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National Cancer Institute®
Ultima Vez Modificado: 1 de marzo del 2002
UI - 11551102
AU - Shtoyerman-Chen R; Friedman E; Figer A; Carmel M; Patael Y; Rath P;
TI - Fidder HH; Bar-Meir S; Theodor L The I1307K APC polymorphism: prevalence in non-Ashkenazi Jews and evidence for a founder effect.
SO - Genet Test 2001 Summer;5(2):141-6
AD - Department of Gastroenterology, Chaim Sheba Medical Center, Tel-Hashomer, Israel. email@example.com
A missense mutation within the APC gene, I1307K, was described in Ashkenazi individuals at risk for colorectal cancer (CRC) and in the general population. The anecdotal reporting of the occurrence of this mutation in some non-Ashkenazi individuals led us to hypothesize that within the Jewish people, the I1307K polymorphism may reflect a founder mutation, and that the mutation is not restricted to ethnic Ashkenazis. To test that notion, and to establish the occurrence rate of the I1307K polymorphism in non-Ashkenazi Jewish populations, we screened Iraqi and Moroccan Jews and consecutive Jewish CRC patients and performed haplotype analysis with APC-linked markers in two I1307K carrier families. We analyzed Jewish individuals: 210 Moroccans, 160 Iraqis, 148 Ashkenazi, and 349 CRC patients (227 Ashkenazi and 122 non-Ashkenazi). The mutation detection scheme included PCR followed by denaturing gradient gel electrophoresis (DGGE) or modified restriction analysis (MRA). Haplotypes were assessed using three intragenic and three flanking markers. The I1307K polymorphism was detected in 29/227 Ashkenazi (12.8%), 2/122 (1.6%) non-Ashkenazi CRC patients, and in 2 individuals each (approximately 1%) within the Moroccan and Iraqi populations. Allelic pattern analysis in all our I1307K carriers, revealed a common haplotype for the three intragenic markers tested, in all mutation carriers, regardless of ethnic origin. The I1307K polymorphism, therefore, exists in all ethnic Jewish populations: Ashkenazi and non-Ashkenazi, with or without colon cancer. Jewish I1307K mutation carriers share a common allelic pattern with APC-linked markers. This strongly supports the notion of a founder mutation for I1307K.
UI - 11793475
AU - Kahmann S; Herter P; Kuhnen C; Muller KM; Muhr G; Martin D; Soddemann M;
TI - Muller O A non-radioactive protein truncation test for the sensitive detection of all stop and frameshift mutations.
SO - Hum Mutat 2002 Feb;19(2):165-72
AD - Max-Planck-Institut fur molekulare Physiologie, Dortmund, Germany.
A new method for mutation detection is described, which is a technical advancement of the protein truncation test. The new technique is non-radioactive and highly sensitive for detection of virtually all sequence mutations, which lead to a stop signal or to the shift of the translation frame. The method includes four steps: 1) capture of the interesting sequence copies out of the sample by binding to an immobilized complementary sequence, 2) PCR amplification of the gene fragment to be analyzed with primers coding both for amino- and carboxy-terminal tags, 3) in vitro transcription and translation, and 4) analysis of the translation products by Western blot. As an evaluation of the new method, we detected mutated gene copies at a dilution of 1 to 40 compared to the non-mutated gene. Using the method, we were able to detect a mutation in the adenomatous polyposis coli tumor suppressor gene (APC) in a stool sample of a colorectal cancer patient. This mutation could not be detected by direct sequencing of the amplified APC gene fragment. Copyright 2002 Wiley-Liss, Inc.
UI - 11830528
AU - Huerta S; Irwin RW; Heber D; Go VL; Koeffler HP; Uskokovic MR; Harris DM
TI - 1alpha,25-(OH)(2)-D(3) and its synthetic analogue decrease tumor load in the Apc(min) Mouse.
SO - Cancer Res 2002 Feb 1;62(3):741-6
AD - University of California-Los Angeles Center for Human Nutrition, Los Angeles, CA 90095, USA.
