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Adenoma prevalence and cancer risk in familial non-polyposis colorectal cancer.

https://arctichealth.org/en/permalink/ahliterature19350
Source
Gut. 2002 Feb;50(2):228-34
Publication Type
Article
Date
Feb-2002
Author
G. Lindgren
A. Liljegren
E. Jaramillo
C. Rubio
A. Lindblom
Author Affiliation
Department of Clinical Genetics, Karolinska Hospital, S 171 76 Stockholm, Sweden.
Source
Gut. 2002 Feb;50(2):228-34
Date
Feb-2002
Language
English
Publication Type
Article
Keywords
Adenoma - epidemiology - genetics - pathology
Adult
Age Distribution
Age of Onset
Analysis of Variance
Chi-Square Distribution
Colonoscopy - methods
Colorectal Neoplasms - epidemiology - genetics - pathology
Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology - genetics - pathology
Cross-Sectional Studies
Female
Humans
Logistic Models
Male
Middle Aged
Pedigree
Prevalence
Research Support, Non-U.S. Gov't
Retrospective Studies
Risk assessment
Risk factors
Sex Distribution
Sweden - epidemiology
Abstract
BACKGROUND AND AIMS: Polypectomy in the colon has been shown to prevent colorectal cancer in both the general population and in familial colorectal cancer. Individuals with a family history of colorectal cancer have an increased risk of the disease. Over a period of 10 years, 304 subjects at risk were included in ongoing surveillance with regular colonoscopies. To compile the medical findings and experience generated during this period, a retrospective cross sectional study was performed. SUBJECTS: Subjects were classified into three family groups: families with hereditary non-polyposis colorectal cancer (HNPCC); families with hereditary colorectal cancer (HCC, non-Lynch syndrome); and a third group of families with only empirical risk estimates based on a family history of two close relatives (TCR) with colorectal cancer. METHODS: The risk population was studied with regard to age at onset, prevalence, number, cancer risk, size, dysplasia, and distribution of adenomas. A comparison was made within the family groups and with a reference group representing the general population. RESULTS: In total, 195 adenomas and six cancers were detected among 85 individuals. The relative risk of having an adenoma in the whole risk population compared with the general population was 2.6. Subjects from TCR families had most adenomas and HNPCC subjects had the least. A shift from proximal adenomas to distal carcinomas in families with HCC and TCR suggested a higher cancer risk in distal adenomas in these syndromes. HNPCC families showed a younger age at onset and adenomas with a higher degree of dysplasia. In HNPCC, there was a similar localisation of adenomas and carcinomas, suggesting a high risk of cancer in all adenomas. CONCLUSIONS: There was clear overrepresentation of adenomas in all three family types compared with the reference population. In HNPCC, we found earlier onset of adenomas and faster progression to cancer. Families with HCC, and even more so TCR subjects, had a later onset and lower risk of cancer from proximal adenomas. Based on these results, surveillance protocols in Sweden have been revised.
Notes
Erratum In: Gut 2002 May;50(5):742
PubMed ID
11788565 View in PubMed
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Alcohol consumption and risk of colorectal cancer: the Findrink study.

