Genomes and Genes
Summary: Tumor suppressor genes located in the 5q21 region on the long arm of human chromosome 5. The mutation of these genes is associated with familial adenomatous polyposis (ADENOMATOUS POLYPOSIS COLI) and GARDNER SYNDROME, as well as some sporadic colorectal cancers.
Publications235 found, 100 shown here
- Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APCP J Morin
Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA
Science 275:1787-90. 1997..The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity...
- Constitutive transcriptional activation by a beta-catenin-Tcf complex in APC-/- colon carcinomaV Korinek
Department of Immunology, University Hospital, Post Office Box 85500, 3508 GA Utrecht, Netherlands
Science 275:1784-7. 1997..Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium...
- Myc deletion rescues Apc deficiency in the small intestineOwen J Sansom
The Beatson Institute, Garscube Estate, Glasgow G61 1BD, UK
Nature 446:676-9. 2007..Array analysis revealed that Myc is required for the majority of Wnt target gene activation following Apc loss. These data establish Myc as the critical mediator of the early stages of neoplasia following Apc loss...
- 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..Our results indicate that CD44 expression is part of a genetic program controlled by the beta-catenin/Tcf-4 signaling pathway and suggest a role for CD44 in the generation and turnover of epithelial cells...
- Association of the APC tumor suppressor protein with cateninsL K Su
Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231
Science 262:1734-7. 1993..A 27-residue fragment of APC containing a 15-amino acid repeat was sufficient for the interaction with the catenins. These results suggest an important link between tumor initiation and cell adhesion...
- Somatic mutations of the APC gene in colorectal tumors: mutation cluster region in the APC geneY Miyoshi
Department of Biochemistry, Cancer Institute, Tokyo, Japan
Hum Mol Genet 1:229-33. 1992..These results strongly suggest that somatic mutations of the APC gene are associated with development of a great majority of colorectal tumors...
- APC, signal transduction and genetic instability in colorectal cancerR Fodde
Department of Human and Clinical Genetics, and Center for Biomedical Genetics, Leiden University Medical Center, The Netherlands
Nat Rev Cancer 1:55-67. 2001..Inactivation of APC--the gene responsible for most cases of colorectal cancer--might fulfil both requirements...
- Association of the APC gene product with beta-cateninB Rubinfeld
Onyx Pharmaceuticals, Richmond, CA 94806
Science 262:1731-4. 1993..An antibody specific to beta-catenin also recognized the 95-kilodalton protein in the immunoprecipitates. These results suggest that APC is involved in cell adhesion...
- Multiple colorectal adenomas, classic adenomatous polyposis, and germ-line mutations in MYHOliver M Sieber
Molecular and Population Genetics Laboratory, London Research Institute, Cancer Research UK, London, United Kingdom
N Engl J Med 348:791-9. 2003..Tumors from affected persons displayed excess somatic transversions of a guanine-cytosine pair to a thymine-adenine pair (G:C-->T:A) in the APC gene...
- Inhibition of intestinal tumorigenesis in Apcmin/+ mice by (-)-epigallocatechin-3-gallate, the major catechin in green teaJihyeung Ju
Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854 8020, USA
Cancer Res 65:10623-31. 2005....
- Inherited variants of MYH associated with somatic G:C-->T:A mutations in colorectal tumorsNada Al-Tassan
Institute of Medical Genetics, University of Wales College of Medicine, Heath Park, Cardiff, CF14 4XN, UK
Nat Genet 30:227-32. 2002..Our findings link the inherited variants in MYH to the pattern of somatic APC mutation in family N and implicate defective base excision repair in predisposition to tumors in humans...
- The Apc 1322T mouse develops severe polyposis associated with submaximal nuclear beta-catenin expressionPatrick Pollard
Molecular and Population Genetics Laboratory, London Research Institute, Cancer Research UK, London, England
Gastroenterology 136:2204-2213.e1-13. 2009..In mice, however, second hits appear to vary with the strain or genetic background used. This suggested the possibility of creating suboptimal Apc genotypes in the mouse...
- Mutation cluster region, association between germline and somatic mutations and genotype-phenotype correlation in upper gastrointestinal familial adenomatous polyposisChristopher Groves
Academic Unit and Polyposis Registry, Saint Mark s Hospital, Harrow, United Kingdom
Am J Pathol 160:2055-61. 2002..Compared with colonic tumors, however, retention of a greater number of beta-catenin binding/degradation repeats is optimal for tumorigenesis in upper gastrointestinal FAP...
- Intestinal tumorigenesis in compound mutant mice of both Dpc4 (Smad4) and Apc genesK Takaku
Banyu Tsukuba Research Institute Merck, Japan
Cell 92:645-56. 1998..These results indicate that mutations in DPC4 (SMAD4) play a significant role in the malignant progression of colorectal tumors...
- Mutations in APC, Kirsten-ras, and p53--alternative genetic pathways to colorectal cancerGillian Smith
Cancer Research United Kingdom Molecular Pharmacology Unit, Biomedical Research Centre, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom
Proc Natl Acad Sci U S A 99:9433-8. 2002....
- Familial adenomatous polyposisPolymnia Galiatsatos
Division of Gastroenterology, Department of Medicine, The Sir Mortimer B Davis Jewish General Hospital, McGill University, Montreal, Quebec, Canada
Am J Gastroenterol 101:385-98. 2006....
- The APC variants I1307K and E1317Q are associated with colorectal tumors, but not always with a family historyI M Frayling
Colorectal Cancer Unit, Imperial Cancer Research Fund, St Mark s and Northwick Park Hospitals National Health Service Trust, Harrow, HA1 3UJ, United Kingdom
Proc Natl Acad Sci U S A 95:10722-7. 1998....
