Genomes and Genes
Gene Symbol: Apc
Description: adenomatosis polyposis coli
Alias: AI047805, AU020952, AW124434, CC1, Min, mAPC, adenomatous polyposis coli protein, multiple intestinal neoplasia
Publications159 found, 100 shown here
- Identification of stem cells in small intestine and colon by marker gene Lgr5Nick Barker
Hubrecht Institute, Uppsalalaan 8, 3584CT Utrecht, The Netherlands
Nature 449:1003-7. 2007..The expression pattern of Lgr5 suggests that it marks stem cells in multiple adult tissues and cancers...
- Crypt stem cells as the cells-of-origin of intestinal cancerNick Barker
Hubrecht Institute for Developmental Biology and Stem Cell Research, Uppsalalaan 8, 3584CT Utrecht and University Medical Centre Utrecht, Netherlands
Nature 457:608-11. 2009Intestinal cancer is initiated by Wnt-pathway-activating mutations in genes such as adenomatous polyposis coli (APC). As in most cancers, the cell of origin has remained elusive...
- Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC geneL K Su
Molecular Genetics Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21231
Science 256:668-70. 1992..Recently, a mouse lineage that exhibits an autosomal dominantly inherited predisposition to multiple intestinal neoplasia (Min) was described...
- Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migrationOwen J Sansom
School of Biosciences, University of Cardiff, Cardiff CF10 3US, Wales
Genes Dev 18:1385-90. 2004Although Apc is well characterized as a tumor-suppressor gene in the intestine, the precise mechanism of this suppression remains to be defined...
- Spindle orientation bias in gut epithelial stem cell compartments is lost in precancerous tissueAaron J Quyn
Cell and Developmental Biology, University of Dundee, Dundee, DD1 5EH, UK
Cell Stem Cell 6:175-81. 2010..label retention are lost in precancerous tissue heterozygous for the adenomatous polyposis coli tumor suppressor (Apc). This loss correlates with cell shape changes specifically in the stem cell compartment...
- Genome-wide screen reveals APC-associated RNAs enriched in cell protrusionsStavroula Mili
Department of Microbiology, Center for Cell Signaling, University of Virginia, HSC, Charlottesville, Virginia 22908 0577, USA
Nature 453:115-9. 2008..RNAs in the granules associate with the adenomatous polyposis coli (APC) tumour suppressor and the fragile X mental retardation protein (FMRP)...
- Pathology of mouse models of intestinal cancer: consensus report and recommendationsGregory P Boivin
Department of Pathology and Laboratory Medicine, University of Cincinnati and Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio 45267, USA
Gastroenterology 124:762-77. 2003
- Mapping Wnt/beta-catenin signaling during mouse development and in colorectal tumorsSilvia Maretto
Histology and Embryology Section, Department of Histology, Microbiology, and Medical Biotechnology, University of Padua, 35131 Padua, Italy
Proc Natl Acad Sci U S A 100:3299-304. 2003..Analyses of BAT-gal expression in the adenomatous polyposis coli (multiple intestinal neoplasia+) background revealed betacatenin transcriptional activity in intestinal adenomas but surprisingly not ..
- A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumorsR Fodde
Department of Genetics, Leiden University, The Netherlands
Proc Natl Acad Sci U S A 91:8969-73. 1994..observed in patients with familial adenomatous polyposis and in mice which carry a mutation called multiple intestinal neoplasia (Min)...
- Complete deletion of Apc results in severe polyposis in miceA F Cheung
Koch Institute and Department of Biology, MIT, Cambridge, MA, USA
Oncogene 29:1857-64. 2010..studies reveal that whole-gene deletion of Apc results in more rapid tumor development than the APC multiple intestinal neoplasia (Apc(Min)) truncation...
- ERK activation drives intestinal tumorigenesis in Apc(min/+) miceSung Hee Lee
Department of Medicine, University of California, San Diego, La Jolla, California, USA
Nat Med 16:665-70. 2010..activation of ERK by epidermal growth factor (EGF) increased p-ERK and c-Myc and restored the multiple intestinal neoplasia (Min) phenotype in Apc(min/+)/Myd88(-/-) mice...
- A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responsesShaoguang Wu
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Nat Med 15:1016-22. 2009..NTBF) chronically colonize mice, only ETBF triggers colitis and strongly induces colonic tumors in multiple intestinal neoplasia (Min) mice...
- Focal adhesion kinase is required for intestinal regeneration and tumorigenesis downstream of Wnt/c-Myc signalingGabrielle H Ashton
The Beatson Institute for Cancer Research, Glasgow, UK
Dev Cell 19:259-69. 2010..following intestinal regeneration, we investigated the functional importance of FAK following deletion of the Apc tumor suppressor protein within the intestinal epithelium...
- Essential role of beta-catenin in postnatal bone acquisitionSheri L Holmen
Laboratory of Cell Signaling and Carcinogenesis, Van Andel Research Institute, Grand Rapids, Michigan 49503, USA
J Biol Chem 280:21162-8. 2005..Wnt signaling pathway in osteogenesis, we generated mice lacking the beta-catenin or adenomatous polyposis coli (Apc) genes in osteoblasts...
- The Apc 1322T mouse develops severe polyposis associated with submaximal nuclear beta-catenin expressionPatrick Pollard
Molecular and Population Genetics Laboratory, London Research Institute, Cancer Research UK, London, England
Gastroenterology 136:2204-2213.e1-13. 2009We previously demonstrated that the 2 APC mutations in human colorectal tumors are coselected, because tumorigenesis requires an optimal level of Wnt signaling...