https://arctichealth.org/en/permalink/ahliterature157764
Source
Eur J Epidemiol. 2008;23(6):395-401
Publication Type
Article
Date
2008
Author
Adetunji T Toriola
Sudhir Kurl
Jari A Laukanen
Charles Mazengo
Jussi Kauhanen
Author Affiliation
School of Public Health and Clinical Nutrition, University of Kuopio, P.O. Box 1627, 70211, Kuopio, Finland. adetunji.toriola@uta.fi
Source
Eur J Epidemiol. 2008;23(6):395-401
Date
2008
Language
English
Publication Type
Article
Keywords
Adult
Alcohol drinking - epidemiology
Alcohol-Related Disorders - epidemiology - genetics
Cohort Studies
Colorectal Neoplasms - epidemiology - genetics
Finland - epidemiology
Humans
Male
Middle Aged
Proportional Hazards Models
Risk factors
Abstract
We investigated the association between alcohol consumption and colorectal cancer because previous studies have yielded conflicting results. As part of the Findrink study, data from the Kuopio Ischaemic Heart Disease (KIHD) Risk Factor Study were analysed. The KIHD study is a cohort of 2,682 men from Eastern Finland with no history of cancer at baseline. The men were grouped into five groups according to their weekly alcohol intake in grams. Association between alcohol and colorectal cancer was examined using Cox proportional hazard models. There were 59 cases of colorectal cancer during an average follow up of 16.7 years. Men within the highest quintile of alcohol consumption had a median weekly alcohol intake of 198.8 g. Age and examination year adjusted risk ratio of colorectal cancer among men within the highest quintile of alcohol consumption was 4.4 (95% CI: 1.6-11.9, P-value = 0.004). After adjusting for potential confounders, such as vegetable consumption, fibre intake, smoking, family history of cancer, socio-economic status, leisure time physical activity, men with the highest amount of alcohol consumption still had a 3.5-fold (95% CI: 1.2-9.9, P-value = 0.021) increased risk of colorectal cancer. Exclusion of men diagnosed with colorectal cancer during the first 2 years of follow up from the analyses did not alter the risk increase. In conclusion, this study gives further evidence of a positive association between alcohol consumption and the risk of colorectal cancer.
PubMed ID
18409007 View in PubMed
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APC I1307K and E1317Q variants are rare or do not occur in Swedish colorectal cancer patients.

https://arctichealth.org/en/permalink/ahliterature19920
Source
Eur J Cancer. 2001 Mar;37(4):499-502
Publication Type
Article
Date
Mar-2001
Author
S. Evertsson
A. Lindblom
X F Sun
Author Affiliation
Department of Oncology, Institute of Biomedicine and Surgery, Linköping University, S-581 85, Linköping, Sweden.
Source
Eur J Cancer. 2001 Mar;37(4):499-502
Date
Mar-2001
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Arabidopsis Proteins
Calcium-Binding Proteins - genetics
Colorectal Neoplasms - epidemiology - genetics
Female
Humans
Male
Middle Aged
Mutation, Missense - genetics
Pedigree
Polymerase Chain Reaction - methods
Research Support, Non-U.S. Gov't
Sweden - epidemiology - ethnology
Abstract
Recently, a germ line mutation of the APC gene, I1307K, was discovered in a subset of Ashkenazi jews. The mutation involves an amino acid exchange and creates a tract consisting of eight contiguous adenosine residues believed to cause hypermutability in this region. Another germ line missense variant, E1317Q, not restricted to a certain ethnic population, could functionally alter the protein. These APC variants have been linked with increased colorectal cancer risk in several studies. However, they have not yet been investigated in Swedish colorectal cancer patients. Thus, our aim was to investigate the prevalence of I1307K and E1317Q in Swedish colorectal cancer patients in order to determine if these genetic variants are important predisposing factors to colorectal cancer in this population. To this end, sequence analysis was carried out of the APC gene in order to identify any I1307K and E1317Q variants in 106 unselected cases and 88 hereditary/familial colorectal cancer cases including 22 cases of hereditary non-polyposis colorectal cancer (HNPCC) fulfilling the Amsterdam criteria. Out of a total of 194 cases examined, we did not find any variants. It seems that these alterations are rare or absent in the Swedish population.
PubMed ID
11267860 View in PubMed
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Association between biallelic and monoallelic germline MYH gene mutations and colorectal cancer risk.

https://arctichealth.org/en/permalink/ahliterature177604
Source
J Natl Cancer Inst. 2004 Nov 3;96(21):1631-4
Publication Type
Article
Date
Nov-3-2004
Author
Marina E Croitoru
Sean P Cleary
Nando Di Nicola
Michael Manno
Teresa Selander
Melyssa Aronson
Mark Redston
Michelle Cotterchio
Julia Knight
Robert Gryfe
Steven Gallinger
Author Affiliation
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, ON, Canada.