Both calcium and vitamin D are thought to be able to inhibit colon carcinogenesis. To better define the effects of vitamin D, we studied 1alpha,25-(OH)(2)-D(3) and a noncalcemic synthetic analogue of vitamin D(3) (VD(3)) in the Apc(min) mouse. Female Apc(min) mice 4-5 weeks old were randomized to four groups: a VD(3)-treated group (n = 11) were given injections of 0.01 microg of 1alpha,25-(OH)(2)-D(3) i.p. three times per week; an analogue-treated group (n = 10) received 5 microg of 1alpha,25-(OH)(2)-16-ene-19-nor-24-oxo-D(3) i.p. three times per week; and a control group (n = 12) received sham injections of PBS. A sulindac-treated group (n = 10) was used as a positive control. Doses of these compounds were chosen based on previous toxicity studies in mice and rats. After 10 weeks of treatment, mice were killed and two observers (S. H., R. W. I.), blinded to treatment, scored polyp number and size. Tumor number was not affected with 1alpha,25-(OH)(2)-D(3) or vitamin D analogue administration. A significant decrease in total tumor load (sum of all polyp areas) over the entire gastrointestinal tract was seen in the analogue (36% decrease; P < 0.05) and the VD(3) groups (46%; P < 0.001). There was a significant decrease in polyp number (49%; P < 0.001) and polyp area (70%; P < 0.001) in the sulindac group. Reverse transcription-PCR of the total RNA derived from intestinal tissue revealed expression of the vitamin D receptor throughout the small intestine and the colon. Serum calcium levels in the analogue group were not elevated at week 4 of treatment and only moderately elevated (22%) by week 8 (P < or =0.001). In contrast, serum calcium in the VD(3) group was significantly elevated (P < or =0.001) at weeks 4 (23%) and 8 (45%). Food intake and growth rate were significantly lower in the VD(3) group (26%, P < 0.001, and 27%, P < 0.001, respectively) at week 10. In contrast, food intake and growth rate were similar for the control, sulindac, and analogue groups. Our results indicate that a noncalcemic analogue of vitamin D can significantly decrease intestinal tumor load in Apc(min) mice without severe toxic side effects and suggest that these compounds may have utility as chemopreventive agents in groups at high-risk for colon cancer.
UI - 11852337
AU - Matsumoto T; Iida M; Kobori Y; Mizuno M; Nakamura S; Hizawa K
TI - Progressive duodenal adenomatosis in a familial adenomatous polyposis pedigree with APC mutation at codon 1556.
SO - Dis Colon Rectum 2002 Feb;45(2):229-33
AD - Department of Endoscopic Diagnostics and Therapeutics, Kyushu University Hospital, Fukuoka, Japan.
PURPOSE: In familial adenomatous polyposis, genotype-duodenal phenotype correlations have not been clearly understood. We identified the adenomatous polyposis coli gene mutation in a family pedigree with severe duodenal adenomatosis. METHODS: Among 53 familial adenomatous polyposis families, we found a pedigree composed of five affected members with severe duodenal adenomatosis. Clinical manifestations of the family members were reviewed. The adenomatous polyposis coli gene of four members were screened by polymerase chain reaction-based single strand conformation polymorphism or protein truncation test. RESULTS: The family was characterized by sparse colorectal polyposis, osteomas, and epidermal cysts. However, there were intrafamilial variabilities in the occurrence of fundic gland polyposis, congenital hypertrophy of the retinal pigment epithelium, and desmoids. All the members had duodenal adenomatosis in their second or third decades, and the adenomatosis in three members progressed during surveillance. A frameshift mutation was found at codon 1556 of the adenomatous polyposis coli gene in two members, and the equivalent mutation was confirmed by protein truncation test in another two. CONCLUSIONS: Distal 3' mutation of the adenomatous polyposis coli gene seems to contribute to severe duodenal adenomatosis in familial adenomatous polyposis. Specification of the adenomatous polyposis coli gene mutation may be a clue for surveillance strategy for duodenal adenomatosis in patients with familial adenomatous polyposis.