- Genetic dissection of differential signaling threshold requirements for the Wnt/beta-catenin pathway in vivoMichael Buchert
Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Parkville, Australia
PLoS Genet 6:e1000816. 2010Contributions of null and hypomorphic alleles of Apc in mice produce both developmental and pathophysiological phenotypes...
- Suppression of intestinal neoplasia by DNA hypomethylationP W Laird
Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142, USA
Cell 81:197-205. 1995..A reduction in the DNA methyltransferase activity in Min mice due to heterozygosity of the DNA methyltransferase gene, in conjunction with a weekly dose of the DNA ..
- Complete genetic suppression of polyp formation and reduction of CpG-island hypermethylation in Apc(Min/+) Dnmt1-hypomorphic MiceCindy A Eads
Department of Biochemistry and Molecular Biology, University of Southern California, Keck School of Medicine, Norris Comprehensive Cancer Center, Room 6418, Los Angeles, California 90089 9176, USA
Cancer Res 62:1296-9. 2002..In this study, we show that low levels of CpG island methylation occur in the normal intestinal mucosa of Apc(Min/+) mice and are increased in Multiple Intestinal Metaplasia (Min) polyps...
- Carcinogenesis in mouse stomach by simultaneous activation of the Wnt signaling and prostaglandin E2 pathwayHiroko Oshima
Division of Genetics, Cancer Research Institute, Kanazawa University, 13 1 Takara machi, Kanazawa 920 0934, Japan
Gastroenterology 131:1086-95. 2006..To investigate the role of Wnt and PGE(2) in gastric cancer, we have generated transgenic mice that activate both pathways and examined their phenotypes...
- Loss of single immunoglobulin interlukin-1 receptor-related molecule leads to enhanced colonic polyposis in Apc(min) miceHui Xiao
Department of Immunology, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
Gastroenterology 139:574-85. 2010....
- DCC constrains tumour progression via its dependence receptor activityMarie Castets
Apoptosis, Cancer and Development Laboratory Equipe labellisée La Ligue, LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052 CNRS UMR5286, Universite de Lyon, Centre Leon Berard, 69008 Lyon, France
Nature 482:534-7. 2012..is also associated with an increase in the number and aggressiveness of intestinal tumours in a predisposing APC mutant context, resulting in the development of highly invasive adenocarcinomas...
- Environmental and genetic activation of a brain-adipocyte BDNF/leptin axis causes cancer remission and inhibitionLei Cao
Department of Molecular Virology, Immunology and Medical Genetics, and Neuroscience and Neurological Surgery and the Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA
Cell 142:52-64. 2010..These results suggest that genetic or environmental activation of this BDNF/leptin axis may have therapeutic significance for cancer...
- Spindle misorientation in tumors from APC(min/+) miceElizabeth S Fleming
Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA
Mol Carcinog 48:592-8. 2009..We found spindle angles were increased in crypts heterozygous for the APC(min) mutation, and further increased in tumors...
- PUMA suppresses intestinal tumorigenesis in miceWei Qiu
Department of Pathology, University of Pittsburgh and Cancer Institute, Pittsburgh, Pennsylvania, USA
Cancer Res 69:4999-5006. 2009..enhanced the formation of spontaneous macroadenomas and microadenomas in the distal small intestine and colon of APC(Min/+) mice...
- Importance of epidermal growth factor receptor signaling in establishment of adenomas and maintenance of carcinomas during intestinal tumorigenesisReade B Roberts
Department of Cell Biology, Vanderbilt University, 1161 21st Avenue South, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 99:1521-6. 2002..allele to genetically examine the impact of impaired epidermal growth factor receptor (Egfr) signaling on the Apc(Min) mouse model of familial adenomatous polyposis...
- Suppression of intestinal neoplasia by deletion of Dnmt3bHaijiang Lin
Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02141, USA
Mol Cell Biol 26:2976-83. 2006..Using conditional inactivation of de novo methyltransferase Dnmt3b in Apc(Min/+) mice, we demonstrate that the loss of Dnmt3b has no impact on microadenoma formation, which is considered ..
- The SIRT1 deacetylase suppresses intestinal tumorigenesis and colon cancer growthRon Firestein
Paul F Glenn Laboratories for the Biological Mechanisms of Aging, Department of Pathology, Harvard Medical School, Boston, Massachusetts, United States of America
PLoS ONE 3:e2020. 2008..Taken together, these observations show that SIRT1 suppresses intestinal tumor formation in vivo and raise the prospect that therapies targeting SIRT1 may be of clinical use in beta-catenin-driven malignancies...
- A dominant mutation that predisposes to multiple intestinal neoplasia in the mouseA R Moser
McArdle Laboratory for Cancer Research, University of Wisconsin Madison 53706
Science 247:322-4. 1990..The mutant gene was found to be dominantly expressed and fully penetrant. Affected mice developed multiple adenomas throughout the entire intestinal tract at an early age...
- The adenomatous polyposis coli-associated exchange factors Asef and Asef2 are required for adenoma formation in Apc(Min/+)miceYoshihiro Kawasaki
Laboratory of Molecular and Genetic Information, Institute of Molecular and Cellular Biosciences, The University of Tokyo, 1 1 1 Yayoi, Bunkyo ku, Tokyo 113, Japan
EMBO Rep 10:1355-62. 2009..We also show that deficiency of either Asef or Asef2 significantly reduces the number and size of adenomas in Apc(Min/+) mice, which are heterozygous for an APC mutation and spontaneously develop adenomas in the intestine...
