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National Cancer Institute®
Ultima Vez Modificado: 21 de noviembre del 2001
UI - 21451200
AU - Burghes AH; Vaessin HE; de La Chapelle A
TI - Genetics. The land between Mendelian and multifactorial inheritance.
SO - Science 2001 Sep 21;293(5538):2213-4
AD - Department of Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH 43210, USA. firstname.lastname@example.org
UI - 21274205
AU - Wittekind C; Tannapfel A
TI - Adenoma of the papilla and ampulla--premalignant lesions?
SO - Langenbecks Arch Surg 2001 Apr;386(3):172-5
AD - Institute of Pathology, University of Leipzig, Germany. email@example.com
Ampullary adenomas arising in the papilla or the ampulla Vateri, are rare, benign, neoplastic lesions. No specific aetiological factors, such as diet, chemical or environmental causes, have been identified yet. An established risk factor which is accompanied by the development of adenoma is the presence of genetically inherited polyposis syndromes, e.g. familial adenomatosis coli (FAP). Adenomas assume tubular, tubulovillous, or villous architecture and are not different from adenomas arising elsewhere in the gastrointestinal tract. The full neoplastic spectrum, ranging from mild to high grade dysplasia, up to invasive carcinoma, resembles the adenoma-carcinoma sequence of the large bowels.
UI - 21437289
AU - Martin-Denavit T; Duthel S; Giraud S; Olschwang S; Saurin JC; Plauchu H
TI - Phenotype variability of two FAP families with an identical APC germline mutation at codon 1465: a potential modifier effect?
SO - Clin Genet 2001 Aug;60(2):125-31
AD - Service de Genetique Clinique, Hospices Civils de Lyon, Hotel Dieu, 69288 Lyon cedex 02, France. firstname.lastname@example.org
We report the cases of two familial adenomatous polyposis (FAP) families who presented with the same 2 base pair deletion (AG) at codon 1465 of the adenomatous polyposis coli (APC) gene, but showed phenotypic variability. The mutation was revealed by a simple nonradioactive method using a heteroduplex analysis and identified by a sequence analysis. This observation suggests the responsibility of modifier genes in FAP patients' phenotype.
UI - 21017799
AU - Hyer W; Beveridge I; Domizio P; Phillips R
TI - Clinical management and genetics of gastrointestinal polyps in children.
SO - J Pediatr Gastroenterol Nutr 2000 Nov;31(5):469-79
AD - Department of Pediatrics, St. Mark's Hospital, Harrow, United Kingdom. email@example.com
UI - 21408664
AU - Fodde R; Smits R
TI - Disease model: familial adenomatous polyposis.
SO - Trends Mol Med 2001 Aug;7(8):369-73
AD - Dept. of Human and Clinical Genetics, Leiden University Medical Center, Sylvius Laboratories, Wassenaarseweg 72, 2333 AL, Leiden, The Netherlands. firstname.lastname@example.org
Mutations in the APC gene are responsible for familial adenomatous polyposis (FAP) and for the majority of sporadic colorectal cancers. The establishment of genotype-phenotype correlations in FAP is often complicated by the great clinical variability observed among carriers of the same APC mutation even within the same kindred. This variability is likely to arise from the interaction of genetic and environmental modifying factors, the dissection of which ideally requires the employment of mouse models where the effects of specific Apc mutations are analyzed in an inbred, homogeneous genetic background and a controlled environment. The availability of different Apc mouse models allows not only the establishment of more precise genotype-phenotype correlations but has also provided very important clues for the understanding of the function of APC in homeostasis and tumorigenesis. Also, the close phenotypic resemblance to the human disease makes these mice unique preclinical models to test chemopreventive and therapeutic interventions.
UI - 21424742
AU - Ryo A; Nakamura M; Wulf G; Liou YC; Lu KP
TI - Pin1 regulates turnover and subcellular localization of beta-catenin by inhibiting its interaction with APC.
SO - Nat Cell Biol 2001 Sep;3(9):793-801
AD - Cancer Biology Program, Division of Hematology/Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, HIM 1047, Boston, MA 02215, USA.