- Colonic tumorigenesis in BubR1+/-ApcMin/+ compound mutant mice is linked to premature separation of sister chromatids and enhanced genomic instabilityChinthalapally V Rao
Department of Medicine, University of Oklahoma Health Science Center, Oklahoma City, OK 73104, USA
Proc Natl Acad Sci U S A 102:4365-70. 2005..Together, our studies suggest that BubR1 and Apc functionally interact in regulating metaphase-anaphase transition, deregulation of which may play a key role in genomic instability and development and progression of colorectal cancer...
- Chemoprevention of spontaneous intestinal adenomas in the Apc Min mouse model by the nonsteroidal anti-inflammatory drug piroxicamR F Jacoby
Department of Medicine Division of Gastroenterology, University of Wisconsin, Madison, Wisconsin 53792, USA
Cancer Res 56:710-4. 1996..The Min mouse model demonstrates that the nonsteroidal anti-inflammatory drug piroxicam has strong biological and therapeutic effects, potentially useful for prevention of the early adenoma stage of tumor development...
- APC gene: database of germline and somatic mutations in human tumors and cell linesP Laurent-Puig
Hôpital Laennec Service de Chirurgie Digestive Générale et Oncologique, 42 rue de Sevres, 75007 Paris, France
Nucleic Acids Res 26:269-70. 1998..It includes both molecular information about the mutations and clinical data about the patients. Software has been designed to analyse all this information in the database...
- Chemopreventive efficacy and pharmacokinetics of curcumin in the min/+ mouse, a model of familial adenomatous polyposisSarah Perkins
Cancer Biomarkers and Prevention Group, Department of Oncology, University of Leicester, Leicester, United Kingdom
Cancer Epidemiol Biomarkers Prev 11:535-40. 2002..6 g of curcumin is required for efficacy in humans. A clear advantage of curcumin over nonsteroidal anti-inflammatory drugs is its ability to decrease intestinal bleeding linked to adenoma maturation...
- 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..These studies suggest that mTOR inhibitors should be further explored as potential colorectal cancer therapies in patients whose tumors do not have activating mutations in KRAS...
- Dextran sodium sulfate strongly promotes colorectal carcinogenesis in Apc(Min/+) mice: inflammatory stimuli by dextran sodium sulfate results in development of multiple colonic neoplasmsTakuji Tanaka
Department of Oncologic Pathology, Kanazawa Medical University, Uchinada, Ishikawa, Japan
Int J Cancer 118:25-34. 2006..The findings also suggest that strong oxidative/nitrosative stress caused by DSS-induced inflammation may contribute to the colonic neoplasms development...
- Targeted expression of oncogenic K-ras in intestinal epithelium causes spontaneous tumorigenesis in miceKlaus Peter Janssen
Cellular Morphogenesis and Signalisation, UMR144, Institut Curie, Paris, France
Gastroenterology 123:492-504. 2002..Ras oncoproteins are mutated in about 50% of human colorectal cancers, but their precise role in tumor initiation or progression is still unclear...
- 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..Upregulation of Ets2 and, potentially, other genes involved in this kind of protective effect may provide a prophylactic effect in all individuals, regardless of ploidy...
- Adenomatous polyposis families that screen APC mutation-negative by conventional methods are genetically heterogeneousElise T Renkonen
Department of Medical Genetics, Institute of Dentistry, Biomedicum Helsinki, PO Box 63 Haartmaninkatu 8, FIN 00014 University of Helsinki, Helsinki, Finland
J Clin Oncol 23:5651-9. 2005..Our purpose was to clarify the genetic basis of polyposis and genotype-phenotype correlations in such families...
- Tumor suppressor gene promoter hypermethylation in serum of breast cancer patientsEssel Dulaimi
Department of Surgical Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA
Clin Cancer Res 10:6189-93. 2004..In this study, we examine serum, a more readily accessible bodily fluid known to contain neoplastic DNA from individuals with cancer, for methylation-based detection of breast neoplasia...
- Haploinsufficiency of Krüppel-like factor 5 rescues the tumor-initiating effect of the Apc(Min) mutation in the intestineBeth B McConnell
Division of Digestive Diseases, Department of Medicine, Department of Pharmacology, and Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA
Cancer Res 69:4125-33. 2009....
- Prognostic DNA methylation marker in serum of cancer patientsHannes M Müller
Department of General and Transplant Surgery, Innsbruck Medical University, A 6020 Innsbruck, Austria
Ann N Y Acad Sci 1022:44-9. 2004..This finding indicates great potential for the use of these epigenetic markers in clinical, routine risk assessment in patients with various malignancies...
- The many ways of Wnt in cancerPaul Polakis
Department of Research, Genentech Inc, 1 DNA Way, South San Francisco, CA 94080, USA
Curr Opin Genet Dev 17:45-51. 2007..This review summarizes the reported genetic defects in the Wnt pathway, with an emphasis on their functional contribution to human tumor progression...
- Somatic APC mosaicism: an underestimated cause of polyposis coliF J Hes
Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
Gut 57:71-6. 2008..The patient with 10 or more adenomas in the colon poses a diagnostic challenge. Beside germline mutations in the APC and MUTYH genes, only four cases of mosaic APC mutations have been reported...
- A target-selected Apc-mutant rat kindred enhances the modeling of familial human colon cancerJames M Amos-Landgraf
Department of Biostatistics and Medical Informatics, Section of Gastroenterology and Hepatology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53726, USA
Proc Natl Acad Sci U S A 104:4036-41. 2007..We believe that the Pirc rat kindred can address many of the current gaps in the modeling of human colon cancer...
- The frequency of founder mutations in the BRCA1, BRCA2, and APC genes in Australian Ashkenazi Jews: implications for the generality of U.S. population dataA Y Bahar
Hereditary Cancer Clinic, Prince of Wales Hospital, Randwick, New South Wales, Australia
Cancer 92:440-5. 2001..DNA extracted from 1200 deidentified blood samples was tested using amplification refractory mutation system polymerase chain reaction...