- Point: From animal models to prevention of colon cancer. Systematic review of chemoprevention in min mice and choice of the model systemDenis E Corpet
UMR Xenobiotiques, Institut National Recherche Agronomique, Ecole Nationale Veterinaire Toulouse, 31076 Toulouse, France
Cancer Epidemiol Biomarkers Prev 12:391-400. 2003The Apc(Min/+) mouse model and the azoxymethane (AOM) rat model are the main animal models used to study the effect of dietary agents on colorectal cancer...
- Apc mice: models, modifiers and mutantsAmy E McCart
Colorectal Cancer Genetics Group, Institute of Cell and Molecular Science, Barts and The London, Queen Mary s School of Medicine and Dentistry, 4 Newark Street, Whitechapel, London E1 2AT, UK
Pathol Res Pract 204:479-90. 2008..The (multiple intestinal neoplasia Min) mouse contains a point mutation in the Apc gene, develops numerous adenomas and was the first ..
- Impact of genetic background on spontaneous or 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced intestinal tumorigenesis in Min/+ miceInger Lise Steffensen
Department of Food Toxicology, Division of Environmental Medicine, Norwegian Institute of Public Health, P O Box 4404 Nydalen, NO 0403 Oslo, Norway
Cancer Lett 240:289-96. 2006..8- and 3.7-fold above the spontaneous levels in multiple intestinal neoplasia (Min)/+ F1 mice with AKR/J and A/J backgrounds, respectively, compared with only 3-fold in C57BL/6J ..
- Intestinal tumorigenesis initiated by dedifferentiation and acquisition of stem-cell-like propertiesSarah Schwitalla
Institute of Molecular Immunology, Klinikum rechts der Isar, Technische Universitat Munchen, 81675 Munich, Germany
Cell 152:25-38. 2013..Thus, our data support the concept of bidirectional conversion and highlight the importance of inflammatory signaling for dedifferentiation and generation of tumor-initiating cells in vivo...
- Crypt-restricted proliferation and commitment to the Paneth cell lineage following Apc loss in the mouse intestinePauline Andreu
Institut Cochin, INSERM U567, CNRS UMR8104, Universite Paris V, 24 rue du Fb St Jacques, 75014 Paris, France
Development 132:1443-51. 2005Loss of Apc appears to be one of the major events initiating colorectal cancer...
- Derivation of conditionally immortalized cell lines containing the Min mutation from the normal colonic mucosa and other tissues of an "Immortomouse"/Min hybridR H Whitehead
Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Australia
Epithelial Cell Biol 3:119-25. 1994The Multiple Intestinal Neoplasia (Min) mouse carries the murine homologue of the human APC gene...
- Intestinal inflammatory cytokine response in relation to tumorigenesis in the Apc(Min/+) mouseJamie L McClellan
Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29209, USA
Cytokine 57:113-9. 2012..the timing and magnitude of the intestinal inflammatory cytokine response in relation to tumorigenesis in the Apc(Min/+) mouse. Apc(Min/+) mice and wildtype mice were sacrificed at one of 4 time-points: 8, 12, 16, and 20 weeks of age...
- Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatmentKenneth E Hung
Division of Gastroenterology, Tufts Medical Center, Boston, MA 02111, USA
Proc Natl Acad Sci U S A 107:1565-70. 2010..Several of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent models for familial cancer predisposition syndromes...
- Plasminogen activator inhibitor-1 (Pai-1) blockers suppress intestinal polyp formation in Min miceMichihiro Mutoh
Cancer Prevention Basic Research Project, National Cancer Center Research Institute, 5 1 1 Tsukiji, Chuo Ku, Tokyo 104 0045, Japan
Carcinogenesis 29:824-9. 2008..We noticed that Min mice, featuring a defect in the adenomatous polyposis coli (Apc) gene, develop intestinal polyps along with high serum triglyceride (TG) levels up to 10-fold those observed in ..
- ApcMin: a mouse model for intestinal and mammary tumorigenesisA R Moser
McArdle Laboratory, University of Wisconsin, Madison 53706, USA
Eur J Cancer 31:1061-4. 1995Min (multiple intestinal neoplasia) is a mutant allele of the murine Apc (adenomatous polyposis coli) locus, encoding a nonsense mutation at codon 850...
- Mouse model of colonic adenoma-carcinoma progression based on somatic Apc inactivationTakao Hinoi
Department of Internal Medicine, The Cancer Center, University of Michigan School of Medicine, Ann Arbor, Michigan 48109 2200, USA
Cancer Res 67:9721-30. 2007Mutations in the adenomatous polyposis coli (APC) gene are pivotal in colorectal tumorigenesis. Existing mouse intestinal tumor models display mainly small intestinal lesions and carcinomas are rare...
- Apc deficiency is associated with increased Egfr activity in the intestinal enterocytes and adenomas of C57BL/6J-Min/+ miceAmy E Moran
Department of Surgery, Weill College of Medicine of Cornell University, and Strang Cancer Prevention Center, New York, New York 10021, USA
J Biol Chem 279:43261-72. 2004..We analyzed the normal mucosa of Min/+ and Apc+/+ (WT) littermate mice together with Apc-null adenomas to gain insight into the roles of Egfr in these intestinal ..