Phosphorylation on a serine or threonine residue preceding proline (Ser/Thr-Pro) is a key regulatory mechanism, and the conformation of certain phosphorylated Ser/Thr-Pro bonds is regulated specifically by the prolyl isomerase Pin1. Whereas the inhibition of Pin1 induces apoptosis, Pin1 is strikingly overexpressed in a subset of human tumours. Here we show that Pin1 regulates beta-catenin turnover and subcellular localization by interfering with its interaction with adenomatous polyposis coli protein (APC). A differential-display screen reveals that Pin1 increases the transcription of several beta-catenin target genes, including those encoding cyclin D1 and c-Myc. Manipulation of Pin1 levels affects the stability of beta-catenin in vitro. Furthermore, beta-catenin levels are decreased in Pin1-deficient mice but are increased and correlated with Pin1 overexpression in human breast cancer. Pin1 directly binds a phosphorylated Ser-Pro motif next to the APC-binding site in beta-catenin, inhibits its interaction with APC and increases its translocation into the nucleus. Thus, Pin1 is a novel regulator of beta-catenin signalling and its overexpression might contribute to the upregulation of beta-catenin in tumours such as breast cancer, in which APC or beta-catenin mutations are not common.
UI - 21424793
AU - Sonoshita M; Takaku K; Sasaki N; Sugimoto Y; Ushikubi F; Narumiya S;
TI - Oshima M; Taketo MM Acceleration of intestinal polyposis through prostaglandin receptor EP2 in Apc(Delta 716) knockout mice.
SO - Nat Med 2001 Sep;7(9):1048-51
AD - Laboratory of Biomedical Genetics, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan.
Arachidonic acid is metabolized to prostaglandin H(2) (PGH(2)) by cyclooxygenase (COX). COX-2, the inducible COX isozyme, has a key role in intestinal polyposis. Among the metabolites of PGH(2), PGE(2) is implicated in tumorigenesis because its level is markedly elevated in tissues of intestinal adenoma and colon cancer. Here we show that homozygous deletion of the gene encoding a cell-surface receptor of PGE(2), EP2, causes decreases in number and size of intestinal polyps in Apc(Delta 716) mice (a mouse model for human familial adenomatous polyposis). This effect is similar to that of COX-2 gene disruption. We also show that COX-2 expression is boosted by PGE(2) through the EP2 receptor via a positive feedback loop. Homozygous gene knockout for other PGE(2) receptors, EP1 or EP3, did not affect intestinal polyp formation in Apc(Delta 716) mice. We conclude that EP2 is the major receptor mediating the PGE2 signal generated by COX-2 upregulation in intestinal polyposis, and that increased cellular cAMP stimulates expression of more COX-2 and vascular endothelial growth factor in the polyp stroma.
UI - 21469634
AU - Buckhaults P; Rago C; St Croix B; Romans KE; Saha S; Zhang L;
TI - Vogelstein B; Kinzler KW Secreted and cell surface genes expressed in benign and malignant colorectal tumors.
SO - Cancer Res 2001 Oct 1;61(19):6996-7001
AD - Howard Hughes Medical Institute, Johns Hopkins Medical Institution, Baltimore, Maryland 21231, USA.
Serial analysis of gene expression was used to identify transcripts encoding secreted or cell surface proteins that were expressed in benign and malignant tumors of the colorectum. A total of 290,394 tags were analyzed from normal, adenomatous, and cancerous colonic epithelium. Of the 21,343 different transcripts observed, 957 were found to be differentially expressed between normal tissue and adenoma or between normal tissue and cancer. Forty-nine transcripts were elevated > or =20-fold in adenomas, 40 transcripts were elevated > or =20-fold in cancers, and 9 transcripts were elevated > or =20-fold in both. Products of six of these nine transcripts (TGFBI, LYS, RDP, MIC-1, REGA, and DEHL) were predicted to be secreted or to reside on the cell surface, and these were analyzed in more detail. The abnormal expression levels predicted by serial analysis of gene expression were confirmed by quantitative PCR analyses of each of these six genes. Moreover, the cell types responsible for the elevated expression were identified by in situ hybridization and by PCR analyses of epithelial cells immunoaffinity purified from primary tumors. This study extends knowledge of the differences in gene expression that underlie various stages of neoplasia and suggests specific diagnostic approaches that may be useful for the early detection of colorectal neoplasia.
