Apc

Summary

Gene Symbol: Apc
Description: adenomatosis polyposis coli
Alias: AI047805, AU020952, AW124434, CC1, Min, mAPC, adenomatous polyposis coli protein, multiple intestinal neoplasia
Species: mouse

Top Publications

  1. ncbi Identification of stem cells in small intestine and colon by marker gene Lgr5
    Nick Barker
    Hubrecht Institute, Uppsalalaan 8, 3584CT Utrecht, The Netherlands
    Nature 449:1003-7. 2007
  2. doi Crypt stem cells as the cells-of-origin of intestinal cancer
    Nick Barker
    Hubrecht Institute for Developmental Biology and Stem Cell Research, Uppsalalaan 8, 3584CT Utrecht and University Medical Centre Utrecht, Netherlands
    Nature 457:608-11. 2009
  3. ncbi Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene
    L K Su
    Molecular Genetics Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 256:668-70. 1992
  4. pmc Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration
    Owen J Sansom
    School of Biosciences, University of Cardiff, Cardiff CF10 3US, Wales
    Genes Dev 18:1385-90. 2004
  5. doi Spindle orientation bias in gut epithelial stem cell compartments is lost in precancerous tissue
    Aaron J Quyn
    Cell and Developmental Biology, University of Dundee, Dundee, DD1 5EH, UK
    Cell Stem Cell 6:175-81. 2010
  6. pmc Genome-wide screen reveals APC-associated RNAs enriched in cell protrusions
    Stavroula Mili
    Department of Microbiology, Center for Cell Signaling, University of Virginia, HSC, Charlottesville, Virginia 22908 0577, USA
    Nature 453:115-9. 2008
  7. ncbi Pathology of mouse models of intestinal cancer: consensus report and recommendations
    Gregory 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
  8. pmc Mapping Wnt/beta-catenin signaling during mouse development and in colorectal tumors
    Silvia 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
  9. pmc A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors
    R Fodde
    Department of Genetics, Leiden University, The Netherlands
    Proc Natl Acad Sci U S A 91:8969-73. 1994
  10. pmc Complete deletion of Apc results in severe polyposis in mice
    A F Cheung
    Koch Institute and Department of Biology, MIT, Cambridge, MA, USA
    Oncogene 29:1857-64. 2010

Detail Information

Publications159 found, 100 shown here

  1. ncbi Identification of stem cells in small intestine and colon by marker gene Lgr5
    Nick 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...
  2. doi Crypt stem cells as the cells-of-origin of intestinal cancer
    Nick Barker
    Hubrecht Institute for Developmental Biology and Stem Cell Research, Uppsalalaan 8, 3584CT Utrecht and University Medical Centre Utrecht, Netherlands
    Nature 457:608-11. 2009
    Intestinal 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...
  3. ncbi Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene
    L 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...
  4. pmc Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration
    Owen J Sansom
    School of Biosciences, University of Cardiff, Cardiff CF10 3US, Wales
    Genes Dev 18:1385-90. 2004
    Although Apc is well characterized as a tumor-suppressor gene in the intestine, the precise mechanism of this suppression remains to be defined...
  5. doi Spindle orientation bias in gut epithelial stem cell compartments is lost in precancerous tissue
    Aaron 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...
  6. pmc Genome-wide screen reveals APC-associated RNAs enriched in cell protrusions
    Stavroula 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)...
  7. ncbi Pathology of mouse models of intestinal cancer: consensus report and recommendations
    Gregory 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
  8. pmc Mapping Wnt/beta-catenin signaling during mouse development and in colorectal tumors
    Silvia 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 ..
  9. pmc A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors
    R 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)...
  10. pmc Complete deletion of Apc results in severe polyposis in mice
    A 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...
  11. pmc ERK activation drives intestinal tumorigenesis in Apc(min/+) mice
    Sung 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...
  12. pmc A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses
    Shaoguang 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...
  13. pmc Focal adhesion kinase is required for intestinal regeneration and tumorigenesis downstream of Wnt/c-Myc signaling
    Gabrielle 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...
  14. ncbi Essential role of beta-catenin in postnatal bone acquisition
    Sheri 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...