- Wnt regulates axon behavior through changes in microtubule growth directionality: a new role for adenomatous polyposis coliSilvia A Purro
Research Department of Cell and Developmental Biology, University College London, London WC1E 6BT, United Kingdom
J Neurosci 28:8644-54. 2008..Wnt signaling directly affects the microtubule cytoskeleton by unexpectedly inducing adenomatous polyposis coli (APC) loss from microtubule plus-ends. Consistently, short hairpin RNA knockdown of APC mimics Wnt3a function...
- Protein kinase C alpha but not PKCzeta suppresses intestinal tumor formation in ApcMin/+ miceHenrik Oster
Laboratory for Signal Transduction, Max Planck Institute of Experimental Endocrinology and Department of Nephrology, Hannover Medical School, Hannover, Germany
Cancer Res 66:6955-63. 2006..Even without an additional Apc mutation, PKCalpha knockout mice showed an elevated tendency to develop spontaneous intestinal tumors...
- Identification of a novel putative gastrointestinal stem cell and adenoma stem cell marker, doublecortin and CaM kinase-like-1, following radiation injury and in adenomatous polyposis coli/multiple intestinal neoplasia miceRandal May
Department of Medicine, University of Oklahoma Health Sciences Center, 920 Stanton L Young Boulevard, WP 1360, Oklahoma City, Oklahoma 73104, USA
Stem Cells 26:630-7. 2008..DCAMKL-1) to examine radiation-induced stem cell apoptosis and adenomatous polyposis coli (APC)/multiple intestinal neoplasia (min) mice to determine the effects of APC mutation on DCAMKL-1 expression...
- Colorectal cancers in a new mouse model of familial adenomatous polyposis: influence of genetic and environmental modifiersSabine Colnot
Departement Genetique, Developpement et Pathologie Moleculaire, Institut Cochin INSERM, CNRS UMR 8104, Universite Paris V, Paris, France
Lab Invest 84:1619-30. 2004Murine models of familial adenomatous polyposis harbor a germinal heterozygous mutation on Apc tumor suppressor gene...
- Homozygosity for the Min allele of Apc results in disruption of mouse development prior to gastrulationA R Moser
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706, USA
Dev Dyn 203:422-33. 1995..Mice carrying Min (multiple intestinal neoplasia), a mutant allele of Apc, develop intestinal and mammary tumors as adults...
- Inactivation of the UNC5C Netrin-1 receptor is associated with tumor progression in colorectal malignanciesAgnès Bernet
Apoptosis, Cancer and Development Laboratory Equipe labellisée La Ligue, Centre National de la Recherche Scientifique, CNRS UMR5238, University of Lyon, Centre Leon Berard, Lyon, France
Gastroenterology 133:1840-8. 2007..We investigate here whether UNC5C acts as a tumor suppressor in colorectal malignancies...
- Dvl2 promotes intestinal length and neoplasia in the ApcMin mouse model for colorectal cancerCiara Metcalfe
Medical Research Council Laboratory of Molecular Biology, Li Ka Shing Centre, Cambridge, United Kingdom
Cancer Res 70:6629-38. 2010..Furthermore, deletion of Dvl2 reduced the intestinal tumor numbers in a dose-dependent way in the Apc(Min) model for colorectal cancer...
- Effect of exercise on biological pathways in ApcMin/+ mouse intestinal polypsKristen A Baltgalvis
Univ of South Carolina, Dept of Exercise Science, Rm 405A Public Health Research Bldg, 921 Assembly St, Columbia, SC 29208, USA
J Appl Physiol (1985) 104:1137-43. 2008..Treadmill training can decrease Apc(Min/+) mouse intestinal polyp number and size, but the mechanisms remain unclear...
- beta-Catenin-accumulated crypts in the colonic mucosa of juvenile ApcMin/+ miceKazuya Hata
BMR Laboratories, Sunplanet Co, Ltd, 4388 Hagiwara, Kamiishidu, Yourou, Gifu 503 1602, Japan
Cancer Lett 239:123-8. 2006Although Apc(Min/+) mice are widely used for an animal model of human familial adenomatous polyposis (FAP), a majority of intestinal polyps locate in the small intestine...
- Shmt1 heterozygosity impairs folate-dependent thymidylate synthesis capacity and modifies risk of Apc(min)-mediated intestinal cancer riskAmanda J MacFarlane
Division of Nutritional Sciences and Department of Biomedical Sciences, Cornell University, Ithaca, New York 14850, USA
Cancer Res 71:2098-107. 2011..Shmt1 hemizygosity was associated with increased risk for intestinal cancer in Apc(min)(/+) mice through a gene-by-diet interaction, indicating that the capacity for thymidylate synthesis modifies ..
- Suppression of polypogenesis in a new mouse strain with a truncated Apc(Delta474) by a novel COX-2 inhibitor, JTE-522H Sasai
Pharmaceutical Frontier Research Laboratories, Japan Tobacco Inc, 1 13 2 Fukuura, Kanazawaku, Yokohama 236 4, Japan
Carcinogenesis 21:953-8. 2000..However, the number of polyps that our mice developed was similar to that of other Apc knockout mice such as Apc(Min) and Apc(1309) mice. Cyclooxygenase-2 (COX-2) has been implicated in colorectal carcinoma...
- Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer developmentAbdolrahman S Nateri
Mammalian Genetics Laboratory, CR UK London Research Institute, Lincoln s Inn Fields Laboratories, 44 Lincoln s Inn Fields, London WC2A 3PX, UK
Nature 437:281-5. 2005..In the Apc(Min) mouse model of intestinal cancer, genetic abrogation of c-Jun N-terminal phosphorylation or gut-specific ..
- Genetic deletion of mPGES-1 accelerates intestinal tumorigenesis in APC(Min/+) miceN Elander
Department of Clinical and Experimental Medicine, Division of Cell Biology, Faculty of Health Sciences, Linkoping University, SE 58185 Linkoping, Sweden
Biochem Biophys Res Commun 372:249-53. 2008..Here we demonstrate that APC(Min/+) mice with genetic deletion of microsomal prostaglandin E synthase-1 (mPGES-1), which catalyses the terminal ..
- Genetic background affects susceptibility to mammary hyperplasias and carcinomas in Apc(min)/+ miceA R Moser
Department of Human Oncology, University of Wisconsin Madison, 600 Highland Avenue, Madison, WI 53792, USA
Cancer Res 61:3480-5. 2001Treatment of female C57BL/6J (B6) mice carrying the mutant Min allele of the adenomatous polyposis coli (Apc) gene with ethylnitrosourea (ENU) results in approximately 90% of mice developing an average of three mammary tumors within 65 ..
- Sulindac treatment alters collagen and matrilysin expression in adenomas of ApcMin/+ miceHector Guillen-Ahlers
W M Keck Center for Transgene Research, University of Notre Dame, Notre Dame, IN 46556, USA
Carcinogenesis 29:1421-7. 2008..However, the mechanisms by which these drugs act are not fully understood. In this study, Apc(Min/+) mice, a genetic model of human familial adenomatous polyposis, were treated with sulindac, and these mice ..
- SirT1-null mice develop tumors at normal rates but are poorly protected by resveratrolG Boily
Center for Cancer Therapeutics, Ottawa Health Research Institute, and Department of Medicine, University of Ottawa, Ontario, Canada
Oncogene 28:2882-93. 2009..The number of intestinal polyps induced in mice carrying the Apc(min) mutation was unaffected by the SirT1 genotype although the average polyp size was slightly smaller in the SirT1-..
- Loss of heterozygosity in spontaneous and X-ray-induced intestinal tumors arising in F1 hybrid min mice: evidence for sequential loss of APC(+) and Dpc4 in tumor developmentJ Haines
Radiation Effects Department, National Radiological Protection Board, Chilton, Oxfordshire, England
Genes Chromosomes Cancer 28:387-94. 2000Min (multiple intestinal neoplasia) mice carry a mutant allele of the murine Apc (adenomatous polyposis coli) locus and are predisposed to intestinal adenoma formation in the intestinal tract...
- Adenomatous polyposis coli on microtubule plus ends in cell extensions can promote microtubule net growth with or without EB1Katsuhiro Kita
Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA
Mol Biol Cell 17:2331-45. 2006In 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...
- Mechanisms of APC-driven tumorigenesis: lessons from mouse modelsR Fodde
MGC Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
Cytogenet Cell Genet 86:105-11. 1999..The adenomatous polyposis coli (APC) gene, originally identified as the gene responsible for familial adenomatous polyposis (FAP), an inherited ..
- Enhanced CpG mutability and tumorigenesis in MBD4-deficient miceCatherine B Millar
Wellcome Trust Centre for Cell Biology, The King s Buildings, Edinburgh University, Edinburgh EH9 3JR, UK
Science 297:403-5. 2002..On a cancer-susceptible Apc(Min/+) background, Mbd4-/- mice showed accelerated tumor formation with CpG --> TpG mutations in the Apc gene...
- Adenomatous polyposis coli protein nucleates actin assembly and synergizes with the formin mDia1Kyoko Okada
Department of Biology, Howard Hughes Medical Institute, Brandeis University, Waltham, MA 02454, USA
J Cell Biol 189:1087-96. 2010The tumor suppressor protein adenomatous polyposis coli (APC) regulates cell protrusion and cell migration, processes that require the coordinated regulation of actin and microtubule dynamics...
- Haploinsufficiency of Flap endonuclease (Fen1) leads to rapid tumor progressionMelanie Kucherlapati
Department of Medicine and Harvard Partners Center for Genetics and Genomics, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 99:9924-9. 2002..However, when combined with a mutation in the adenomatous polyposis coli (Apc) gene, double heterozygous animals have increased numbers of adenocarcinomas and decreased survival...
- Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) miceDenis Alferez
Cancer Research UK, Histopathology Unit, London Research Institute, London, UK
Mol Cancer Ther 7:590-8. 2008..The Apc(Min/+) mouse is a well-characterized in vivo model of intestinal tumorigenesis, and animals with this genetic ..
- Somatic genetic events linked to the Apc locus in intestinal adenomas of the Min mouseC Luongo
McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin Medical School, Madison 53706, USA
Genes Chromosomes Cancer 17:194-8. 1996We have found previously that all spontaneous intestinal adenomas from Apc+/ApcMin mice lose the wild type Apc marker on two genetic backgrounds...