UI - 21217696
AU - Attard TM; Giardiello FM; Argani P; Cuffari C
TI - Fundic gland polyposis with high-grade dysplasia in a child with attenuated familial adenomatous polyposis and familial gastric cancer.
SO - J Pediatr Gastroenterol Nutr 2001 Feb;32(2):215-8
AD - Department of Pediatrics, The Johns Hopkins Hospital, Baltimore, Maryland 21287-2631, USA.
UI - 21367432
AU - Olschwang S
TI - [Intestinal polyposis]
SO - Ann Med Interne (Paris) 2001 Jun;152(4):267-72
AD - INSERM U434, Fondation Jean-Dausset-CEPH, 27, rue Juliette-Dodu, 75010 Paris, France. email@example.com
UI - 21481727
AU - Church J; Lowry A; Simmang C; The Standards Task Force; American Society
TI - of Colon and Rectal Surgeons Practice parameters for the identification and testing of patients at risk for dominantly inherited colorectal cancer--supporting documentation.
SO - Dis Colon Rectum 2001 Oct;44(10):1404-12
UI - 93278969
AU - Evans G
TI - Ethical issues: the geneticist's view point.
SO - Dis Markers 1992 Jul-Aug;10(4):199-203; discussion 211-28
AD - Department of Medical Genetics, St Mary's Hospital, Manchester.
UI - 96282904
AU - Michie S; McDonald V; Bobrow M; McKeown C; Marteau T
TI - Parents' responses to predictive genetic testing in their children: report of a single case study.
SO - J Med Genet 1996 Apr;33(4):313-8
AD - Psychology and Genetics Research Group, United Medical School, Guy's Hospital, London, UK.
There is a widely held view among health professionals that predictive genetic testing of children for late onset diseases is not desirable clinical practice. Yet, little is known about the views of parents, or their responses, to predictive genetic testing in their children. Since such testing is being carried out in some genetic centres, the opportunity was taken to conduct a single case study of the parents of 2 and 4 year old sisters who were tested for the gene for familial adenomatous polyposis. Interviews before testing, after, and 15 months later showed a stable attitude, that parental responsibility included making decisions about such testing, and that the role of health professionals should be one of information giving rather than decision making. These parents had no regrets about having their children tested and reported no changes in their behaviour towards either the child who tested positively or the child who tested negatively. Using standardised scales, mood was found to be within the normal range both before and after testing in the mother and father. This case study is a first step towards systematic empirical studies determining the consequences of acquiescing to parents' requests for genetic testing in their children.
UI - 97212608
AU - Giardiello FM; Brensinger JD; Petersen GM; Luce MC; Hylind LM; Bacon JA;
TI - Booker SV; Parker RD; Hamilton SR The use and interpretation of commercial APC gene testing for familial adenomatous polyposis.
SO - N Engl J Med 1997 Mar 20;336(12):823-7
AD - Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
BACKGROUND: The use of commercially available tests for genes linked to familial cancer has aroused concern about the impact of these tests on patients. Familial adenomatous polyposis is an autosomal dominant disease caused by a germ-line mutation of the adenomatous polyposis coli (APC) gene that causes colorectal cancer if prophylactic colectomy is not performed. We evaluated the clinical use of commercial APC gene testing. METHODS: We assessed indications for APC gene testing, whether informed consent was obtained and genetic counseling was offered before testing, and the interpretation of the results through telephone interviews with physicians and genetic counselors in a nationwide sample of 177 patients from 125 families who underwent testing during 1995. RESULTS: Of the 177 patients tested, 83.0 percent had clinical features of familial adenomatous polyposis or were at risk for the disease-both valid indications for being tested. The appropriate strategy for presymptomatic testing was used in 79.4 percent (50 of 63 patients). Only 18.6 percent (33 of 177) received genetic counseling before the test, and only 16.9 percent (28 of 166) provided written informed consent. In 31.6 percent of the cases the physicians misinterpreted the test results. Among the patients with unconventional indications for testing, the rate of positive results was only 2.3 percent (1 of 44). CONCLUSIONS: Patients who underwent genetic tests for familial adenomatous polyposis often received inadequate counseling and would have been given incorrectly interpreted results. Physicians should be prepared to offer genetic counseling if they order genetic tests.