Source
J Natl Cancer Inst. 2004 Nov 3;96(21):1631-4
Date
Nov-3-2004
Language
English
Publication Type
Article
Keywords
Adenomatous Polyposis Coli - genetics
Aspartic Acid
Base Pair Mismatch
Case-Control Studies
Colorectal Neoplasms - epidemiology - genetics
Colorectal Neoplasms, Hereditary Nonpolyposis - genetics
Cysteine
DNA Glycosylases - genetics
DNA Mutational Analysis
DNA, Neoplasm - analysis
Gene Frequency
Genetic Predisposition to Disease
Germ-Line Mutation
Glycine
Humans
Loss of Heterozygosity
Ontario - epidemiology
Phenotype
Risk factors
Tumor Markers, Biological - genetics
Tyrosine
Abstract
The MutY human homologue (MYH) gene encodes a member of the base excision repair pathway that is involved in repairing oxidative damage to DNA. Two germline MYH gene mutations that result in Myh proteins containing amino acid substitutions Y165C and G382D (hereafter called the Y165C and G382D mutations) are associated with adenomatous poly-posis and colorectal cancer among patients from several European poly-posis registries. We used a population-based series of 1238 colorectal cancer patients and 1255 healthy control subjects from Ontario, Canada, to examine the risk of colorectal cancer among biallelic and monoallelic germline MYH Y165C and G382D mutation carriers. The entire MYH gene coding region was screened in all MYH Y165C and G382D mutation carriers. Compared with noncarriers, biallelic and monoallelic germline MYH gene mutation carriers had an increased risk of colorectal cancer and were more likely to have first-or second-degree relatives with colorectal cancer (relative risk = 1.54, 95% confidence interval = 1.10 to 2.16). The increased risk of colorectal cancer in biallelic and monoallelic MYH gene mutation carriers was not consistently associated with the development of multiple adenomatous polyps. Loss of heterozygosity in at least one of four loci in MYH was detected in eight (47%) of 17 colorectal tumors from monoallelic MYH gene mutation carriers but in only two (20%) of 10 colorectal tumors from biallelic MYH gene mutation carriers. These two MYH gene mutations may account for a substantial fraction of hereditary colorectal cancer.
Notes
Comment In: J Natl Cancer Inst. 2005 Feb 16;97(4):320-1; author reply 321-215713969
PubMed ID
15523092 View in PubMed
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Association studies on 11 published colorectal cancer risk loci.

https://arctichealth.org/en/permalink/ahliterature142026
Source
Br J Cancer. 2010 Aug 10;103(4):575-80
Publication Type
Article
Date
Aug-10-2010
Author
S. von Holst
S. Picelli
D. Edler
C. Lenander
J. Dalén
F. Hjern
N. Lundqvist
U. Lindforss
L. Påhlman
K. Smedh
A. Törnqvist
J. Holm
M. Janson
M. Andersson
S. Ekelund
L. Olsson
S. Ghazi
N. Papadogiannakis
A. Tenesa
S M Farrington
H. Campbell
M G Dunlop
A. Lindblom
Author Affiliation
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm S17176, Sweden.
Source
Br J Cancer. 2010 Aug 10;103(4):575-80
Date
Aug-10-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Colorectal Neoplasms - epidemiology - genetics
Female
Genetic Association Studies
Genetic Loci
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Risk factors
Sweden
Abstract
Recently, several genome-wide association studies (GWAS) have independently found numerous loci at which common single-nucleotide polymorphisms (SNPs) modestly influence the risk of developing colorectal cancer. The aim of this study was to test 11 loci, reported to be associated with an increased or decreased risk of colorectal cancer: 8q23.3 (rs16892766), 8q24.21 (rs6983267), 9p24 (rs719725), 10p14 (rs10795668), 11q23.1 (rs3802842), 14q22.2 (rs4444235), 15q13.3 (rs4779584), 16q22.1 (rs9929218), 18q21.1 (rs4939827), 19q13.1 (rs10411210) and 20p12.3 (rs961253), in a Swedish-based cohort.
The cohort was composed of 1786 cases and 1749 controls that were genotyped and analysed statistically. Genotype-phenotype analysis, for all 11 SNPs and sex, age of onset, family history of CRC and tumour location, was performed.