UI - 11748858
AU - Hutter P; Rey-Berthod C; Chappuis PO; Couturier A; Membrez V; Murphy A;
TI - Joris F; Schorderet DF; Delozier-Blanchet C; Soravia C Molecular and clinical characteristics in 32 families affected with familial adenomatous polyposis.
SO - Hum Mutat 2001 Dec;18(6):550
AD - Unite de Genetique, Institut Central des Hopitaux Valaisans, Av. Grand-Champsec, 1951 Sion, Switzerland. firstname.lastname@example.org.
Germ-line mutations in the 5' half of the Adenomatous Polyposis Coli (APC) gene are found in about 80% of the patients affected with familial adenomatous polyposis (FAP). The vast majority of these are nonsense or frameshift mutations which result in the loss of the carboxyl terminus of the APC protein. Using an in vivo assay in yeast, we have identified pathogenic germ-line mutations in 26 of 32 (81%) unrelated Swiss families affected with FAP. Nine mutations were novel and eight families were shown to harbor two recurrent mutations. Correlations were attempted between the location of APC germ-line mutations and clinical manifestations of the disease. Copyright 2001 Wiley-Liss, Inc.
UI - 11768390
AU - Montera M; Piaggio F; Marchese C; Gismondi V; Stella A; Resta N; Varesco
TI - L; Guanti G; Mareni C A silent mutation in exon 14 of the APC gene is associated with exon skipping in a FAP family.
SO - J Med Genet 2001 Dec;38(12):863-7
UI - 11818567
AU - Roberts RB; Min L; Washington MK; Olsen SJ; Settle SH; Coffey RJ;
TI - Threadgill DW Importance of epidermal growth factor receptor signaling in establishment of adenomas and maintenance of carcinomas during intestinal tumorigenesis.
SO - Proc Natl Acad Sci U S A 2002 Feb 5;99(3):1521-6
AD - Department of Cell Biology, Vanderbilt University, 1161 21st Avenue South, Nashville, TN 37232, USA.
We used the hypomorphic Egfr(wa2) allele to genetically examine the impact of impaired epidermal growth factor receptor (Egfr) signaling on the Apc(Min) mouse model of familial adenomatous polyposis. Transfer of the Apc(Min) allele onto a homozygous Egfr(wa2) background results in a 90% reduction in intestinal polyp number relative to Apc(Min) mice carrying a wild-type Egfr allele. This Egfr effect is potentially synergistic with the actions of the modifier-of-min (Mom1) locus. Surprisingly, the size, expansion, and pathological progression of the polyps appear Egfr-independent. Histological examination of the ilea of younger animals revealed no differences in the number of microadenomas, the presumptive precursor lesions to gross intestinal polyps. Pharmacological inhibition with EKI-785, an Egfr tyrosine kinase inhibitor, produced similar results in the Apc(Min) model. These data suggest that normal Egfr activity is required for establishment of intestinal tumors in the Apc(Min) model between initiation and subsequent expansion of initiated tumors. The role of Egfr signaling during later stages of tumorigenesis was examined by using nude mice xenografts of two human colorectal cancer cell lines. Treatment with EKI-785 produced a dose-dependent reduction in tumor growth, suggesting that Egfr inhibitors may be useful for advanced colorectal cancer treatment.
UI - 11848471
AU - Greco C; Alvino S; Buglioni S; Assisi D; Lapenta R; Grassi A; Stigliano
TI - V; Mottolese M; Casale V Activation of c-MYC and c-MYB proto-oncogenes is associated with decreased apoptosis in tumor colon progression.