UI - 97297366
AU - DudokdeWit AC; Tibben A; Duivenvoorden HJ; Frets PG; Zoeteweij MW;
TI - Losekoot M; van Haeringen A; Niermeijer MF; Passchier J Psychological distress in applicants for predictive DNA testing for autosomal dominant, heritable, late onset disorders. The Rotterdam/Leiden Genetics Workgroup.
SO - J Med Genet 1997 May;34(5):382-90
AD - Department of Medical Psychology, Erasmus University Rotterdam, The Netherlands.
In a comparative study on the effects of predictive DNA testing for late onset disorders, pre-test psychological distress was assessed in people at risk for Huntington's disease (HD, n = 41), cerebral haemorrhage (HCHWA-D, n = 9), breast and ovarian cancer (HBOC, n = 24), and polyposis coli (FAP, n = 45). Partners, if available, also participated in the study. Distress was measured with the subscales Intrusion and Avoidance of the Impact of Event Scale. People at risk for the neurodegenerative disorders reported more avoidance than those at risk for the cancer syndromes. People at risk for FAP and partners of those at risk for HBOC reported less intrusion than the others at risk and the other partners. Subjects who were more distressed reported more experiences with the disease in close relatives, the disease having a great impact on their lives, having considerations against predictive testing, expecting that being identified as a gene carrier would have adverse effects, and expecting relief after being identified as a non-carrier. Test candidates who expected an increase of personal problems showed higher avoidance, whereas those who could better anticipate future life as a carrier had higher intrusion levels. Generally, subjects with high distress levels are of more concern to the healthcare professional than those with low distress levels. However, high distress may reflect worrying as a mental preparation for the test result, whereas low distress may indicate denial-avoidance behaviour and poor anticipation of the test outcome. In pre-test counselling sessions, this should be acknowledged and addressed.
UI - 21236249
AU - Joint Test and Technology Transfer Committee Working Group, American
TI - College of Medical Genetics, 9650 Rockville Pike, Bethesda, MD 20814-3998, United States. Genetic testing for colon cancer: joint statement of the American College of Medical Genetics and American Society of Human Genetics. Joint Test and Technology Transfer Committee Working Group.
SO - Genet Med 2000 Nov-Dec;2(6):362-6
UI - 21396470
AU - Liao PH; Lee TL; Yang LC; Yang SH; Chen SL; Chou MY
TI - Adenomatous polyposis coli gene mutation and decreased wild-type p53 protein expression in oral submucous fibrosis: a preliminary investigation.
SO - Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001 Aug;92(2):202-7
AD - Departmnent of Dentistry, Chung Shan Medical and Dental College, Taichung, Taiwan, ROC.
OBJECTIVE: The purpose of this study was to identify the adenomatous polyposis coli (APC) tumor suppressor gene mutation and level of wild-type p53 protein expression in patients with oral submucous fibrosis (OSF). STUDY DESIGN: Cells from OSF and control subjects were cultured in Dulbecco modified Eagle medium with 10% fetal bovine serum at 37 degrees C. Genomic DNA was extracted from cultured cells and used as a template for polymerase chain reaction amplification of the APC tumor suppressor gene. The presence of wild-type p53 protein in cell lysates of cultured cells was analyzed by Western blot. Data were analyzed by the sign test for nonparametric samples and by analysis of variance. RESULTS: The results showed that the APC gene of explant cultured cells from OSF patients (8/8) had a CGA-to-GGA transition mutation at codon 498 that resulted in an Arg-to-Gly missense mutation (P <.01). All (8/8) normal HGF cultures revealed expression of the wild-type APC protein. Cells cultured from 7 of 8 OSF patients were also found to have a single nucleotide deletion at nucleotide 1494 that resulted in creating a stop codon (TGA) at codon 504 (P <.01). This created a premature signal for the endpoint of translation and thus resulted in the generation of a truncated protein product that encodes a polypeptide of 503 amino acid residue. It was found that wild- type p53 protein in human gingival fibroblast cell cultures was significantly higher than in OSF cells (P <.01). CONCLUSION: Alterations of the APC and wild-type p53 tumor suppressor genes in OSF may imply a risk for progression to oral cancer.
