Genomes and Genes
Gene Symbol: Apc
Description: adenomatosis polyposis coli
Alias: AI047805, AU020952, AW124434, CC1, Min, mAPC, adenomatous polyposis coli protein, multiple intestinal neoplasia
Publications112 found, 100 shown here
- 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...
- 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 ..
- 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...
- 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...
- 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...
- 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...
- 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
- 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...
- 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...
- 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...
- 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 ..
- 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 ..
- 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 ..
- 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...
- 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 ..
- 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...
- 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...
- 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...
- 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...
- 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...
- 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...
- 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...
- 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.
- 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)...
- 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...
- 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..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...
- 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...
- 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...
- 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 ..
- 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...
- 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 ..
- 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...
- Plasminogen activator inhibitor-1 (PAI-1) modifies the formation of aggressive fibromatosis (desmoid tumor)Catherine Fen Li
Program in Developmental Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8
Oncogene 24:1615-24. 2005..deletion in Pai-1 was crossed with a mouse that develops aggressive fibromatosis and gastrointestinal tumors (Apc/Apc1638N mouse)...
- Liver-targeted disruption of Apc in mice activates beta-catenin signaling and leads to hepatocellular carcinomasS Colnot
Institut Cochin, Institut National de la Sante et de la Recherche Medicale U567, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8104, Universite Paris V, 24 rue du Faubourg St Jacques, 75014 Paris, France
Proc Natl Acad Sci U S A 101:17216-21. 2004..To investigate this issue, we constructed a mutant mouse strain, Apc(lox/lox), in which exon 14 of the tumor-suppressor gene adenomatous polyposis coli (Apc) is flanked by loxP ..
- 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...
- EphB receptor activity suppresses colorectal cancer progressionEduard Batlle
Hubrecht Laboratory, Center for Biomedical Genetics, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands
Nature 435:1126-30. 2005..Furthermore, reduction of EphB activity accelerates tumorigenesis in the colon and rectum of Apc(Min/+) mice, and results in the formation of aggressive adenocarcinomas...
- TGF-beta receptor inactivation and mutant Kras induce intestinal neoplasms in mice via a beta-catenin-independent pathwayPatty Trobridge
Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
Gastroenterology 136:1680-8.e7. 2009..The RAS-RAF-ERK pathway is frequently up-regulated in colon cancer via mutational activation of KRAS or BRAF. We assessed how these pathways interact in vivo and affect formation of colorectal tumors...
- 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...
- 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...
- 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..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 ..
- APC inactivation associates with abnormal mitosis completion and concomitant BUB1B/MAD2L1 up-regulationMiguel Abal
Morphogenesis and intracellular signalling, UMR 144, Institut Curie CNRS, Paris, France
Gastroenterology 132:2448-58. 2007..A role for the tumor suppressor gene APC has been proposed in colorectal cancer that leads to compromised chromosome segregation even though the molecular ..
- 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...
- 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...
- 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...
- 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..b>Apc(Min)-mediated tumour number was determined in aneuploid mouse models Ts65Dn, Ts1Rhr and Ms1Rhr...
- 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...
- Synergy between LRH-1 and beta-catenin induces G1 cyclin-mediated cell proliferationOronza A Botrugno
Institut de Genetique et de Biologie Moleculaire et Cellulaire, Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Universite Louis Pasteur, 67404 Illkirch, France
Mol Cell 15:499-509. 2004..The implication of LRH-1 in cell proliferation highlights an unanticipated crosstalk between LRH-1 and the beta-catenin/Tcf4 signaling pathway, which is relevant for the renewal of intestinal crypt cells...
- Dnmt1N/+ reduces the net growth rate and multiplicity of intestinal adenomas in C57BL/6-multiple intestinal neoplasia (Min)/+ mice independently of p53 but demonstrates strong synergy with the modifier of Min 1(AKR) resistance alleleR T Cormier
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706, USA
Cancer Res 60:3965-70. 2000..5-cytosine DNA methyltransferase gene (Dnmt1(N/+)) diminishes intestinal tumorigenesis in C57BL/6-multiple intestinal neoplasia (Min)/+ mice...
- 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...
- Tumor-associated Apc mutations in Mlh1-/- Apc1638N mice reveal a mutational signature of Mlh1 deficiencyM Kuraguchi
Strang Cancer Research Laboratory at The Rockefeller University, New York, NY 10021, USA
Oncogene 19:5755-63. 2000Apc1638N mice, which are heterozygous for a germline mutation in Apc, typically develop three to five spontaneous intestinal tumors per animal. In most cases this is associated with allelic loss of wildtype Apc...