- Apc modulates embryonic stem-cell differentiation by controlling the dosage of beta-catenin signalingMenno F Kielman
Center for Human and Clinical Genetics, Leiden University Medical Center, Sylvius Laboratory, Wassenaarseweg 72, 2333 RA Leiden, The Netherlands
Nat Genet 32:594-605. 2002..The adenomatous polyposis coli gene (APC) is a major controller of the Wnt pathway and is essential to prevent tumorigenesis in a variety of tissues and ..
- Apc tumor suppressor gene is the "zonation-keeper" of mouse liverSamira Benhamouche
Institut Cochin, Département GDPM, INSERM U567, CNRS, UMR S 8104, Paris, F 75014, France
Dev Cell 10:759-70. 2006..we show the complementary localization of activated beta-catenin in the perivenous area and the negative regulator Apc in periportal hepatocytes...
- Altered dynamics of intestinal cell maturation in Apc1638N/+ miceDonghai Wang
Department of Medicine, Montefiore Medical Center, Bronx, New York 10467, USA
Cancer Res 70:5348-57. 2010..of activation of these genes were displaced along this axis in the histologically normal intestinal mucosa of Apc(1638N/+) mice before tumor development...
- A genetic study of the role of the Wnt/beta-catenin signalling in Paneth cell differentiationPauline Andreu
Institut Cochin, Universite Paris Descartes, CNRS UMR 8104, Paris, France
Dev Biol 324:288-96. 2008..de novo specification of Paneth cells in both the small intestine and colon and that colon cancers resulting from Apc mutations expressed many genes involved in Paneth cell differentiation...
- Rapid colorectal adenoma formation initiated by conditional targeting of the Apc geneH Shibata
Department of Cell Biology, Cancer Institute, Toshima ku, Tokyo 170, Japan
Science 278:120-3. 1997..by the development of multiple colorectal adenomas, and affected individuals carry germline mutations in the APC gene...
- NGF-induced axon growth is mediated by localized inactivation of GSK-3beta and functions of the microtubule plus end binding protein APCFeng Quan Zhou
UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
Neuron 42:897-912. 2004..kinases control axon growth via regulation of a microtubule plus end binding protein, adenomatous polyposis coli (APC)...
- Chemopreventive efficacy of combined piroxicam and difluoromethylornithine treatment of Apc mutant Min mouse adenomas, and selective toxicity against Apc mutant embryosR F Jacoby
University of Wisconsin Comprehensive Cancer Center, Madison 53792, USA
Cancer Res 60:1864-70. 2000..We used the Apc mutant Min mouse model to test combinations of agents that might maximize preventive benefit with minimal toxicity ..
- Functional interaction of an axin homolog, conductin, with beta-catenin, APC, and GSK3betaJ Behrens
Max Delbruck Center for Molecular Medicine, Robert Rossle Strasse 10, 13122 Berlin, Germany
Science 280:596-9. 1998..found to form a complex with both beta-catenin and the tumor suppressor gene product adenomatous polyposis coli (APC)...
- Atonal homolog 1 is a tumor suppressor geneWouter Bossuyt
Laboratory of Neurogenetics, Department of Molecular and Developmental Genetics, VIB, Leuven, Belgium
PLoS Biol 7:e39. 2009..Our data indicate that ATOH1 may be an early target for oncogenic mutations in tissues where it instructs cellular differentiation...
- Roles of arrest-defective protein 1(225) and hypoxia-inducible factor 1alpha in tumor growth and metastasisMi Ni Lee
Division of Life and Pharmaceutical Sciences, Ewha Women s University, Seoul, Korea
J Natl Cancer Inst 102:426-42. 2010..Murine arrest-defective protein 1A (mARD1A(225)) acetylates HIF-1alpha, triggering its degradation, and thus may play a role in decreased expression of VEGFA...
- Apc(MIN) modulation of vitamin D secosteroid growth controlHaibo Xu
Centre for Cancer Research and Cell Biology, Queen s University of Belfast, Northern Ireland, UK
Carcinogenesis 31:1434-41. 2010..Most sporadic CRCs arise from adenomatous polyposis coli (APC) gene mutation but understanding of its effects on vitamin D growth control is limited...
- Curcumin modifies Apc(min) apoptosis resistance and inhibits 2-amino 1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induced tumour formation in Apc(min) miceG P Collett
Department of Surgery, The Cancer Centre, Queen s University Belfast
Carcinogenesis 22:821-5. 2001..This study investigates the effects of curcumin on apoptosis and tumorigenesis in male Apc(min) mice treated with the human dietary carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)...
- The CAST/Ei strain confers significant protection against Apc(Min) intestinal polyps, independent of the resistant modifier of Min 1 (Mom1) locusRevati Koratkar
Department of Microbiology and Immunology, Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA
Cancer Res 62:5413-7. 2002Intestinal adenoma development in Apc(Min) mice is influenced by genetic background...
- Dietary soy sphingolipids suppress tumorigenesis and gene expression in 1,2-dimethylhydrazine-treated CF1 mice and ApcMin/+ miceHolly Symolon
Program in Nutrition and Health Science, Emory University, Atlanta, GA 30322, USA
J Nutr 134:1157-61. 2004..colon tumorigenesis in CF1 mice treated with a colon carcinogen [1,2-dimethylhydrazine (DMH)] and in multiple intestinal neoplasia (Min) mice, which develop intestinal tumors spontaneously...