- Therapeutic utility of aspirin in the ApcMin/+ murine model of colon carcinogenesisBrian K Reuter
Center for Cardiovascular Sciences, Albany Medical College, New York 12208, USA
BMC Cancer 2:19. 2002..The present study examines the ability of aspirin to treat established polyposis in Min/+ mice...
- 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..Our data demonstrate that loss of EphB expression represents a critical step in colorectal cancer progression...
- Detection of dysplastic intestinal adenomas using a fluorescent folate imaging probeWei Tsung Chen
Center for Molecular Imaging Research, Harvard Medical School, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 92129, USA
Mol Imaging 4:67-74. 2005..2.2%), and confirmed the source of FFP-positive cells to be primarily an F4/80-positive macrophage subpopulation. Taken together, these results indicate that probe potentially can be used to image dysplastic intestinal adenomas in vivo...
- 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..Similarities with cancer of the breast, prostate, lung, and other sites raise the possibility of broader roles for regulatory lymphocytes in prevention and treatment of epithelial cancers in humans...
- A CpG island hypermethylation profile of primary colorectal carcinomas and colon cancer cell linesGuro E Lind
Department of Genetics, Institute for Cancer Research, The Norwegian Radium Hospital, 0310 Oslo, Norway
Mol Cancer 3:28. 2004..We compared the DNA methylation profiles of the cell lines with those of the primary tumors. Finally, we examined if the epigenetic changes were associated with known genetic markers and/or clinicopathological variables...
- Beef induces and rye bran prevents the formation of intestinal polyps in Apc(Min) mice: relation to beta-catenin and PKC isozymesM Mutanen
Department of Applied Chemistry and Microbiology Nutrition, PO Box 27, University of Helsinki, Helsinki, FIN 00014, Finland
Carcinogenesis 21:1167-73. 2000..43). No differences between groups in expression of protein kinase C (PKC) alpha, betaII, delta and zeta were found. The four PKC isozymes were positively correlated with cytosolic beta-catenin levels (r = 0.62-0.68; P < 0.0001)...
- Regulation of spontaneous intestinal tumorigenesis through the adaptor protein MyD88Seth Rakoff-Nahoum
Howard Hughes Medical Institute and Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA
Science 317:124-7. 2007..This study thus reveals the important role of an innate immune signaling pathway in intestinal tumorigenesis...
- Guanylyl cyclase C suppresses intestinal tumorigenesis by restricting proliferation and maintaining genomic integrityPeng Li
Department of Pharmacology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
Gastroenterology 133:599-607. 2007..However, the role of GCC in neoplasia remains obscure...
- Intestinal tumorigenesis is suppressed in mice lacking the metalloproteinase matrilysinC L Wilson
Department of Cell Biology, Vanderbilt University, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 94:1402-7. 1997..These results argue for the use of MMP inhibitors in the treatment and prevention of early-stage colon cancer...
- Suppression of intestinal and mammary neoplasia by lifetime administration of aspirin in Apc(Min/+) and Apc(Min/+), Msh2(-/-) miceO J Sansom
Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3US, United Kingdom
Cancer Res 61:7060-4. 2001..Thus embryonic and perinatal exposure to aspirin suppresses neoplasia specifically associated with the loss of Apc function, opening a potential window of opportunity for nonsteroidal anti-inflammatory drug intervention...
- Involvement of APC and K-ras mutation in non-polypoid colorectal tumorigenesisN Umetani
Department of Surgical Oncology, School of Medicine, The University of Tokyo, Japan
Br J Cancer 82:9-15. 2000..In this non-polypoid pathway, APC mutation seems to be requisite but K-ras mutation not. It is possible that new APC mutations are acquired after the development of superficial depressed adenomas...
- Pathogenesis of non-familial colorectal carcinomas with high microsatellite instabilityK Shitoh
Department of Surgery, Jichi Medical School, 3311 1 Yakushiji, Minamikawachimachi, Tochigi 324 0498, Japan
J Clin Pathol 53:841-5. 2000..The relation between MSI and cancer associated genes in non-familial colorectal carcinomas has yet to be evaluated. To clarify this matter, changes in cancer associated genes were examined in non-familial colorectal carcinomas...
- Enhanced CpG mutability and tumorigenesis in MBD4-deficient miceCatherine B Millar
Wellcome Trust Centre for Cell Biology, The King s Buildings, Edinburgh University, Edinburgh EH9 3JR, UK
Science 297:403-5. 2002..On a cancer-susceptible Apc(Min/+) background, Mbd4-/- mice showed accelerated tumor formation with CpG --> TpG mutations in the Apc gene. Thus MBD4 suppresses CpG mutability and tumorigenesis in vivo...
- Different familial adenomatous polyposis phenotypes resulting from deletions of the entire APC exon 15Li Kuo Su
Department of Molecular and Cellular Oncology, Box 79, The University of Texas M D Anderson Cancer Center, 1515 Holcombe Boulevard, Houston 77030, USA
Hum Genet 111:88-95. 2002..A surprising finding was that one proband had the typical FAP phenotype, whereas the other had a phenotype consistent with that of AFAP...
- A Drosophila APC tumour suppressor homologue functions in cellular adhesionFumihiko Hamada
MRC Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 2QH, UK
Nat Cell Biol 4:208-13. 2002..These results indicate that Drosophila APC functions in cellular adhesion; these results could have implications for colorectal adenoma formation and tumour progression in humans...