- Targeted inactivation of the p21(WAF1/cip1) gene enhances Apc-initiated tumor formation and the tumor-promoting activity of a Western-style high-risk diet by altering cell maturation in the intestinal mucosalW C Yang
Albert Einstein Cancer Center, Bronx, New York 10467, USA
Cancer Res 61:565-9. 2001..increases the frequency and size of intestinal tumors in Apc1638+/- mice that inherit a mutant allele of the Apc gene, and intermediate effects are seen if a single p21 allele is inactivated...
- Apc1638N: a mouse model for familial adenomatous polyposis-associated desmoid tumors and cutaneous cystsR Smits
Medical Genetics Center South West Netherlands, Department of Human Genetics, Leiden University
Gastroenterology 114:275-83. 1998Germline mutations in the adenomatous polyposis coli (APC) gene are responsible for familial adenomatous polyposis (FAP), an autosomal dominant predisposition to the formation of multiple colorectal adenomas...
- 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(-/-..
- 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...
- 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...
- 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...
- Genotype-phenotype correlation in murine Apc mutation: differences in enterocyte migration and response to sulindacN N Mahmoud
The New York Hospital Cornell Medical Center, New York 10021, USA
Cancer Res 59:353-9. 1999The adenomatous polyposis coli (APC) gene product mediates coordinated cell growth in the intestinal mucosa...
- Cyclin D1 genetic heterozygosity regulates colonic epithelial cell differentiation and tumor number in ApcMin miceJames Hulit
The Lombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University, Research Building Room E501, 3970 Reservoir Rd, N W, Box 571468, Washington, DC 20057 1468, USA
Mol Cell Biol 24:7598-611. 2004..activity, the primary transforming events in colorectal carcinoma, occurs through induction of the Wnt pathway or APC gene mutations that cause familial adenomatous polyposis...
- 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...
- Peroxisome proliferator-activated receptor ligand MCC-555 suppresses intestinal polyps in ApcMin/+ mice via extracellular signal-regulated kinase and peroxisome proliferator-activated receptor-dependent pathwaysKiyoshi Yamaguchi
Department of Pathobiology, College of Veterinary Medicine, The University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA
Mol Cancer Ther 7:2779-87. 2008..In this study, we explored the antitumorigenic effects of MCC-555 both in cell culture and in Apc-deficient mice, an animal model for human familial adenomatous polyposis...
- The pleiotropic phenotype of Apc mutations in the mouse: allele specificity and effects of the genetic backgroundRichard B Halberg
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, Wisconsin 53706, USA
Genetics 180:601-9. 2008..Afflicted individuals are heterozygous for mutations in the APC gene...
- The tumor suppressor protein APC colocalizes with beta-catenin in the colon epithelial cellsT Senda
Department of Anatomy I, Nagoya University School of Medicine, Japan
Biochem Biophys Res Commun 223:329-34. 1996The APC gene is mutated in familial adenomatous polyposis and sporadic colorectal tumors. The product of this gene is a 300 kDa cytoplasmic protein associated with catenin...
- 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...
- 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)...
- Mouse models for hereditary nonpolyposis colorectal cancerN de Wind
Division of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam
Cancer Res 58:248-55. 1998..To develop a model for intestinal tumorigenesis in HNPCC, we introduced the Min allele of the Apc tumor suppressor gene...
- Inactivation of both APC alleles in human and mouse tumorsD B Levy
Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231
Cancer Res 54:5953-8. 1994..coli (APC) gene lead to multiple intestinal tumors in familial adenomatous polyposis patients and in multiple intestinal neoplasia (Min) mice...
- 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...
- 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)...
- Interaction of Muc2 and Apc on Wnt signaling and in intestinal tumorigenesis: potential role of chronic inflammationKan Yang
Strang Cancer Center at New York Blood Bank, New York, USA
Cancer Res 68:7313-22. 2008Somatic mutations of the adenomatous polyposis coli (APC) gene are initiating events in the majority of sporadic colon cancers...
- Dietary induction of colonic tumors in a mouse model of sporadic colon cancerKan Yang
Strang Cancer Research Laboratory, Department of Medicine, Gastroenterology and Hepatology, Weill Medical College of Cornell University, New York, New York 10467, USA
Cancer Res 68:7803-10. 2008..of colonic epithelial cells in the flat mucosa by the NWD was similar to that initiated by inheritance of a mutant Apc allele...