SO - Anticancer Res 2001 Sep-Oct;21(5):3185-92
AD - Clinical Pathology Service, Regina Elena Cancer Institute, Rome, Italy. email@example.com
BACKGROUND: An increasing amount of evidence suggests that progression from normal mucosa to colorectal cancer is accompanied by morphological and genetic alterations. Genetic abnormalities affect malignant transformation via a gradual imbalance of normal tissue homeostasis involving programmed cell death (PCD) or apoptosis. Therefore, it has been hypothesized that alterations in apoptosis may contribute to carcinogenesis. The aim of the present work was to investigate the relationship between frequency of spontaneous apoptosis during transition adenoma-to-carcinoma of the colorectal tract and the incidence of activation of c-myc and c-myb proto-oncogenes, involved both in colon tumorigenesis and apoptosis. MATERIALS AND METHODS: Ninety-five tissue specimens (60 polyps and 35 adenocarcinomas) were removed with autologous normal adjacent mucosa from colon cancer patients. Genomic DNA was extracted and analyzed for both apoptosis frequency (DNA fragmentation assay) and proto-oncogene activation (Southern blot analysis). On the same samples, Bcl-2 protein expression was evaluated by immunohistochemistry. RESULTS: Our results showed that: i) a significant relationship exists between apoptosis and genesis of colorectal cancer since, compared to adenomatous polyps and adjacent normal mucosa, cell death is markedly inhibited in tumors (p = 0.01); ii) during colon tumor progression, apoptosis and amplifications of c-myc/c-myb genes are inversely related; iii) Bcl-2 expression is retained in colon tumors even though at a significantly lower level with respect to adenomatous polyps. CONCLUSION: These results indicate that failure of the normal apoptotic process together with de-regulation of c-myc and c-myb proto-oncogenes might promote the development of colorectal tumors.
UI - 11848484
AU - Paulsen JE; Alexander J
TI - Growth stimulation of intestinal tumours in Apc(Min/+) mice by dietary L-methionine supplementation.
SO - Anticancer Res 2001 Sep-Oct;21(5):3281-4
AD - Department of Environmental Medicine, National Institute of Public Health, Oslo, Norway. firstname.lastname@example.org
We studied the effects of extra dietary methionine on the formation and growth of intestinal adenomas in the Min (Apc+/-) mouse, which is a murine model of the human familial adenomatous syndrome. The AIN-76A diet was supplemented with 0.7% L-methionine from week 4 after birth and the animals were killed at week 8. The number of tumours in Min mice was apparently not affected by the addition of extra methionine. However, the dietary methionine supplementation increased the surface area of small intestinal tumours by 41% (p=0.009). In the colon, extra methionine did not affect tumour size. In conclusion, extra dietary methionine promotes the growth of adenomas in the small intestine of Min mice.
UI - 11815870
AU - de Chadarevian JP; Dunn S; Malatack JJ; Ganguly A; Blecker U; Punnett HH
TI - Chromosome rearrangement with no apparent gene mutation in familial adenomatous polyposis and hepatocellular neoplasia.
SO - Pediatr Dev Pathol 2002 Jan-Feb;5(1):69-75
AD - Department of Pathology and Laboratory Medicine. (Anatomical Pathology, Cytogenetics), MCP Hahnemann University School of Medicine and St. Christopher's Hospital for Children, Erie Avenue at Front Street, Philadelphia, PA 19134, USA.
We have identified a constitutional inversion in chromosome 5 associated with familial adenomatous polyposis in three generations of a Mexican family. Two of three siblings developed hepatic neoplasia in infancy. The gene truncation assay failed to demonstrate a truncated protein in the segment harboring the adenomatous polyposis coli (APC) genes. Polymerase chain reaction (PCR) amplification of APC gene coding exons and sequencing of PCR products did not reveal any significant mutation. The data suggest that in this family, the phenotype may be the result of a "position effect."
UI - 11824361
AU - Herfarth C
TI - [Surgery and molecular biology: new insight or stray path?]
SO - Kongressbd Dtsch Ges Chir Kongr 2001;118():769-85
Surgery has the optimal possibility for theoretical-clinical transfer of molecular biological knowledge. On the basis of the existing research emphasis on clinical molecular biology at the Department of Surgery, University of Heidelberg, this is shown by the example of colorectal cancer: Establishment of a large clinical register for hereditary colorect cancer, use of molecular biological methods to improve phenotype/genotype correlations, definition of risk groups, decision on surgical therapeutical concepts for hereditary cancers and considerations on the creation of problem-orientated centers for hereditary cancer. A further example for the application of molecular methods is the detection of minimal residual disease or tumor cells in the different compartments (blood, lymph nodes, bone marrow and peritoneum) in order to achieve a better risk evaluation exceeding the standard pathohistological stage definition. The goal is an individualized or more focused therapy for each patient. Transfer of research from the basic sciences into the clinical setting, integrated into the daily clinical work, is possible in a so-called tandem model.