- Chemopreventive efficacy of combined piroxicam and difluoromethylornithine treatment of Apc mutant Min mouse adenomas, and selective toxicity against Apc mutant embryosR F Jacoby
University of Wisconsin Comprehensive Cancer Center, Madison 53792, USA
Cancer Res 60:1864-70. 2000..28:1. Thus, these agents are effective against adenomas that have homozygous mutation of the APC gene and also select against fetuses bearing a heterozygous mutation in the APC gene...
- Epigenetic alterations of CDH1 and APC genes: relationship with activation of Wnt/beta-catenin pathway in invasive ductal carcinoma of breastChandra P Prasad
Department of Biochemistry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India
Life Sci 83:318-25. 2008..The concordance between CDH1 and APC methylation in IDCs and paired circulating DNA underscores the utility of serum DNA as a non-invasive tool for methylation analysis in IDC patients...
- Evaluation of dHPLC in mutation screening of the APC gene in a Greek FAP cohortMarkos Mihalatos
Molecular Biology Research Center HYGEIA, Antonis Papayiannis, Kifissias Ave and Erythrou Stavrou 4 Str, 15123 Maroussi, Athens, Greece
Anticancer Res 23:2691-5. 2003..A multitude of mutations, dispersed throughout the gene, have been described. We wanted to evaluate the usefulness of denaturing high performance liquid chromatography (dHPLC) for mutation screening...
- 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..The adenomas showed deletion of Apc exon 14, indicating that the loss of Apc function was caused by Cre-loxP-mediated recombination...
- The type of somatic mutation at APC in familial adenomatous polyposis is determined by the site of the germline mutation: a new facet to Knudson's 'two-hit' hypothesisH Lamlum
Molecular and Population Genetics Laboratory, Imperial Cancer Research Fund, 44, Lincoln s Inn Fields, London WC2A 3PX, UK
Nat Med 5:1071-5. 1999..Our findings also indicate a new mechanism for disease severity: if a broader spectrum of mutations is selected in tumors, the somatic mutation rate is effectively higher and more tumors grow...
- Truncating APC mutations have dominant effects on proliferation, spindle checkpoint control, survival and chromosome stabilityAnthony Tighe
Faculty of Life Sciences, University of Manchester, The Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK
J Cell Sci 117:6339-53. 2004..We suggest therefore that the initial APC mutation acts as a 'double whammy', destabilising the genome and setting the stage for deregulated proliferation upon loss of the second APC allele...
- Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc geneM Oshima
Banyu Tsukuba Research Institute Merck, Japan
Proc Natl Acad Sci U S A 92:4482-6. 1995..It is therefore unlikely that the truncated product interacts directly with the wild-type protein and causes the microadenomas by a dominant negative mechanism...
- Extensive characterization of genetic alterations in a series of human colorectal cancer cell linesJ Gayet
INSERM U434 - CEPH, Paris, France
Oncogene 20:5025-32. 2001..Our results may prove to be very useful for understanding the different biological pathways involved in the development of colon cancer, and for groups studying cellular biology and pharmacology on the same cell lines...
- Guidelines for the clinical management of familial adenomatous polyposis (FAP)H F A Vasen
Department of Gastroenterology and Hepatology, Leiden University Medical Centre, Rijnsburgerweg 10, 2333 AA Leiden, The Netherlands
Gut 57:704-13. 2008..The guidelines described herein may be helpful in the appropriate management of FAP families. In order to improve the care of these families further, prospective controlled studies should be undertaken...
- DNA methylation markers and early recurrence in stage I lung cancerMalcolm V Brock
Johns Hopkins Hospital, Baltimore, USA
N Engl J Med 358:1118-28. 2008..Despite optimal and early surgical treatment of non-small-cell lung cancer (NSCLC), many patients die of recurrent NSCLC. We investigated the association between gene methylation and recurrence of the tumor...
- Methylation of adenomatous polyposis coli in endometrial cancer occurs more frequently in tumors with microsatellite instability phenotypeMichele Zysman
Samuel Lunenfeld Research Institute, Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, M5G 1X5, Canada
Cancer Res 62:3663-6. 2002..Our results demonstrate APC methylation in endometrial cancer for the first time and show that APC hypermethylation occurs at an increased frequency in MSI+ endometrial tumors (P = 0.01)...
- Analysis of chromosomal instability in human colorectal adenomas with two mutational hits at APCO M Sieber
Molecular and Population Genetics Laboratory, FACS Laboratory, Cancer Research UK
Proc Natl Acad Sci U S A 99:16910-5. 2002..Regarding the model in which APC mutations lead directly to CIN, if APC mutations do have this effect in vivo, it must be subtle. Alternatively, CIN associated with APC mutations might be essentially an in vitro phenomenon...
- Detection of dysplastic intestinal adenomas using enzyme-sensing molecular beacons in miceKatharina Marten
Center for Molecular Imaging Research, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
Gastroenterology 122:406-14. 2002..Proteases play key roles in the pathogenesis of tumor growth and invasion. This study assesses the expression of cathepsin B in dysplastic adenomatous polyps...
- Evidence for genetic predisposition to desmoid tumours in familial adenomatous polyposis independent of the germline APC mutationN J H Sturt
Polyposis Registry, St Mark s Hospital, Harrow, Middlesex HA1 3UJ, UK
Gut 53:1832-6. 2004..We have suggested that because families with germline mutations in this region already have the requisite change, they are more likely to develop desmoids. However, there are families with 5' germline mutations where desmoids are common...
- Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or "multiple" colorectal adenomasO M Sieber
Molecular and Population Genetics Laboratory, Imperial Cancer Research Fund, 44 Lincoln s Inn Fields, London WC2A 3PX, United Kingdom
Proc Natl Acad Sci U S A 99:2954-8. 2002..Screening for germ-line deletions in APC mutation-negative individuals with classical polyposis seems warranted...