- A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of ArmadilloS Hayashi
Department of Molecular Biology, Princeton University, NJ 08540, USA
Proc Natl Acad Sci U S A 94:242-7. 1997Mutations in the adenomatous polyposis coli gene (which encodes a protein called APC) are associated with the formation of intestinal polyps and colon cancers...
- Manipulation of the mouse germline in the study of Min-induced neoplasiaA Bilger
Laboratory of Genetics, University of Wisconsin Medical School, Madison 53706, USA
Semin Cancer Biol 7:249-60. 1996The Min mouse, generated by random germline mutagenesis, carries a mutation in the mouse homolog of APC and is a model of inherited human intestinal tumorigenesis...
- PKCalpha tumor suppression in the intestine is associated with transcriptional and translational inhibition of cyclin D1Marybeth A Pysz
Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, New York 14263, USA
Exp Cell Res 315:1415-28. 2009..Loss of PKCalpha and effects of its re-expression were independent of the status of the APC/beta-catenin signaling pathway or known genetic alterations, indicating that they are a general characteristic of ..
- Expression of transgenic carcinoembryonic antigen (CEA) in tumor-prone mice: an animal model for CEA-directed tumor immunotherapyJ A Thompson
Institute of Immunobiology, University of Freiburg, Germany
Int J Cancer 72:197-202. 1997..As a model for colorectal tumors, mice bearing a mutation in the Apc gene (Min mice) and the CEA transgene developed multiple intestinal adenomas with strong CEA expression in all ..
- Transgenic expression of VEGF in intestinal epithelium drives mesenchymal cell interactions and epithelial neoplasiaAmelie Boquoi
Department of Medicine, Fox Chase Cancer Center, Philadelphia, Pennsylvania, USA
Gastroenterology 136:596-606.e4. 2009..We used a transgenic approach to directly test the hypothesis that augmented VEGF expression can drive progression of intestinal neoplasia...
- Alkylation-induced colon tumorigenesis in mice deficient in the Mgmt and Msh6 proteinsJ M Bugni
Biological Engineering Department and Center for Environmental Health Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
Oncogene 28:734-41. 2009..AOM and dextran sulfate sodium (DSS)-induced colorectal adenomas and against spontaneous intestinal adenomas in Apc(Min) mice...
- Long-lived Min mice develop advanced intestinal cancers through a genetically conservative pathwayRichard B Halberg
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, Wisconsin 53706, USA
Cancer Res 69:5768-75. 2009C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenomas along the entire length of the intestine and consequently die at an early age...
- Balancing between antitumor efficacy and autoimmune pathology in T-cell-mediated targeting of carcinoembryonic antigenRinke Bos
Department of Immunohematology and Blood Transfusion, Tumor Immunology Group, Leiden University Medical Center, Leiden, The Netherlands
Cancer Res 68:8446-55. 2008....
- Comparative analysis of 1196 orthologous mouse and human full-length mRNA and protein sequencesW Makałowski
National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland 20894, USA
Genome Res 6:846-57. 1996..Also, they should prove useful in estimating the additional sampling diversity provided by mouse EST sequencing projects designed to complement the existing human cDNA collection...
- Glucagon-like peptide-2 does not modify the growth or survival of murine or human intestinal tumor cellsJacqueline A Koehler
Department of Medicine, Samuel Lunenfeld Research Institute, Mt Sinai Hospital, University of Toronto, Toronto, Ontario, Canada
Cancer Res 68:7897-904. 2008..The importance of the GLP-2R for tumor growth was also examined in Apc(Min/+) mice chronically treated with exogenous GLP-2 and in Apc(Min/+):Glp2r(-/-) mice...
- Disruption of estrogen receptor signaling enhances intestinal neoplasia in Apc(Min/+) miceAlicia G Cleveland
Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198, USA
Carcinogenesis 30:1581-90. 2009..Through crosses between an ERalpha knockout and Apc(Min) mouse strains, we demonstrate that ERalpha deficiency is associated with a significant increase in intestinal ..
- Pax-2 expression defines a subset of GABAergic interneurons and their precursors in the developing murine cerebellumS M Maricich
Alzheimer Research Laboratory, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, Ohio 44106, USA
J Neurobiol 41:281-94. 1999..Finally, our data support the hypothesis that the basket and stellate cells arise from neuronally restricted, migratory precursors located in the early postnatal cerebellar white matter...