Of eleven loci, 5 showed statistically significant odds ratios similar to previously published findings: 8q23.3, 8q24.21, 10p14, 15q13.3 and 18q21.1. The remaining loci 11q23.1, 16q22.1, 19q13.1 and 20p12.3 showed weak trends but somehow similar to what was previously published. The loci 9p24 and 14q22.2 could not be confirmed. We show a higher number of risk alleles in affected individuals compared to controls. Four statistically significant genotype-phenotype associations were found; the G allele of rs6983267 was associated to older age, the G allele of rs1075668 was associated with a younger age and sporadic cases, and the T allele of rs10411210 was associated with younger age.
Our study, using a Swedish population, supports most genetic variants published in GWAS. More studies are needed to validate the genotype-phenotype correlations.
Notes
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PubMed ID
20648012 View in PubMed
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Awareness of heredity in colorectal cancer patients is insufficient among clinicians: a Norwegian population-based study.

https://arctichealth.org/en/permalink/ahliterature95224
Source
Colorectal Dis. 2009 Jun;11(5):456-61
Publication Type
Article
Date
Jun-2009
Author
Tranø G.
Wasmuth H H
Sjursen W.
Hofsli E.
Vatten L J
Author Affiliation
Department of Gastrointestinal Surgery, Hamar Hospital, Sykehuset Innlandet Hospital Trust, Hamar, Norway. gerd.trano@ntnu.no
Source
Colorectal Dis. 2009 Jun;11(5):456-61
Date
Jun-2009
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Cohort Studies
Colorectal Neoplasms - epidemiology - genetics
Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology - genetics
Documentation - statistics & numerical data
Family Health
Female
Genetic Predisposition to Disease - epidemiology - genetics
Humans
Male
Middle Aged
Norway
Practice Guidelines as Topic
Abstract
OBJECTIVE: The assessment of family history and medical data is crucial in identifying families with Lynch syndrome (LS). Among consecutive colorectal cancer (CRC) patients, we aimed at identifying all patients with a hereditary predisposition, and to study a possible discrepancy with assessments made by the responsible clinicians. METHOD: All consecutively diagnosed patients with CRC from two Norwegian hospitals were included, and information on family history was collected in a detailed interview. We assessed information in medical records, and tumours were examined for LS-associated histopathological features. RESULTS: Among 562 patients, there was no documentation of family history in 388 (69.0%) medical records, and in 174 (31.0%) patients, there was no clinical assessment of the information that was collected on family history. Based on detailed interviews and extended pathological examination, we found that 137 (24.4%) of the 562 patients could be classified as possible LS according to the Revised Bethesda Guidelines (RBG); and that 46 (33.6%) of these patients could be identified by family history alone. CONCLUSION: Family history and relevant information in patient records can identify patients with possible LS. However, clinicians often fail to include information on hereditary factors and to assess relevant data in medical records. Familial CRC is therefore not acknowledged, and genetic counselling is not offered.
Notes
Comment In: Colorectal Dis. 2009 Jun;11(5):461-319508539
PubMed ID
19508550 View in PubMed
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Cancer risk in HFE C282Y homozygotes: results from the HUNT 2 study.

https://arctichealth.org/en/permalink/ahliterature117608
Source
Scand J Gastroenterol. 2013 Feb;48(2):189-95
Publication Type
Article
Date
Feb-2013
Author
Arne Asberg
Ketil Thorstensen
Wenche Ø Irgens
Pål R Romundstad
Kristian Hveem
Author Affiliation
Department of Clinical Chemistry, Trondheim University Hospital, Trondheim, Norway. arne.aasberg@stolav.no
Source
Scand J Gastroenterol. 2013 Feb;48(2):189-95
Date
Feb-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Breast Neoplasms - epidemiology - genetics
Carcinoma, Hepatocellular - epidemiology - genetics
Colorectal Neoplasms - epidemiology - genetics
Female
Follow-Up Studies
Genetic markers
Histocompatibility Antigens Class I - genetics
Homozygote
Humans
Incidence
Liver Neoplasms - epidemiology - genetics
Male
Membrane Proteins - genetics
Middle Aged
Multivariate Analysis
Mutation
Norway - epidemiology
Proportional Hazards Models
Registries
Risk factors
Abstract
In addition to hepatocellular cancer, HFE C282Y homozygotes are reported to have increased risk of colorectal cancer and breast cancer. This study was done to further explore the cancer risk in C282Y homozygotes.