UI - 11824368
AU - Pistorius S; Schackert HK; Saeger HD
TI - [Can molecular genetic knowledge from studies of hereditary carcinoma be applied to sporadic colorectal carcinoma?]
SO - Kongressbd Dtsch Ges Chir Kongr 2001;118():820-4
AD - Klinik und Poliklinik fur Viszeral-, Thorax- und Gefasschirurgie, Universitatsklinikum Carl Gustav Carus, TU Dresden, Fetscherstrasse 74, 01307 Dresden.
Colorectal carcinomas without a family history are considered to be "sporadic" carcinomas, however, also have a genetic basis. Within the hereditary forms there are 15-50% of patients without a family history being carriers of de novo germline mutations. In addition, non-pathogenic polymorphisms in these tumorsyndrome-genes as well as in genes involved in the carcinogen metabolism (GST, NAT, CYP, MTHFR) are associated with an increased or decreased colorectal cancer risk. Identification of these genetic risk factors will enable individually tailored surveillance and recommendations for prophylaxis as well as individually tailored treatment.
UI - 11839722
AU - Matsumoto T; Iida M; Kobori Y; Mizuno M; Nakamura S; Hizawa K; Yao T
TI - Serrated adenoma in familial adenomatous polyposis: relation to germline APC gene mutation.
SO - Gut 2002 Mar;50(3):402-4
AD - Department of Endoscopic Diagnostics and Therapeutics, Kyushu University Hospital, Fukuoka, Japan. email@example.com
BACKGROUND: Serrated adenoma is a precursor of colorectal cancer. AIM: To clarify possible genotype-phenotype correlations of serrated adenomas in familial adenomatous polyposis (FAP). Patients: Eleven patients from eight families with FAP. METHODS: We performed total colonoscopy with multiple biopsies in patients. Neoplasia with a serrated glandular structure was regarded as a serrated adenoma. In each patient, germline mutations of the APC gene were determined. Colonic phenotype was compared with germline mutations of the APC gene. RESULTS: Serrated adenomas were found in three patients. These patients had macroscopic polyps <100 in number. Pedigrees with serrated adenomas had the truncating germline APC mutation at codon 161, 332, or 1556 while in the other pedigrees mutations were found between codons 554 and 1324. CONCLUSIONS: In FAP, serrated adenoma may be a phenotype characteristic of the attenuated form.
UI - 11713587
AU - Humar B; D'Orazio D; Albrecht C; Bauerfeind P; Muller H; Dobbie Z;
TI - Bendik I Expression of putative anticancer targets in familial adenomatous polyposis and its association with the APC mutation status.
SO - Int J Oncol 2001 Dec;19(6):1179-86
AD - Division of Medical Genetics, DKBW, Research Group Human Genetics, University Hospital, Basel, Switzerland.
Several substances interfering with colorectal carcinogenesis may reduce or prevent adenoma formation in familial adenomatous polyposis (FAP), an inherited predisposition to colorectal cancer. This study determined the expression of genes coding for putative anticancer targets (COX-2, iNOS, MMP-7, ODC, PKCbeta, PPARgamma, RXRalpha, RXRbeta, RXRgamma) in FAP patients to provide one of the rationales for the design of chemotherapy and -prevention strategies. Gene expression was assessed by TaqMan analysis in colonic tissue of 9 FAP patients with mutations in the APC gene (APCpos), 5 FAP patients without identified genetic defect (APCneg), and 3 healthy individuals. Among the examined genes, PKCbeta and MMP-7 were most consistently altered in adenoma tissue relative to matched mucosa. Intriguingly, ODC was clearly overexpressed in polyps from APCpos but not APCneg patients. Furthermore, PKCbeta, MMP-7, ODC, and COX-2 as well as all RXRs displayed altered expression in apparently healthy FAP mucosa as opposed to that of healthy individuals. Our data suggests PKCbeta and MMP-7 to be the most suited as anticancer targets among the genes studied.