- Activation of the beta-catenin gene by interstitial deletions involving exon 3 in primary colorectal carcinomas without adenomatous polyposis coli mutationsK Iwao
Department of Medical Genetics, Biomedical Research Center, Osaka University Medical School, Suita City, Japan
Cancer Res 58:1021-6. 1998..This result suggested that, in the absence of a peptide encoded by exon 3, beta-catenin is stabilized and has a dominant oncogenic effect on colorectal tumorigenesis...
- The sulfide metabolite of sulindac prevents tumors and restores enterocyte apoptosis in a murine model of familial adenomatous polyposisN N Mahmoud
The New York Hospital Cornell University Medical Center, NY 10021, USA
Carcinogenesis 19:87-91. 1998..001). These data suggest that the anti-tumor effect of sulindac in Apc-deficient animals is mediated by the sulfide metabolite and correlates with suppression of tissue prostaglandin synthesis...
- Top-down morphogenesis of colorectal tumorsI M Shih
The Howard Hughes Medical Institute, Johns Hopkins Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
Proc Natl Acad Sci U S A 98:2640-5. 2001..Genetically altered cells in the superficial portions of the mucosae spread laterally and downward to form new crypts that first connect to preexisting normal crypts and eventually replace them...
- A molecular variant of the APC gene at codon 1822: its association with diet, lifestyle, and risk of colon cancerM L Slattery
Department of Family and Preventive Medicine University of Utah, Salt Lake City, 84112, USA
Cancer Res 61:1000-4. 2001..These results suggest that the codon 1,822 variant of the APC gene may have functional significance. Individuals who have the valine/valine variant of this gene may be at reduced risk of colon cancer if they eat a low-fat diet...
- Tumorigenesis in the multiple intestinal neoplasia mouse: redundancy of negative regulators and specificity of modifiersR B Halberg
McArdle Laboratory for Cancer Research, Department of Biostatistics, University of Wisconsin, Madison, WI 53706, USA
Proc Natl Acad Sci U S A 97:3461-6. 2000..The ensemble of tumor suppressors and modifiers of a neoplastic process can be usefully analyzed in respect to tissue specificity and synergy...
- Molecular nature of colon tumors in hereditary nonpolyposis colon cancer, familial polyposis, and sporadic colon cancerM Konishi
Department of Biochemistry, Tokyo Metropolitan Institute of Medical Science, Japan
Gastroenterology 111:307-17. 1996..To clarify the nature of HNPCC tumors, RER and genetic changes were compared between HNPCC and non-HNPCC tumors...
- APC mutations in familial adenomatous polyposis families in the Northwest of EnglandJ G Armstrong
Department of Medical Genetics, St Mary s Hospital, Manchester, UK
Hum Mutat 10:376-80. 1997..Although the frequency of the most common mutation appears low, it is not dissimilar to that reported by other groups...
- Loss of Apc and the entire chromosome 18 but absence of mutations at the Ras and Tp53 genes in intestinal tumors from Apc1638N, a mouse model for Apc-driven carcinogenesisR Smits
MGC Department of Human Genetics, Leiden University, The Netherlands
Carcinogenesis 18:321-7. 1997....
- Mutation analysis of the adenomatous polyposis coli (APC) gene in northwest Spanish patients with familial adenomatous polyposis (FAP) and sporadic colorectal cancerC Ruiz-Ponte
Unidad de Medicina Molecular INGO, SERGAS, 15706 Universidad de Santiago de Compostela, Spain
Hum Mutat 18:355. 2001..Differences in the recurrence of pathological mutations in APC could exist among populations. However, epidemiological studies must be performed to confirm this hypothesis...
- Periampullary adenomas and adenocarcinomas in familial adenomatous polyposis: cumulative risks and APC gene mutationsJ Bjork
Department of Gastroenterology and Hepatology, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden
Gastroenterology 121:1127-35. 2001..The genotype of patients with stage IV periampullary adenomas and periampullary adenocarcinomas was also investigated...
- The I1307K APC polymorphism: prevalence in non-Ashkenazi Jews and evidence for a founder effectR Shtoyerman-Chen
Department of Gastroenterology, Chaim Sheba Medical Center, Tel Hashomer, Israel
Genet Test 5:141-6. 2001..Jewish I1307K mutation carriers share a common allelic pattern with APC-linked markers. This strongly supports the notion of a founder mutation for I1307K...
- Microadenomatous lesions involving loss of Apc heterozygosity in the colon of adult Apc(Min/+) miceYasuhiro Yamada
Department of Pathology, Gifu University School of Medicine, Gifu 500 8705, Japan
Cancer Res 62:6367-70. 2002..Our results may give an account for the low incidence of colonic tumors in Apc(Min/+) mice...
- Enhanced stem cell survival in familial adenomatous polyposisKyoung Mee Kim
Department of Pathology, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA
Am J Pathol 164:1369-77. 2004..Heterozygous APC mutations may change stem cell survival during colorectal pretumor progression...
- Molecular changes in the Ki-ras and APC genes in primary colorectal carcinoma and synchronous metastases compared with the findings in accompanying adenomasP Zauber
Saint Barnabas Medical Center, 22 Old Short Hill Road, Livingstone, NJ 07039, USA
Mol Pathol 56:137-40. 2003....
- R-flurbiprofen chemoprevention and treatment of intestinal adenomas in the APC(Min)/+ mouse model: implications for prophylaxis and treatment of colon cancerW J Wechter
Laboratory of Chemical Endocrinology, Loma Linda University School of Medicine, California 92350, USA
Cancer Res 57:4316-24. 1997..i.d.. Both drug-treated groups demonstrated tumor numbers significantly less than that of the vehicle control (P < 0.01). Our results suggest that prophylaxis and treatment trials of R-FB should be extended to humans...