  15. doi The Apc 1322T mouse develops severe polyposis associated with submaximal nuclear beta-catenin expression
    Patrick Pollard
    Molecular and Population Genetics Laboratory, London Research Institute, Cancer Research UK, London, England
    Gastroenterology 136:2204-2213.e1-13. 2009
    We previously demonstrated that the 2 APC mutations in human colorectal tumors are coselected, because tumorigenesis requires an optimal level of Wnt signaling...
  16. pmc Genetic dissection of differential signaling threshold requirements for the Wnt/beta-catenin pathway in vivo
    Michael Buchert
    Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Parkville, Australia
    PLoS Genet 6:e1000816. 2010
    Contributions of null and hypomorphic alleles of Apc in mice produce both developmental and pathophysiological phenotypes...
  17. ncbi Suppression of intestinal neoplasia by DNA hypomethylation
    P 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 ..
  18. ncbi Complete genetic suppression of polyp formation and reduction of CpG-island hypermethylation in Apc(Min/+) Dnmt1-hypomorphic Mice
    Cindy 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...
  19. ncbi Carcinogenesis in mouse stomach by simultaneous activation of the Wnt signaling and prostaglandin E2 pathway
    Hiroko 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...
  20. pmc Loss of single immunoglobulin interlukin-1 receptor-related molecule leads to enhanced colonic polyposis in Apc(min) mice
    Hui Xiao
    Department of Immunology, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Gastroenterology 139:574-85. 2010
    ....
  21. doi DCC constrains tumour progression via its dependence receptor activity
    Marie 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...
  22. pmc Environmental and genetic activation of a brain-adipocyte BDNF/leptin axis causes cancer remission and inhibition
    Lei 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...
  23. doi Spindle misorientation in tumors from APC(min/+) mice
    Elizabeth S Fleming
    Center for Molecular Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA
    Mol Carcinog 48:592-8. 2009
    The adenomatous polyposis coli (APC) tumor suppressor gene is mutated in the majority of colon cancers, and its mutation may initiate cancer by multiple mechanisms...
  24. pmc PUMA suppresses intestinal tumorigenesis in mice
    Wei 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...
  25. pmc Importance of epidermal growth factor receptor signaling in establishment of adenomas and maintenance of carcinomas during intestinal tumorigenesis
    Reade 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...
  26. pmc Suppression of intestinal neoplasia by deletion of Dnmt3b
    Haijiang 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 ..
  27. pmc The SIRT1 deacetylase suppresses intestinal tumorigenesis and colon cancer growth
    Ron 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...
  28. ncbi A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse
    A 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...
  29. pmc The adenomatous polyposis coli-associated exchange factors Asef and Asef2 are required for adenoma formation in Apc(Min/+)mice
    Yoshihiro 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
    Sporadic and familial colorectal tumours usually harbour biallelic adenomatous polyposis coli (APC)-associated mutations that result in constitutive activation of Wnt signalling...
  30. pmc Point: From animal models to prevention of colon cancer. Systematic review of chemoprevention in min mice and choice of the model system
    Denis E Corpet
    UMR Xenobiotiques, Institut National Recherche Agronomique, Ecole Nationale Veterinaire Toulouse, 31076 Toulouse, France
    Cancer Epidemiol Biomarkers Prev 12:391-400. 2003
    The 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...
  31. doi Apc mice: models, modifiers and mutants
    Amy 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 ..
  32. ncbi Impact of genetic background on spontaneous or 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced intestinal tumorigenesis in Min/+ mice
    Inger 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 ..
  33. doi Intestinal tumorigenesis initiated by dedifferentiation and acquisition of stem-cell-like properties
    Sarah 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...
  34. ncbi Crypt-restricted proliferation and commitment to the Paneth cell lineage following Apc loss in the mouse intestine
    Pauline Andreu
    Institut Cochin, INSERM U567, CNRS UMR8104, Universite Paris V, 24 rue du Fb St Jacques, 75014 Paris, France
    Development 132:1443-51. 2005
    Loss of Apc appears to be one of the major events initiating colorectal cancer...
  35. ncbi Derivation of conditionally immortalized cell lines containing the Min mutation from the normal colonic mucosa and other tissues of an "Immortomouse"/Min hybrid
    R H Whitehead
    Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Australia
    Epithelial Cell Biol 3:119-25. 1994
    The Multiple Intestinal Neoplasia (Min) mouse carries the murine homologue of the human APC gene...
