full-title] Sheng li xue bao : [Acta physiologica Sinica]
  • [ISO-abbreviation] Sheng Li Xue Bao
  • [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; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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100. Barth AI, Caro-Gonzalez HY, Nelson WJ: Role of adenomatous polyposis coli (APC) and microtubules in directional cell migration and neuronal polarization. Semin Cell Dev Biol; 2008 Jun;19(3):245-51
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] Role of adenomatous polyposis coli (APC) and microtubules in directional cell migration and neuronal polarization.
  • These signals lead to modifications of microtubule-associated proteins (MAPs) and point to glycogen synthase kinase (GSK) 3beta as a key regulator of microtubule function during directional migration.
  • This review will summarize these results and then focus on the role of microtubule-binding protein adenomatous polyposis coli (APC) in neuronal polarization and directed migration, and on its regulation by GSK3beta.

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  • (PMID = 18387324.001).
  • [ISSN] 1084-9521
  • [Journal-full-title] Seminars in cell & developmental biology
  • [ISO-abbreviation] Semin. Cell Dev. Biol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM078270-03; United States / NIGMS NIH HHS / GM / GM078270; United States / NIGMS NIH HHS / GM / GM35527; United States / NIGMS NIH HHS / GM / R01 GM035527; United States / NIGMS NIH HHS / GM / R01 GM078270-03; United States / NIGMS NIH HHS / GM / R37 GM035527; United States / NIGMS NIH HHS / GM / R01 GM078270
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Microtubule-Associated Proteins
  • [Number-of-references] 95
  • [Other-IDs] NLM/ NIHMS49460; NLM/ PMC2673958
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