- Mlh1 deficiency enhances several phenotypes of Apc(Min)/+ miceA R Shoemaker
McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin Medical School, Madison, Wisconsin, WI 53706, USA
Oncogene 19:2774-9. 2000Defects in APC and DNA mismatch repair genes are associated with a strong predisposition to colon cancer in humans, and numerous mouse strains with mutations in these genes have been generated...
- A Robertsonian translocation suppresses a somatic recombination pathway to loss of heterozygosityKevin M Haigis
McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin Madison, 1400 University Avenue, Madison, Wisconsin 53706, USA
Nat Genet 33:33-9. 2003In mammals, loss of APC/Apc gatekeeper function initiates intestinal tumorigenesis...
- Transcriptional profiling of the transition from normal intestinal epithelia to adenomas and carcinomas in the APCMin/+ mouseNicholas F Paoni
W M Keck Center for Transgene Research, Walther Cancer Center, and Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, Indiana 46556, USA
Physiol Genomics 15:228-35. 2003Mutations in the adenomatous polyposis coli (APC) gene that result in excessive beta-catenin-induced cell signaling are implicated in the risk of colon cancer...
- Negative energy balance induced by voluntary wheel running inhibits polyp development in APCMin miceLisa H Colbert
Department of Kinesiology, University of Wisconsin Madison, WI, USA
Carcinogenesis 27:2103-7. 2006..9 km/day has had inconsistent effects on spontaneous intestinal polyp development in C57BL/6J-Apc(Min)/J (Min) mice; the amount of energy expenditure and/or a lack of hormonal changes could account for this ..
- Dietary EPA reduces tumor load in ApcMin/+ mice by altering arachidonic acid metabolism, but conjugated linoleic acid, gamma--and alpha-linolenic acids have no effectJay Whelan
Department of Nutrition, 229 Jessie Harris Building, University of Tennessee, Knoxville, TN 37996-1900, USA
Adv Exp Med Biol 507:579-84. 2002
- CXCL1 induced by prostaglandin E2 promotes angiogenesis in colorectal cancerDingzhi Wang
Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA
J Exp Med 203:941-51. 2006..Collectively, our findings show for the first time that CXCL1 is regulated by PGE2 and indicate that CXCL1 inhibitors should be evaluated further as potential anti-angiogenic agents for treatment of CRC...
- The plant lignans matairesinol and secoisolariciresinol administered to Min mice do not protect against intestinal tumor formationAnne Maria Pajari
Department of Applied Chemistry and Microbiology, Division of Nutrition, University of Helsinki, P O Box 66, 00014 Helsinki, Finland
Cancer Lett 233:309-14. 2006The lignans matairesinol (MAT) and secoisolariciresinol (SECO) were fed to Min mice at 0.02% (w/w) in diet to study their effects on intestinal tumor development. The mean number (67 vs. 51, P=0.052) and size (1.4 vs. 1.2 mm, P=0...
- Genetic deletion of receptor for hyaluronan-mediated motility (Rhamm) attenuates the formation of aggressive fibromatosis (desmoid tumor)Cornelia Tolg
Departments of Oncology and Biochemistry, The University of Western Ontario, Canada
Oncogene 22:6873-82. 2003..Rhamm-/- mice were crossed with Apc/Apc1638N mice, which harbor a targeted mutation in the Apc gene predisposing animals to gastrointestinal and ..
- CD4+CD25+ regulatory lymphocytes induce regression of intestinal tumors in ApcMin/+ miceSusan E Erdman
Division of Comparative Medicine and Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
Cancer Res 65:3998-4004. 2005..in humans results from sequential genetic changes in intestinal epithelia commencing with inactivation of the APC tumor suppressor gene. Roles for host immunity in epithelial tumorigenesis are poorly understood...
- Peroxisome proliferator-activated receptor gamma agonist troglitazone induces colon tumors in normal C57BL/6J mice and enhances colonic carcinogenesis in Apc1638 N/+ Mlh1+/- double mutant miceKan Yang
Strang Cancer Research Laboratory at The Rockefeller University, New York, NY, USA
Int J Cancer 116:495-9. 2005..This observation indicates that preexisting mutational events are not necessary for induction of colonic tumors by activated PPAR-gamma in vivo...
- Promotion of colon tumors in C57BL/6J-APC(min)/+ mice by thiazolidinedione PPARgamma agonists and a structurally unrelated PPARgamma agonistMichael V Pino
Aventis Inc, Drug Safety Evaluation, Bridgewater, New Jersey 08807, USA
Toxicol Pathol 32:58-63. 2004..agonists (troglitazone and rosiglitazone) were previously shown to promote colon tumor formation in C57BL/6J-APC(min)/+ mice, a model for human familial adenomatous polyposis...