UI - 11773864
AU - Lamberti C; Jungck M; Laarmann M; Knapp M; Caspari R; Friedl W;
TI - Sauerbruch T; Propping P; Kruse R Arylamine N-acetyltransferase type 2 and glutathione S-transferases M1 and T1 polymorphisms in familial adenomatous polyposis.
SO - Pharmacogenetics 2002 Jan;12(1):49-54
AD - Institute of Human Genetics, University of Bonn, Bonn, Germany. firstname.lastname@example.org
Familial adenomatous polyposis (FAP) exhibits a variable phenotype even in carriers of the same adenomatous polyposis coli germline mutation. Xenobiotic-metabolizing enzymes such as N-acetyltransferases (NATs) and glutathione S-transferases (GSTs) were reported to modify the individual risk for colorectal cancer. We examined whether the polymorphisms of the NAT2, GSTM1, and GSTT1 enzymes affect age at diagnosis of first colorectal adenomas or extracolonic manifestations in 411 FAP patients. Neither age at diagnosis of colorectal adenomas nor occurrence of extra-intestinal tumors differed significantly between genotypes at the NAT2 and GSTM1 loci, whereas GSTT1 polymorphism showed an uncertain association with extra-intestinal manifestations. Combinations of supposed at risk genotypes of the three enzymes showed no significant differences either. Thus, NAT2, GSTM1, or GSTT1 are unlikely to modify the disease phenotype in FAP patients.
UI - 11751493
AU - Keller JJ; Offerhaus GJ; Drillenburg P; Caspers E; Musler A; Ristimaki
TI - A; Giardiello FM Molecular analysis of sulindac-resistant adenomas in familial adenomatous polyposis.
SO - Clin Cancer Res 2001 Dec;7(12):4000-7
AD - Department of Pathology, Academic Medical Center, 1100 DD Amsterdam, the Netherlands. email@example.com
PURPOSE: Sulindac causes the reduction of adenomas in familial adenomatous polyposis (FAP) patients, but complete regression is unusual, and breakthrough of colorectal carcinoma during sulindac treatment has been described. The molecular features related to sulindac resistance are unknown. Therefore, we investigated molecular alterations in adenomas from FAP patients with complete adenoma regression on sulindac (responsive patients) and from FAP patients with sulindac-resistant adenomas (resistant patients). DESIGN: Fourteen baseline adenomas (removed before sulindac treatment) from six responsive patients were studied. Also, 9 baseline adenomas and 34 resistant adenomas (removed during sulindac treatment) from three resistant patients were analyzed. Using immunohistochemistry, we evaluated the expression of beta-catenin, cyclooxygenase-2 (Cox-2), p53, Bcl-2, and Bax. K-ras codon 12 mutations, loss of heterozygosity at 5q (APC locus), and microsatellite instability were studied with PCR-based techniques. RESULTS: There were no significant differences between baseline adenomas from sulindac-responsive and -resistant patients (P > 0.05). There was less loss of membranous beta-catenin staining and less nuclear beta-catenin accumulation in resistant adenomas compared with baseline adenomas from the same (sulindac-resistant) patients (P < 0.01) or baseline adenomas from responsive patients (P < 0.01). Epithelial Cox-2 expression was less, though not significant, in resistant adenomas compared with baseline adenomas from resistant patients, but was significantly less in baseline adenomas from responsive patients (P < 0.01). K-ras mutations were found in 8 of 34 resistant adenomas (24%) and in none of the baseline adenomas (P < 0.05). Stromal Cox-2 expression, staining of p53 and Bcl-2, and loss of heterozygosity at 5q were comparable in both groups. Loss of Bax staining and microsatellite instability were not found in any adenoma. CONCLUSIONS: Sulindac-resistant adenomas display less alteration in beta-catenin staining and less epithelial Cox-2 expression when compared with adenomas removed before sulindac treatment. K-ras mutations may contribute to sulindac-resistance. Continued research is needed to investigate molecular alterations related to sulindac resistance.
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