UI - 21443504
AU - Crabtree MD; Tomlinson IP; Talbot IC; Phillips RK
TI - Variability in the severity of colonic disease in familial adenomatous polyposis results from differences in tumour initiation rather than progression and depends relatively little on patient age.
SO - Gut 2001 Oct;49(4):540-3
AD - Molecular and Population Genetics Laboratory, Imperial Cancer Research Fund, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. firstname.lastname@example.org
INTRODUCTION: As large scale genetic analysis becomes increasingly efficient, attention is turning to problems arising from inaccurate measurement of the phenotype. We have investigated the underlying basis of variation in disease severity in the large intestine of familial adenomatous polyposis (FAP) patients. The development of objective and reproducible measures may have future use in genetic studies, such as analysis of modifier genes. METHODS: We examined the ratio of adenomas to crypts from microscopic slides taken from all parts of the colon of 44 resected FAP specimens. These findings were compared with a carefully reported macroscopic polyp count. Age dependency of adenoma counts (in the period around colectomy) was also analysed. RESULTS: The adenoma:crypt ratio strongly correlated with reported macroscopic polyp count (r=0.82, p<0.001) with no significant residual variation. Polyp density measured using the adenoma: crypt ratio did not vary significantly within an individual colon. Apparent visible variation in polyp density within any colon was not found at the microscopic level. There was no detectable age related increase in macroscopic adenoma count between siblings over the age range at which colectomies were performed. DISCUSSION: The severity of colonic polyposis in FAP can be determined accurately by counting the adenoma:crypt ratio in sections derived from stored tissue blocks. Variation between patients-dependent on APC genotype and, probably, modifier genes-is manifest at both the microscopic and macroscopic levels. Thus variation in disease severity is more likely to result from different rates of tumour initiation than from differences in progression of microadenomas to macroscopic tumours. The absence of a detectable relationship between adenoma number and age (over the range studied) suggests that most tumours may be initiated relatively early in the patient's life, perhaps at a time of particular susceptibility.
UI - 21477322
AU - Marotta A; Tan C; Gray V; Malik S; Gallinger S; Sanghera J; Dupuis B;
TI - Owen D; Dedhar S; Salh B Dysregulation of integrin-linked kinase (ILK) signaling in colonic polyposis.
SO - Oncogene 2001 Sep 27;20(43):6250-7
AD - Jack Bell Research Center, 2660 Oak Street, Vancouver, BC, Canada V6H 3Z6.
Mutation of the adenomatous polyposis coli (APC) gene and the subsequent dysregulation of beta-catenin are well-documented abnormalities in familial adenomatous polyposis (FAP), as well as sporadic polyposis. Intriguingly, overexpression of the integrin-linked kinase (ILK) has been shown to modulate beta-catenin subcellular localization and function. However, the significance of this finding for human carcinogenesis remains unclear. Here, we report the increased biochemical activity and expression of ILK protein in polyps from FAP patients. Furthermore, dramatic increases in ILK immunoreactivity were observed in all abnormal crypts from sporadic polyps, when compared with the normal appearing crypts within the same resected specimens. As sulindac and aspirin are the two most important therapeutic/chemopreventative agents demonstrated in colorectal carcinogenesis, in both humans and animals, further investigation revealed that these non-steroidal anti-inflammatory drugs (NSAIDs) target ILK and ILK-mediated events in vivo. These include inhibition of, both the biochemical activation of ILK, inhibition of serine 9 GSK3beta phosphorylation and the enhancement of TCF-4 transcriptional activity. In conclusion, ILK protein hyperexpression appears to be an early event in colonic polyposis. Additionally, ILK signaling is shown to undergo modulation by sulindac (and aspirin) for the first time, indicating that it is likely to be one of the targets affected by these agents in vivo.
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