  36. pmc Intestinal inflammatory cytokine response in relation to tumorigenesis in the Apc(Min/+) mouse
    Jamie 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...
  37. pmc Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment
    Kenneth 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...
  38. doi Plasminogen activator inhibitor-1 (Pai-1) blockers suppress intestinal polyp formation in Min mice
    Michihiro 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 ..
  39. ncbi ApcMin: a mouse model for intestinal and mammary tumorigenesis
    A R Moser
    McArdle Laboratory, University of Wisconsin, Madison 53706, USA
    Eur J Cancer 31:1061-4. 1995
    Min (multiple intestinal neoplasia) is a mutant allele of the murine Apc (adenomatous polyposis coli) locus, encoding a nonsense mutation at codon 850...
  40. ncbi Mouse model of colonic adenoma-carcinoma progression based on somatic Apc inactivation
    Takao 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. 2007
    Mutations 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...
  41. ncbi Apc deficiency is associated with increased Egfr activity in the intestinal enterocytes and adenomas of C57BL/6J-Min/+ mice
    Amy 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 ..
  42. pmc Wnt regulates axon behavior through changes in microtubule growth directionality: a new role for adenomatous polyposis coli
    Silvia 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...
  43. ncbi Protein kinase C alpha but not PKCzeta suppresses intestinal tumor formation in ApcMin/+ mice
    Henrik 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...
  44. ncbi 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 mice
    Randal 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...
  45. ncbi Colorectal cancers in a new mouse model of familial adenomatous polyposis: influence of genetic and environmental modifiers
    Sabine Colnot
    Departement Genetique, Developpement et Pathologie Moleculaire, Institut Cochin INSERM, CNRS UMR 8104, Universite Paris V, Paris, France
    Lab Invest 84:1619-30. 2004
    Murine models of familial adenomatous polyposis harbor a germinal heterozygous mutation on Apc tumor suppressor gene...
  46. ncbi Homozygosity for the Min allele of Apc results in disruption of mouse development prior to gastrulation
    A 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...
  47. pmc Inactivation of the UNC5C Netrin-1 receptor is associated with tumor progression in colorectal malignancies
    Agnès 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...
  48. pmc Dvl2 promotes intestinal length and neoplasia in the ApcMin mouse model for colorectal cancer
    Ciara Metcalfe
    Medical Research Council Laboratory of Molecular Biology, Li Ka Shing Centre, Cambridge, United Kingdom
    Cancer Res 70:6629-38. 2010
    b>APC mutations cause activation of Wnt/beta-catenin signaling, which invariably leads to colorectal cancer. Similarly, overexpressed Dvl proteins are potent activators of beta-catenin signaling...
  49. doi Effect of exercise on biological pathways in ApcMin/+ mouse intestinal polyps
    Kristen 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...
  50. ncbi beta-Catenin-accumulated crypts in the colonic mucosa of juvenile ApcMin/+ mice
    Kazuya Hata
    BMR Laboratories, Sunplanet Co, Ltd, 4388 Hagiwara, Kamiishidu, Yourou, Gifu 503 1602, Japan
    Cancer Lett 239:123-8. 2006
    Although Apc(Min/+) mice are widely used for an animal model of human familial adenomatous polyposis (FAP), a majority of intestinal polyps locate in the small intestine...
  51. pmc Shmt1 heterozygosity impairs folate-dependent thymidylate synthesis capacity and modifies risk of Apc(min)-mediated intestinal cancer risk
    Amanda 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 ..
  52. ncbi Suppression of polypogenesis in a new mouse strain with a truncated Apc(Delta474) by a novel COX-2 inhibitor, JTE-522
    H Sasai
    Pharmaceutical Frontier Research Laboratories, Japan Tobacco Inc, 1 13 2 Fukuura, Kanazawaku, Yokohama 236 4, Japan
    Carcinogenesis 21:953-8. 2000
    Mutations of the adenomatous polyposis coli gene (Apc) have been implicated in the occurrence of sporadic colon cancer. Various Apc knockout strains of mice have been created to better understand the function of this gene...
  53. ncbi Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer development
    Abdolrahman 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 ..
  54. doi Genetic deletion of mPGES-1 accelerates intestinal tumorigenesis in APC(Min/+) mice
    N 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 ..