- Loss of Apc+ in intestinal adenomas from Min miceC Luongo
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison 53706
Cancer Res 54:5947-52. 1994..Only one copy of the homologue carrying ApcMin remained in the intestinal adenomas. Possible reasons for the difference in the mechanism of Apc+ loss between human and Min mouse intestinal adenomas are discussed...
- The adenomatous polyposis coli protein: in the limelight out at the edgeD Dikovskaya
Division of Cell and Developmental Biology, School of Life Sciences, WTB/MSI Complex, University of Dundee, DD1 5EH, Dundee, UK
Trends Cell Biol 11:378-84. 2001..Here, we integrate recent information describing the association between APC and the cytoskeleton to illustrate how this multifaceted protein might link different cytoskeletal elements to each other and to cellular signaling pathways...
- The distinct spectra of tumor-associated Apc mutations in mismatch repair-deficient Apc1638N mice define the roles of MSH3 and MSH6 in DNA repair and intestinal tumorigenesisM Kuraguchi
Strang Cancer Research Laboratory at The Rockefeller University, New York, New York 10021, USA
Cancer Res 61:7934-42. 2001..Our analysis therefore has revealed distinct mutational spectra and clarified the roles of Msh3 and Msh6 in DNA repair and intestinal tumorigenesis...
- Mutations in Apc and p53 synergize to promote mammary neoplasiaValerie Meniel
School of Biological Sciences, Cardiff University, Cardiff, United Kingdom
Cancer Res 65:410-6. 2005..We therefore show clear synergy between these two mutations in mammary gland neoplasia and present data to suggest that at least one mechanism for this acceleration is the p53-dependent loss of Apc-deficient cells...
- [Promoter methylation profile in breast cancer]Juan Carlos Roa
Departamento de Anatomia Patologica, Facultad de Medicina, Universidad de La Frontera, Temuco, Chile
Rev Med Chil 132:1069-77. 2004..Genomic DNA methylation, mutations and allelic deletions explain the inactivation of genes involved in cell proliferation and cell cycle control mechanisms...
- Increased frequency of p53 mutation in sporadic colorectal cancer from cigarette smokersMichiko Miyaki
Hereditary Tumor Research Project, Tokyo Metropolitan Komagome Hospital, Japan
Jpn J Clin Oncol 32:196-201. 2002..Cigarette smoking has been shown to increase the risk of colorectal cancer. However, the relation between smoking and genetic alterations has not been clarified in this type of cancer...
- [Methylation status and protein expression of adenomatous polyposis coli (APC) gene in breast cancer]Zhen Liu
First Department of General Surgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning 110004, P R China
Ai Zheng 26:586-90. 2007....
- Suppression of intestinal polyp development by low-fat and high-fiber diet in Apc(delta716) knockout miceK Hioki
Central Institute for Experimental Animals, Kawasaki, Japan
Carcinogenesis 18:1863-5. 1997..This is likely to be due to a decreased frequency of loss of heterozygosity, rather than a retarded growth of the polyp adenomas...
- Tumor regionality in the mouse intestine reflects the mechanism of loss of Apc functionKevin M Haigis
McArdle Laboratory for Cancer Research, 1400 University Avenue, Madison, WI 53706, USA
Proc Natl Acad Sci U S A 101:9769-73. 2004..Perhaps, the power of mouse genetics and biology can be harnessed to identify genetic and other factors that contribute to tumor regionality...
- Chromosome instability in colorectal tumor cells is associated with defects in microtubule plus-end attachments caused by a dominant mutation in APCRebecca A Green
Section of Molecular and Cellular Biology, University of California, Davis, Davis, CA 95616, USA
J Cell Biol 163:949-61. 2003..We propose that APC functions to modulate microtubule plus-end attachments during mitosis, and that a single mutant APC allele predisposes cells to increased mitotic abnormalities, which may contribute to tumor progression...
- Promoter methylation inhibits APC gene expression by causing changes in chromatin conformation and interfering with the binding of transcription factor CCAAT-binding factorGuoren Deng
Gastrointestinal Research Laboratory, Veteran Affairs Medical Center and Department of Medicine, University of California San Francisco, San Francisco, California, USA
Cancer Res 64:2692-8. 2004..In summary, methylation of CpG sites around CCAAT box in APC promoter inhibits the gene expression by changing the chromatin conformation and interfering with the binding of transcription factor CBF to CCAAT box...
- Regulation of caspase expression and apoptosis by adenomatous polyposis coliTingan Chen
Department of Interdisciplinary Oncology and Surgery, University of South Florida, Tampa, FL 33612, USA
Cancer Res 63:4368-74. 2003..These data provide support for the hypothesis that one of the functions of APC is the regulation of caspase activity and other apoptotic proteins by controlling their expression levels in the cell...
- Frequency and parental origin of de novo APC mutations in familial adenomatous polyposisStefan Aretz
Institute of Human Genetics, University of Bonn, Germany
Eur J Hum Genet 12:52-8. 2004..Sex-related differences of mutation types could be observed: large deletions and single-base substitutions were exclusively of paternal origin, whereas the small deletions were equally distributed (maternal/paternal ratio 4:4)...
- Genotype and phenotype of patients with both familial adenomatous polyposis and thyroid carcinomaBrindusa Truta
University California San Francisco, Department of Medicine, Comprehensive Cancer Center, San Francisco, California, USA
Fam Cancer 2:95-9. 2003..Additionally, thyroid cancer in our patients occurred in the setting of classic FAP phenotype. Germline mutations were located predominantly outside the APC mutation cluster region...