- Chemoprevention of familial adenomatous polyposis by low doses of atorvastatin and celecoxib given individually and in combination to APCMin miceMalisetty V Swamy
Department of Medicine, Hem Onc Section, University of Oklahoma Cancer Institute, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA
Cancer Res 66:7370-7. 2006..These observations show that atorvastatin inhibits intestinal tumorigenesis and that, importantly, when given together with low doses of celecoxib, it significantly increases the chemopreventive efficacy in an APC(min) mice.
- Intestinal microbiota: a potential diet-responsive prevention target in ApcMin miceVolker Mai
Department of Epidemiology and Preventive Medicine, The University of Maryland School of Medicine, Baltimore, Maryland 21201 1192, USA
Mol Carcinog 46:42-8. 2007..with a freeze-dried fruit and vegetable extract (OFV), reduced the development of intestinal adenomas in Apc(Min) mice by 57% and 33%, respectively, compared to control mice fed a defined diet ad libitum...
- Defective acute apoptotic response to genotoxic carcinogen in small intestine of APC(Min/+) mice is restored by sulindacYing Hu
Department of Medicine, Flinders University of South Australia, Adelaide, Australia
Cancer Lett 248:234-44. 2007The effect of APC loss on azoxymethane (AOM)-induced apoptosis and cell proliferation, as well as their regulation by sulindac was examined in colon and small intestine in APC(Min/+) mice...
- Expression of guanylin is downregulated in mouse and human intestinal adenomasK A Steinbrecher
Division of Pediatric Gastroenterology and Nutrition, Children s Hospital Medical Center, Cincinnati, Ohio 45229, USA
Biochem Biophys Res Commun 273:225-30. 2000..guanylin expression increases adenoma susceptibility in an animal model of intestinal cancer, the multiple intestinal neoplasia (Min) mouse...
- Chemoprevention of familial adenomatous polyposis by natural dietary compounds sulforaphane and dibenzoylmethane alone and in combination in ApcMin/+ mouseGuoxiang Shen
Center for Cancer Prevention Research, Department of Pharmaceutics, and Susan Lehman Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey 08854, USA
Cancer Res 67:9937-44. 2007..In conclusion, our results showed that both SFN and DBM alone as well as their combination are potent natural dietary compounds for chemoprevention of gastrointestinal cancers...
- Transforming Colorectal Cancer Screening through Multimodal Spectral MarkersVadim 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. ..
- Spectral Markers for Early Detection of Colon NeoplasiaHemant 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. ..
- Improving colonoscopic miss rate by real time microvascular blood analysisHemant Roy; Fiscal Year: 2007..This could have major importance for colon cancer prevention efforts in the United States. ..
- 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. ..
- HMG-CoA Reductase and Polyamine Inhibitors for Prevention of Colorectal CancerChinthalapally V Rao; Fiscal Year: 2010....
- Role of IL10 and TGFb1 in colon cancerSUSAN 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. ..
- HMG CoA REDUCTASE AND COX2 INHIBITORS IN COLON CANCERCHINTHALAPALLY RAO; Fiscal Year: 2006..Finally, we will study the effects of these agents on cell proliferation, and apoptosis during different stages of colon carcinogenesis. ..
- PREVENTION OF COLORECTAL CANCER BY iNOS AND COX-2 SELECTIVE INHIBITORSCHINTHALAPALLY RAO; Fiscal Year: 2007..iNOS-selective inhibitors suppress chemically-induced colon carcinogenesis and also tumor formation in transgenic APC min mice...
- Role of IL10 and TGFb1 in colon cancerSusan 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. ..
- 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. ..
- Cell adhesion, signal transduction and cytoskeletal regulation in DrosophilaMark 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. ..
- A model system to study the tumor suppressor APCMark 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...
- Fatty Liver Preventive Effects and High Dose Hepatotoxicity of Tea PolyphenolsJoshua D Lambert; Fiscal Year: 2010..e. preexisting fatty liver disease) in which individuals may be sensitized to the hepatotoxic effects of EGCG. ..
- 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. ..
- Analyses of Progression to Colon Cancer in a Spectrum of PathwaysWilliam 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...
- A model system to study the tumor suppressor APCMark 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...
- 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. ..
- CELL ADHESION AND SIGNAL TRANSDUCTION IN DROSOPHILAMark 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. ..
- RESEARCH TRAINING IN GASTROENTEROLOGYJean 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 ..
- 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 ..