- Generating somatic mosaicism with a Cre recombinase-microsatellite sequence transgeneAytekin Akyol
Department of Internal Medicine, University of Michigan Medical School, 109 Zina Pitcher, Ann Arbor, Michigan 48109, USA
Nat Methods 5:231-3. 2008..We demonstrated the utility of this approach by inducing colonic polyposis after Cre-mediated bi-allelic inactivation of the Apc gene.
- Requirement for tumor suppressor Apc in the morphogenesis of anterior and ventral mouse embryoTomo o Ishikawa
Department of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto, 606 8501, Japan
Dev Biol 253:230-46. 2003Tumor suppressor Apc (adenomatous polyposis coli) is implicated in the Wnt signaling pathway that is involved in the early embryonic development and tumorigenesis in vertebrates...
- Sulindac suppresses tumorigenesis in the Min mouseY Beazer-Barclay
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
Carcinogenesis 17:1757-60. 1996The Min mouse provides a genetically defined model for inherited and sporadic forms of human colorectal tumorigenesis...
- A reciprocal relationship exists between non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) and cyclooxygenase-2Genzo Iguchi
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T W Alexander Drive, RTP, NC 27709, USA
Cancer Lett 282:152-8. 2009..expression, we investigated the expression of NAG-1 and COX-2 in normal and tumor tissue from human patients, Apc(Min/+) mice, and COX-2(-/-) mice. While COX-2 expression is highly induced in tumor tissue, NAG-1 expression is reduced...
- Generation of a unique strain of multiple intestinal neoplasia (Apc(+/Min-FCCC)) mice with significantly increased numbers of colorectal adenomasHarry S Cooper
Department of Pathology, Division of Medical Science, Fox Chase Cancer Center, Philadelphia, PA 19111, USA
Mol Carcinog 44:31-41. 2005The relevance of the Apc(+/Min) mouse model in the study of human colorectal cancer remains uncertain due to the predominance of small intestinal adenomas and few, if any, colorectal adenomas...
- Genetic disruption of Ptgs-1, as well as Ptgs-2, reduces intestinal tumorigenesis in Min miceP C Chulada
Laboratory of Experimental Carcinogenesis and Mutagenesis, NIH, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Cancer Res 60:4705-8. 2000..disruption of either Ptgs-1 or Ptgs-2 (genes coding for COX-1 or COX-2, respectively) reduced polyp formation in Min/+ mice by approximately 80%...
- Expression of CD44 in Apc and Tcf mutant mice implies regulation by the WNT pathwayV J Wielenga
Department of Pathology, Academic Medical Center, University of Amsterdam, The Netherlands
Am J Pathol 154:515-23. 1999..This suggests a link with disruption of APC tumor suppressor protein-mediated regulation of beta-catenin/Tcf-4 signaling, which is crucial in initiating ..
- Lack of adenomatous polyposis coli protein correlates with a decrease in cell migration and overall changes in microtubule stabilityKarin Kroboth
Division of Cell and Developmental Biology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, United Kingdom
Mol Biol Cell 18:910-8. 2007Most 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...
- Deficiency of SPARC suppresses intestinal tumorigenesis in APCMin/+ miceOwen J Sansom
Beatson Institute of Cancer Research, Glasgow, Scotland, UK
Gut 56:1410-4. 2007..More recently, it has been shown to be upregulated in human gastric and colorectal cancer. We therefore wished to address the functional importance of SPARC upregulation to intestinal tumorigenesis in vivo...
- Loss of cathepsin L activity promotes claudin-1 overexpression and intestinal neoplasiaFrancois Boudreau
Département d Anatomie et de Biologie Cellulaire, Faculte de Medecine et des Sciences de la Sante, 3001 12e Ave Nord, Fleurimont, QC, Canada, J1H 5N4
FASEB J 21:3853-65. 2007..Loss of cathepsin L activity leads to a marked increase in tumor multiplicity in the intestine of Apc(Min) mice...
- Loss of cannabinoid receptor 1 accelerates intestinal tumor growthDingzhi Wang
Departments of Medicine, Vanderbilt University Medical Center, Nashville, Tenessee, USA
Cancer Res 68:6468-76. 2008..and pharmacologic studies reveal that loss or inhibition of CB1 accelerated intestinal adenoma growth in Apc(Min/+) mice whereas activation of CB1 attenuated intestinal tumor growth by inducing cell death via down-regulation of ..
- Trisomy represses Apc(Min)-mediated tumours in mouse models of Down's syndromeThomas E Sussan
Department of Physiology and The Institute for Genetic Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Nature 451:73-5. 2008..Apc(Min)-mediated tumour number was determined in aneuploid mouse models Ts65Dn, Ts1Rhr and Ms1Rhr...
- Insulin receptor substrate-1 deficiency promotes apoptosis in the putative intestinal crypt stem cell region, limits Apcmin/+ tumors, and regulates Sox9Nicole M Ramocki
Department of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, North Carolina 27599 7545, USA or
Endocrinology 149:261-7. 2008..the hypothesis that reduced IRS-1 expression increases apoptosis of intestinal crypt cells and protects against Apc(min/+) (Min)/beta-catenin-driven intestinal tumors...
- Loss of Apc allows phenotypic manifestation of the transforming properties of an endogenous K-ras oncogene in vivoOwen J Sansom
Beatson Institute for Cancer Research, Glasgow G61 1BD, United Kingdom
Proc Natl Acad Sci U S A 103:14122-7. 2006..expressed an oncogenic K-ras(V12) allele in the small intestine of adult mice either alone or in the context of Apc deficiency...