- Intestinal-specific PPARgamma deficiency enhances tumorigenesis in ApcMin/+ miceChristen A McAlpine
Department of Biochemistry and Molecular Biology, University of Minnesota Medical School, Duluth, USA
Int J Cancer 119:2339-46. 2006..Our results suggest that PPARgamma functions as a tumor resistance factor in the mouse intestine and warrant further investigation of the PPARgamma-dependent and independent actions of TZDs in cancer...
- Genetic anthropology of the colorectal cancer-susceptibility allele APC I1307K: evidence of genetic drift within the AshkenazimBethany L Niell
Department of Internal Medicine, Division of Molecular Medicine and Genetics, University of Michigan Medical School, Ann Arbor, MI 48109 0638, USA
Am J Hum Genet 73:1250-60. 2003..This research underscores the importance of the migratory patterns of ancestral populations in the ethnic and geographic distribution of APC I1307K...
- The complex genotype-phenotype relationship in familial adenomatous polyposisHeikki J Jarvinen
Department of Gastroenterological Surgery, Helsinki University Central Hospital, Helsinki, Finland
Eur J Gastroenterol Hepatol 16:5-8. 2004..The clinical applications of genotype-phenotype correlation on the management of patients with familial adenomatous polyposis remain limited apart from predictive genetic testing...
- Dietary factors and truncating APC mutations in sporadic colorectal adenomasBrenda Diergaarde
Division of Human Nutrition and Epidemiology, Wageningen University, Wageningen, The Netherlands
Int J Cancer 113:126-32. 2005..However, most examined dietary factors do not appear to be specifically associated with the occurrence of truncating APC mutations in colorectal adenomas but seem to affect both pathways equally...
- Inhibition of intestinal polyposis with reduced angiogenesis in ApcMin/+ mice due to decreases in c-Myc expressionKrishna Yekkala
Department of Cell and Developmental Biology and Anatomy, University of South Carolina School of Medicine, 6439 Garners Ferry Road, Building 1, C 57, Columbia, SC 29209, USA
Mol Cancer Res 5:1296-303. 2007..This study shows that c-Myc is critical for Apc-dependent intestinal tumorigenesis in mice and provides a potential therapeutic target in the treatment of colorectal cancer...
- Attenuated familial adenomatous polyposis: a case report with mixed features and review of genotype-phenotype correlationDiana N Ionescu
Department of Pathology and Laboratory Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA 15232, USA
Arch Pathol Lab Med 129:1401-4. 2005..Differences in the APC mutation sites alone cannot completely account for intrafamilial and interfamilial variation in the polyposis phenotypes...
- Thyroid cancer in two siblings with FAP syndrome and APC mutationI Brozek
Int J Colorectal Dis 23:331-2. 2008
- 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..Although EX affected IGF-1 and corticosterone, neither marker was related to total polyp number...
- Large submicroscopic genomic APC deletions are a common cause of typical familial adenomatous polyposisS Aretz
J Med Genet 42:185-92. 2005
- Timing of Rectal Cancer Response to ChemoradiationJulio Garcia Aguilar; Fiscal Year: 2009..cells microdissected from pre-chemoradiation biopsy specimens will be tested for mutations in the p53, k-ras and APC genes, BAT26 deletions, and p16 promoter methylation...
- Early Events in Colitis-Associated Colorectal CancerWen Chi Chang; Fiscal Year: 2003..The gatekeeper function of the p53 and APC genes in colitis-associated CRC will be determined by mutational analysis of these genes in microdissected inflamed ..
- Beta-catenin regulation by tumor suppressor APCChunming Liu; Fiscal Year: 2006..Mutations in APC genes result in B-catenin accumulation that activates other oncogenes...
- MINORITY PREDOCTORAL FELLOWSHIP PROGRAMCARILUZ SANTIAGO ORTIZ; Fiscal Year: 2006..The central hypothesis of this proposal is that mutations in p53, K-ras and APC genes promote the formation of malignant cells that can result in tumors in UC-associated cancer...
- role of adipokines in colon epithelial cell homeostasisJENIFER FENTON; Fiscal Year: 2008..unreadable] [unreadable] [unreadable]..
- AUSTRALASIAN C0L0RECTAL CANCER FAMILY STUDYJeremy Jass; Fiscal Year: 2002..These characteristics include manageable yet sufficient size, ethnically diverse, highly localised, stable, and with families that are intact and large. ..
- PREVENTION OF COLORECTAL CANCER BY iNOS AND COX-2 SELECTIVE INHIBITORSCHINTHALAPALLY RAO; Fiscal Year: 2008..abstract_text> ..
- 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. ..
- Inhibiting Survivin for Chemoprevention of Colon CancerSERGIO LAMPRECHT; Fiscal Year: 2005..abstract_text> ..
- The molecular basis of planarian regenerationALEJANDRO SANCHEZ ALVARADO; Fiscal Year: 2006..abstract_text> ..
- Wnt and beta-Catenin Signaling in Development/DiseaseMariann Bienz; Fiscal Year: 2006..Basic researchers and the pharmaceutical and biotechnology industry are invited to discuss how to exploit model systems and how to translate knowledge from these into drug development. [unreadable] [unreadable]..
- Molecular Basis of Young Onset Colorectal CancerLisa Boardman; Fiscal Year: 2006..Following achievement of these goals, I am confident that I will be ready to continue my career as a successful independent investigator committed to colerectal cancer prevention and control. ..
- RAGE and modulation of tumor propertiesEmina Huang; Fiscal Year: 2006..A range of tools will be employed in order to accomplish these goals, both in in vitro assay systems, and in vivo, using RAGE null mice and a murine model of familial adenomatous polyposis (FAP). ..
- SIGNALING IN INTESTINAL CANCERLeonard H Augenlicht; Fiscal Year: 2010..abstract_text> ..
- The Mammalian Cell Cycle Control and Tumor GenesisYue Xiong; Fiscal Year: 2009..abstract_text> ..