  55. ncbi Genetic background affects susceptibility to mammary hyperplasias and carcinomas in Apc(min)/+ mice
    A R Moser
    Department of Human Oncology, University of Wisconsin Madison, 600 Highland Avenue, Madison, WI 53792, USA
    Cancer Res 61:3480-5. 2001
    Treatment 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 ..
  56. pmc Sulindac treatment alters collagen and matrilysin expression in adenomas of ApcMin/+ mice
    Hector 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 ..
  57. doi SirT1-null mice develop tumors at normal rates but are poorly protected by resveratrol
    G 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 ..
  58. ncbi 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 development
    J Haines
    Radiation Effects Department, National Radiological Protection Board, Chilton, Oxfordshire, England
    Genes Chromosomes Cancer 28:387-94. 2000
    Min (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...
  59. pmc Adenomatous polyposis coli on microtubule plus ends in cell extensions can promote microtubule net growth with or without EB1
    Katsuhiro Kita
    Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Mol Biol Cell 17:2331-45. 2006
    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...
  60. ncbi Mechanisms of APC-driven tumorigenesis: lessons from mouse models
    R 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 ..
  61. ncbi Enhanced CpG mutability and tumorigenesis in MBD4-deficient mice
    Catherine 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...
  62. pmc Adenomatous polyposis coli protein nucleates actin assembly and synergizes with the formin mDia1
    Kyoko Okada
    Department of Biology, Howard Hughes Medical Institute, Brandeis University, Waltham, MA 02454, USA
    J Cell Biol 189:1087-96. 2010
    The tumor suppressor protein adenomatous polyposis coli (APC) regulates cell protrusion and cell migration, processes that require the coordinated regulation of actin and microtubule dynamics...
  63. pmc Haploinsufficiency of Flap endonuclease (Fen1) leads to rapid tumor progression
    Melanie 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...
  64. doi Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) mice
    Denis 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 ..
  65. ncbi Somatic genetic events linked to the Apc locus in intestinal adenomas of the Min mouse
    C Luongo
    McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin Medical School, Madison 53706, USA
    Genes Chromosomes Cancer 17:194-8. 1996
    We have found previously that all spontaneous intestinal adenomas from Apc+/ApcMin mice lose the wild type Apc marker on two genetic backgrounds...
  66. ncbi Apc modulates embryonic stem-cell differentiation by controlling the dosage of beta-catenin signaling
    Menno 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 ..
  67. ncbi Apc tumor suppressor gene is the "zonation-keeper" of mouse liver
    Samira 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...
  68. pmc Altered dynamics of intestinal cell maturation in Apc1638N/+ mice
    Donghai 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...
  69. doi A genetic study of the role of the Wnt/beta-catenin signalling in Paneth cell differentiation
    Pauline 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...
  70. ncbi Rapid colorectal adenoma formation initiated by conditional targeting of the Apc gene
    H 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...
  71. ncbi NGF-induced axon growth is mediated by localized inactivation of GSK-3beta and functions of the microtubule plus end binding protein APC
    Feng 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)...
  72. ncbi Chemopreventive efficacy of combined piroxicam and difluoromethylornithine treatment of Apc mutant Min mouse adenomas, and selective toxicity against Apc mutant embryos
    R 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 ..
  73. ncbi Functional interaction of an axin homolog, conductin, with beta-catenin, APC, and GSK3beta
    J 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)...
  74. pmc Atonal homolog 1 is a tumor suppressor gene
    Wouter 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...
  75. pmc Roles of arrest-defective protein 1(225) and hypoxia-inducible factor 1alpha in tumor growth and metastasis
    Mi 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...
  76. pmc Apc(MIN) modulation of vitamin D secosteroid growth control
    Haibo 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...
  77. ncbi 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) mice
    G 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)...
  78. ncbi The CAST/Ei strain confers significant protection against Apc(Min) intestinal polyps, independent of the resistant modifier of Min 1 (Mom1) locus
    Revati Koratkar
    Department of Microbiology and Immunology, Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA
    Cancer Res 62:5413-7. 2002
    Intestinal adenoma development in Apc(Min) mice is influenced by genetic background...
  79. ncbi Dietary soy sphingolipids suppress tumorigenesis and gene expression in 1,2-dimethylhydrazine-treated CF1 mice and ApcMin/+ mice
    Holly 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...