- EphB-ephrin-B interactions suppress colorectal cancer progression by compartmentalizing tumor cellsCarme Cortina
Oncology Programme, Institute for Research in Biomedicine IRB, Josep Samitier 1 5, 08028 Barcelona Spain
Nat Genet 39:1376-83. 2007..Our results indicate that CRC cells must silence EphB expression to avoid repulsive interactions imposed by normal ephrin-B1-expressing intestinal cells at the onset of tumorigenesis...
- Intracellular role for sphingosine kinase 1 in intestinal adenoma cell proliferationMasataka Kohno
Center for Vascular Biology, Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06030, USA
Mol Cell Biol 26:7211-23. 2006..Here, we show that Sphk1 is expressed and is required for small intestinal tumor cell proliferation in Apc Min/+ mice. Adenoma size but not incidence was dramatically reduced in Apc Min/+ Sphk(-/-) mice...
- 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induces genetic changes in murine intestinal tumours and cells with ApcMin mutationA Andreassen
Division of Environmental Medicine, Norwegian Institute of Public Health, P O Box 4404, Nydalen, NO 0403 Oslo, Norway
Mutat Res 604:60-70. 2006..animal studies, spontaneous tumour formation in B6(Min/+) mice was associated with somatic loss of the wild-type Apc+ allele by loss of the entire chromosome 18 or by recombination...
- The PDZ protein tax-interacting protein-1 inhibits beta-catenin transcriptional activity and growth of colorectal cancer cellsMutsumi Kanamori
Laboratory for Genome Exploration Research Group, RIKEN Genomic Sciences Center, 1 7 22 Suehiro cho, Tsurumi ku, Yokohama 230 0045, Japan
J Biol Chem 278:38758-64. 2003..These data suggest that TIP-1 may represent a novel regulatory element in the Wnt/beta-catenin signaling pathway...
- Thrombospondin 1--a regulator of adenoma growth and carcinoma progression in the APC(Min/+) mouse modelLinda S Gutierrez
Walther Cancer Research Center, W M Keck Center for Transgene Research, Department of Chemistry and Biochemistry, Freimann Life Sciences Center University of Notre Dame, Notre Dame, IN 46556, USA
Carcinogenesis 24:199-207. 2003..TSP-1 on adenoma formation and development into cancerous lesions has been evaluated in the Min(/+) (multiple intestinal neoplasia) mouse model...
- Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formationEdmund Wong
Department of Cell Biology, Biostatistics Core, Albert Einstein Cancer Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
Proc Natl Acad Sci U S A 99:14937-42. 2002..The combination of Mbd4 deficiency with a germ line mutation in the adenomatous polyposis coli (Apc) gene increased the tumor number in the GI tract and accelerated tumor progression...
- Cyclin D1 is not an essential target of beta-catenin signaling during intestinal tumorigenesis, but it may act as a modifier of disease severity in multiple intestinal neoplasia (Min) miceJenny Wilding
Cancer and Immunogenetics Laboratory, Cancer Research UK, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom
Cancer Res 62:4562-5. 2002..We tested the hypothesis that cyclin D1 gene activation is important for intestinal tumorigenesis. Multiple intestinal neoplasia mice (a model for human familial adenomatous polyposis) were crossed with cyclin D1 knockout (Ccnd1(-/-..
- Aspirin prevents tumors in a murine model of familial adenomatous polyposisN N Mahmoud
New York Hospital Cornell University Medical Center, NY 10021, USA
Surgery 124:225-31. 1998..Both human and murine studies suggest that anti-inflammatory drugs prevent intestinal neoplasia. The purpose of this study was to investigate the role of aspirin as a chemopreventive agent for colorectal cancer...
- MECHANISMS FOR CHEMOPREVENTION OF COLON CANCERCHINTHALAPALLY RAO; Fiscal Year: 2004..Tissue distribution and comparative metabolism studies of curcumin and PEMC will be studied with synthetic [3H] curcumin and [3H]-PEMC in vivo in male F-344 rats. ..
- PREVENTION OF COLORECTAL CANCER BY iNOS AND COX-2 SELECTIVE INHIBITORSCHINTHALAPALLY RAO; Fiscal Year: 2008..inhibitors suppress chemically-induced colon carcinogenesis and also tumor formation in transgenic APC min mice...
- Role of PPARbeta in colon carcinogenesisJeffrey Peters; Fiscal Year: 2007..in response to topical application of a tumor promoter (TPA), in human colon tumor cells with an inactivated APC gene, and in human and azoxymethane-induced rodent colon tumors providing the first evidence suggesting that this ..
- Physical Activity Measurement in Older AdultsLisa Colbert; Fiscal Year: 2007..This methodology can then be incorporated into future studies examining the associations between doses of physical activity and various health outcomes. [unreadable] [unreadable]..
- Bile acid-induced colon cancer cell proliferationJean Pierre Raufman; Fiscal Year: 2009..3c) The mechanism whereby bile acids activate metalloproteases will be determined by exploring the roles of PKC, Ca2+, and Src in bile acid-induced HB-EGF release. ..
- PATHOLOGICAL CONSEQUENCES OF THE PLASMINOGEN SYSTEMVictoria Ploplis; Fiscal Year: 2010..The hypothesis is that cardiac fibrosis will be regulated by urokinase activity and other functions of PAI-I which will be further pursued in future studies of mice expressing functional mutations of PAI-1. ..