We studied cancer incidence in 292 homozygotes and 62,568 others that participated in the HUNT 2 population screening in 1995-1997. Using Cox proportional hazard models, we estimated cancer hazard ratio as a function of C282Y homozygosity and several screening variables including serum transferrin saturation, alcohol consumption and daily smoking.
Cancer was diagnosed in 36 homozygotes, five of which had two cancer diagnoses. The overall cancer incidence was not increased in C282Y homozygotes (hazard ratio 1.10 [95% CI 0.60-2.03] in women and 0.94 [95% CI 0.53-1.66] in men). However, homozygous men had increased risk of colorectal cancer (hazard ratio 3.03 [95% CI 1.17-7.82], p = 0.022) and primary liver cancer (hazard ratio 54.0 [95% CI 2.68-1089], p = 0.009). The risk of breast cancer in homozygous women was not increased (hazard ratio 1.13 [95% CI 0.35-3.72]). Adjusted for other variables including C282Y homozygosity, very low and very high serum transferrin saturation were associated with increased overall cancer incidence.
C282Y homozygosity is associated with increased risk of colorectal cancer and hepatocellular cancer in men. In the general population, individuals with a very low or a very high serum transferrin saturation may have increased cancer risk.
PubMed ID
23281741 View in PubMed
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Colonoscopic screening examination of relatives of patients with colorectal cancer. I. A comparison with an endoscopically screened normal population.

https://arctichealth.org/en/permalink/ahliterature24396
Source
Scand J Gastroenterol. 1992 Aug;27(8):661-6
Publication Type
Article
Date
Aug-1992
Author
J. Sauar
T. Hausken
G. Hoff
A. Bjørkheim
A. Foerster
P. Mowinckel
Author Affiliation
Dept. of Medicine, Telemark Central Hospital, Skien, Norway.
Source
Scand J Gastroenterol. 1992 Aug;27(8):661-6
Date
Aug-1992
Language
English
Publication Type
Article
Keywords
Adenoma - diagnosis - epidemiology
Adult
Aged
Carcinoma - epidemiology - prevention & control
Colonic Polyps - epidemiology - prevention & control
Colonoscopy
Colorectal Neoplasms - epidemiology - genetics - prevention & control
Comparative Study
Female
Follow-Up Studies
Humans
Male
Middle Aged
Norway - epidemiology
Prevalence
Risk factors
Abstract
First-degree relatives (n = 206) of patients operated on for colorectal cancer (CRC) (n = 181) were offered a colonoscopic screening examination; 169 relatives (82%) attended. The findings were compared with those in a normal population sample with no CRC in first-degree relatives (n = 308), aged 50-59 years, who had been screened by means of flexible sigmoidoscopy. Three carcinomas and 176 polyps were found in 56 of 95 male relatives (57%) and 34 of 74 female relatives (46%). The adenoma prevalence rate was 37 (39%) and 26 (35%) for male and female relatives, respectively. In the 50- to 59-year age group, the adenoma prevalence rates for both sexes collectively and for women separately were significantly higher among relatives than among the population without CRC relatives. Hyperplastic polyps were larger, whereas adenomas were similar in size among relatives compared with the normal population. Colonoscopy may be a suitable method of choice for screening first-degree relatives of patients with CRC.
PubMed ID
1439548 View in PubMed
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Colorectal cancer rates among first-degree relatives of patients with inflammatory bowel disease: a population-based cohort study.