  80. pmc Generating somatic mosaicism with a Cre recombinase-microsatellite sequence transgene
    Aytekin 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.
  81. ncbi Requirement for tumor suppressor Apc in the morphogenesis of anterior and ventral mouse embryo
    Tomo o Ishikawa
    Department of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto, 606 8501, Japan
    Dev Biol 253:230-46. 2003
    Tumor suppressor Apc (adenomatous polyposis coli) is implicated in the Wnt signaling pathway that is involved in the early embryonic development and tumorigenesis in vertebrates...
  82. ncbi Sulindac suppresses tumorigenesis in the Min mouse
    Y Beazer-Barclay
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Carcinogenesis 17:1757-60. 1996
    The Min mouse provides a genetically defined model for inherited and sporadic forms of human colorectal tumorigenesis...
  83. doi A reciprocal relationship exists between non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) and cyclooxygenase-2
    Genzo 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
    ..NAG-1 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...
  84. ncbi Generation of a unique strain of multiple intestinal neoplasia (Apc(+/Min-FCCC)) mice with significantly increased numbers of colorectal adenomas
    Harry S Cooper
    Department of Pathology, Division of Medical Science, Fox Chase Cancer Center, Philadelphia, PA 19111, USA
    Mol Carcinog 44:31-41. 2005
    The 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...
  85. ncbi Genetic disruption of Ptgs-1, as well as Ptgs-2, reduces intestinal tumorigenesis in Min mice
    P 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%...
  86. pmc Expression of CD44 in Apc and Tcf mutant mice implies regulation by the WNT pathway
    V 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 ..
  87. pmc Lack of adenomatous polyposis coli protein correlates with a decrease in cell migration and overall changes in microtubule stability
    Karin 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. 2007
    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...
  88. pmc Deficiency of SPARC suppresses intestinal tumorigenesis in APCMin/+ mice
    Owen 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...
  89. ncbi Loss of cathepsin L activity promotes claudin-1 overexpression and intestinal neoplasia
    Francois 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...
  90. pmc Loss of cannabinoid receptor 1 accelerates intestinal tumor growth
    Dingzhi Wang
    Departments of Medicine, Vanderbilt University Medical Center, Nashville, Tenessee, USA
    Cancer Res 68:6468-76. 2008
    ..genetic 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 ..
  91. doi Trisomy represses Apc(Min)-mediated tumours in mouse models of Down's syndrome
    Thomas 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
    ..b>Apc(Min)-mediated tumour number was determined in aneuploid mouse models Ts65Dn, Ts1Rhr and Ms1Rhr...
  92. pmc Insulin receptor substrate-1 deficiency promotes apoptosis in the putative intestinal crypt stem cell region, limits Apcmin/+ tumors, and regulates Sox9
    Nicole 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...
  93. pmc Loss of Apc allows phenotypic manifestation of the transforming properties of an endogenous K-ras oncogene in vivo
    Owen 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...
  94. ncbi EphB-ephrin-B interactions suppress colorectal cancer progression by compartmentalizing tumor cells
    Carme 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...
  95. pmc Intracellular role for sphingosine kinase 1 in intestinal adenoma cell proliferation
    Masataka 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...
  96. ncbi 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induces genetic changes in murine intestinal tumours and cells with ApcMin mutation
    A 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...
  97. ncbi The PDZ protein tax-interacting protein-1 inhibits beta-catenin transcriptional activity and growth of colorectal cancer cells
    Mutsumi 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...
  98. ncbi Thrombospondin 1--a regulator of adenoma growth and carcinoma progression in the APC(Min/+) mouse model
    Linda 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...
  99. pmc Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formation
    Edmund 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...
  100. ncbi 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) mice
    Jenny 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(-/-..
  101. ncbi Aspirin prevents tumors in a murine model of familial adenomatous polyposis
    N 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...

Research Grants68

  1. Transforming Colorectal Cancer Screening through Multimodal Spectral Markers
    Vadim Backman; Fiscal Year: 2011
    ..Our approach is to develop a minimally intrusive, highly accurate pre-screen that would allow tailoring timing/intensity of screening and surveillance. ..