- Scutellaria baicalensis and Colon Cancer ChemopreventionDiane Harris; Fiscal Year: 2005..abstract_text> ..
- CURCUMIN--MECHANISMS OF CHEMOPREVENTIONLeonard Augenlicht; Fiscal Year: 2001..On the other hand, differences in mechanism could suggest a study design in which curcumin was combined with sulindac or to other NSAIDs in a prevention trial to test whether the two agents give additive, or synergistic, effects. ..
- COLON CANCER--MOLECULAR BIOLOGY OF CELL RESPONSE TO DIETLeonard Augenlicht; Fiscal Year: 2001....
- Nutritional mechanisms and intestinal tumorigenesisLeonard Augenlicht; Fiscal Year: 2009....
- Mechanisms of Growth Inhibition by Helicobacter PylorHassan Ashktorab; Fiscal Year: 2003..These studies will help to establish how bacteria can increase apoptosis possibly through generation of ROS and in specific circumstances this may alter one's risk of developing cancer. ..
- Gordon Research Conference of PolyamineEugene Gerner; Fiscal Year: 2005..abstract_text> ..
- BAALC in neurogenesis and hematopoiesisAlbert de la Chapelle; Fiscal Year: 2007..It is postulated that the high degree of evolutionary conservation of BAALC in mammals will allow observations in mice to be applicable to humans. ..
- Proteomic Validation of the Min Mouse Model of Colon CancerAnthony Yeung; Fiscal Year: 2007..The Min mouse model genetically mimics humans for colon cancer. The proposed work will demonstrate whether it is a perfect model for the human disease. ..
- FATTY ACID MODULATION OF COLON CELL TRANSFORMATIONLeonard Augenlicht; Fiscal Year: 2008..unreadable] [unreadable] [unreadable]..
- GENE INTERACTIONS IN COLON CANCERLeonard Augenlicht; Fiscal Year: 2003....
- The Role of Beta-catenin/Tcf Pathway Defects in CancerEric Fearon; Fiscal Year: 2009..Insights into new diagnostic markers and novel therapeutic targets and approaches for cancer are also expected. ..
- Role of IRS-2 in Diabetes and Beta Cell FunctionXueying Lin; Fiscal Year: 2003..abstract_text> ..
- Proteomic Biomarkers in Pancreatic Cyst FluidsAnthony Yeung; Fiscal Year: 2006..abstract_text> ..
- MOLECULAR CLASSIFICATION OF COLON TUMORSLeonard Augenlicht; Fiscal Year: 2004..abstract_text> ..
- Modulation of Intestinal TumorigenesisLeonard Augenlicht; Fiscal Year: 2006..abstract_text> ..
- Colorectal Cancer Screening: Fecal Blood vs DNADavid Ahlquist; Fiscal Year: 2004..If the DNA-based test proves to have greater screening accuracy than fecal blood testing, this could translate into more effective cancer control and more efficient use of our limited health care resources. ..
- beta-Catenin/NF-kappaBeta and Colon CancerShahid Umar; Fiscal Year: 2004..By studying a mechanistic basis of NF-kappaB and beta-catenin mediated increases in cell census, in the absence and presence of chronic inflammation, we may identify new treatment strategies for reducing cancer risk. ..
- APOPTOSIS IN COLON CANCER CHEMOPREVENTIONEugene Gerner; Fiscal Year: 2005..abstract_text> ..
- INCIDENCE AND MOLECULAR SCREENING FOR HEREDITARY CANCERAlbert de la Chapelle; Fiscal Year: 2004..abstract_text> ..
- INHERITED MSH6 MUTATIONS IN DIVERSE COLORECTAL CANCERSSapna Syngal; Fiscal Year: 2004..Evidence that MSH6 is a moderately penetrant, later-onset hereditary colorectal cancer gene would imply the existence of similar genes for other common cancers that await discovery. ..
- SITE SPECIFICITY OF GASTROINTESTINAL TUMORIGENESISLeonard Augenlicht; Fiscal Year: 2004..Lastly, using microarray analyses, the profiles of gene expression that characterize genetic and dietary modulation of risk will be defined. ..
- Characterization of the Chromosome 17q23 AmpliconFergus Couch; Fiscal Year: 2006..Thus, the project may involve a complete transition from benchtop to bedside. Finally, the amplified and overexpressed genes may prove useful as important targets of gene, pharmacological, and immunological therapy in the future. ..
- Paracrine Regulation of IGF-I in the Developing IleumPhillip Gordon; Fiscal Year: 2006..abstract_text> ..
- Coordination of Proliferation and ApoptosisLeonard Augenlicht; Fiscal Year: 2002..Understanding the mechanism by which mitochondrial function coordinates cell maturation pathways in the intestinal mucosa has profound implications for understanding tumorigenesis and for effecting chemoprevention. ..
- CANCER SCREENING COMPLIANCE IN HEREDITARY COLON CANCERSapna Syngal; Fiscal Year: 2005....
- Nuclear functions of the tumor suppressor protein APCKRISTI NEUFELD; Fiscal Year: 2008..Greater knowledge of APC function in normal cells will improve our understanding of APC's role in tumorigenesis and ultimately illuminate new points for therapeutic intervention. ..
- METHYLATION PROFILING AND RISK OF COLORECTAL CANCERHassan Ashktorab; Fiscal Year: 2007..These studies will help in the detection and _rofiling of genetic changes in the pathway of CRC in AA. ..
- P21 INDUCTION BY BRCA2Fergus Couch; Fiscal Year: 2002....
- 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. ..
- Physical Activity Measurement in Older AdultsLisa Colbert; Fiscal Year: 2007..This methodology can then be incorporated into future studies examining the associations between doses of physical activity and various health outcomes. [unreadable] [unreadable]..