  2. Spectral Markers for Early Detection of Colon Neoplasia
    Hemant Roy; Fiscal Year: 2007
    ..In the future these spectral markers may be assayed with a 4D-ELF probe during rectal examination, thus providing a practical and accurate means of determining the optimal CRC screening regimen. ..
  3. Improving colonoscopic miss rate by real time microvascular blood analysis
    Hemant Roy; Fiscal Year: 2007
    ..This could have major importance for colon cancer prevention efforts in the United States. ..
  4. MECHANISMS FOR CHEMOPREVENTION OF COLON CANCER
    CHINTHALAPALLY 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. ..
  5. HMG-CoA Reductase and Polyamine Inhibitors for Prevention of Colorectal Cancer
    Chinthalapally V Rao; Fiscal Year: 2010
    ....
  6. Role of IL10 and TGFb1 in colon cancer
    SUSAN ERDMAN; Fiscal Year: 2007
    ..Information gained from these studies may elucidate pivotal mechanisms and uncover novel strategies for prevention and treatment of human colon cancer. ..
  7. HMG CoA REDUCTASE AND COX2 INHIBITORS IN COLON CANCER
    CHINTHALAPALLY RAO; Fiscal Year: 2006
    ..Finally, we will study the effects of these agents on cell proliferation, and apoptosis during different stages of colon carcinogenesis. ..
  8. PREVENTION OF COLORECTAL CANCER BY iNOS AND COX-2 SELECTIVE INHIBITORS
    CHINTHALAPALLY RAO; Fiscal Year: 2007
    ..iNOS-selective inhibitors suppress chemically-induced colon carcinogenesis and also tumor formation in transgenic APC min mice...
  9. Role of IL10 and TGFb1 in colon cancer
    Susan E Erdman; Fiscal Year: 2010
    ..We propose to build upon our recent scientific breakthroughs and test strategies in mice that will stimulate potent and highly beneficial Treg to prevent cancer and impart healthful longevity in humans. ..
  10. Bile acid-induced colon cancer cell proliferation
    Jean 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. ..
  11. Cell adhesion, signal transduction and cytoskeletal regulation in Drosophila
    Mark Peifer; Fiscal Year: 2009
    ..We hypothesize that Ena helps generate distinct actin structures using different domains and partners, and that Ena is integrated with other actin regulators in filopodia. We will test these hypotheses. ..
  12. A model system to study the tumor suppressor APC
    Mark Peifer; Fiscal Year: 2010
    ..Its role in human cancer was first identified through the tumor suppressor Adenomatous polyposis coli (APC), mutated in most colon cancers. We now know that APC is a critical negative regulator of Wnt signaling...
  13. Fatty Liver Preventive Effects and High Dose Hepatotoxicity of Tea Polyphenols
    Joshua D Lambert; Fiscal Year: 2010
    ..e. preexisting fatty liver disease) in which individuals may be sensitized to the hepatotoxic effects of EGCG. ..
  14. PATHOLOGICAL CONSEQUENCES OF THE PLASMINOGEN SYSTEM
    Victoria 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. ..
  15. Analyses of Progression to Colon Cancer in a Spectrum of Pathways
    William Dove; Fiscal Year: 2009
    ..changes (loss-of-heterozygosity), to that involving stochastic epigenetic silencing of the tumor suppressor locus Apc, and to another involving induced inflammation...
  16. A model system to study the tumor suppressor APC
    Mark Peifer; Fiscal Year: 2009
    ..Its role in human cancer was first identified through the tumor suppressor Adenomatous polyposis coli (APC), mutated in most colon cancers. We now know that APC is a critical negative regulator of Wnt signaling...
  17. Physical Activity Measurement in Older Adults
    Lisa 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. ..
  18. CELL ADHESION AND SIGNAL TRANSDUCTION IN DROSOPHILA
    Mark Peifer; Fiscal Year: 2002
    ..Aim IV. Complete the genetic screen for genes which interact with arm in cell adhesion, signaling or other functions, and characterize the interactors. ..
  19. RESEARCH TRAINING IN GASTROENTEROLOGY
    Jean Pierre Raufman; Fiscal Year: 2007
    ..We therefore submit this application to address these goals and to impact upon the shortage of physician-scientists and other researchers in the field of Gastroenterology ..
  20. Role of PPARbeta in colon carcinogenesis
    Jeffrey 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 ..