https://arctichealth.org/en/permalink/ahliterature19991
Source
Lancet. 2001 Jan 27;357(9252):262-6
Publication Type
Article
Date
Jan-27-2001
Author
J. Askling
P W Dickman
P. Karlén
O. Broström
A. Lapidus
R. Löfberg
A. Ekbom
Author Affiliation
Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden. johan.askling@mep.ki.se
Source
Lancet. 2001 Jan 27;357(9252):262-6
Date
Jan-27-2001
Language
English
Publication Type
Article
Keywords
Adult
Colorectal Neoplasms - epidemiology - genetics
Family
Female
Humans
Incidence
Inflammatory Bowel Diseases - epidemiology - genetics
Male
Middle Aged
Registries
Sweden - epidemiology
Abstract
BACKGROUND: Inflammatory bowel disease (IBD) and colorectal cancer might share a common cause and, therefore, relatives of patients with IBD could be at increased risk of this malignant disease. We aimed to assess cancer rates among first-degree relatives of patients with IBD to try to determine whether an association between the two diseases exists. METHODS: In a population-based study, we identified 114,102 first-degree relatives by registry linkage and followed them up for cancer occurrence. We used standardised incidence ratio (SIR) of cancer as relative risk. FINDINGS: 560 colorectal cancers were identified among relatives. First-degree relatives of patients with Crohn's disease or ulcerative colitis were not at increased risk of cancer (SIR 0.90, 95% CI 0.82-0.97). The relative risk was 0.96 (0.87-1.06, n=379) for colon cancer and 0.78 (0.68-0.91, 181) for rectal cancer. The SIRs were not affected by age, relation to patient, or type or extent of IBD in the patient. Relatives of patients with both IBD and colorectal cancer had an 80% increased risk of colorectal cancer. INTERPRETATION: Our results do not endorse a common cause of IBD and colorectal cancer. The slightly decreased relative risk for colorectal cancer among relatives could indicate the proportion of all colorectal cancer cases attributable to IBD.
Notes
Comment In: Lancet. 2001 Jan 27;357(9252):246-711214121
PubMed ID
11214128 View in PubMed
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Common variants in human CRC genes as low-risk alleles.

https://arctichealth.org/en/permalink/ahliterature98081
Source
Eur J Cancer. 2010 Apr;46(6):1041-8
Publication Type
Article
Date
Apr-2010
Author
Simone Picelli
Pawel Zajac
Xiao-Lei Zhou
David Edler
Claes Lenander
Johan Dalén
Fredrik Hjern
Nils Lundqvist
Ulrik Lindforss
Lars Påhlman
Kennet Smedh
Anders Törnqvist
Jörn Holm
Martin Janson
Magnus Andersson
Susanne Ekelund
Louise Olsson
Joakim Lundeberg
Annika Lindblom
Author Affiliation
Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden.
Source
Eur J Cancer. 2010 Apr;46(6):1041-8
Date
Apr-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Alleles
Case-Control Studies
Colorectal Neoplasms - epidemiology - genetics
Female
Genetic Predisposition to Disease - epidemiology - genetics
Genome-Wide Association Study
Genotype
Germ-Line Mutation - genetics
Humans
Male
Middle Aged
Penetrance
Polymorphism, Genetic
Risk factors
Sweden - epidemiology
Young Adult
Abstract
The genetic susceptibility to colorectal cancer (CRC) has been estimated to be around 35% and yet high-penetrance germline mutations found so far explain less than 5% of all cases. Much of the remaining variations could be due to the co-inheritance of multiple low penetrant variants. The identification of all the susceptibility alleles could have public health relevance in the near future. To test the hypothesis that what are considered polymorphisms in human CRC genes could constitute low-risk alleles, we selected eight common SNPs for a pilot association study in 1785 cases and 1722 controls. One SNP, rs3219489:G>C (MUTYH Q324H) seemed to confer an increased risk of rectal cancer in homozygous status (OR=1.52; CI=1.06-2.17). When the analysis was restricted to our 'super-controls', healthy individuals with no family history for cancer, also rs1799977:A>G (MLH1 I219V) was associated with an increased risk in both colon and rectum patients with an odds ratio of 1.28 (CI=1.02-1.60) and 1.34 (CI=1.05-1.72), respectively (under the dominant model); while 2 SNPs, rs1800932:A>G (MSH6 P92P) and rs459552:T>A (APC D1822V) seemed to confer a protective effect. The latter, in particular showed an odds ratio of 0.76 (CI=0.60-0.97) among colon patients and 0.73 (CI=0.56-0.95) among rectal patients. In conclusion, our study suggests that common variants in human CRC genes could constitute low-risk alleles.
PubMed ID
20149637 View in PubMed
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54 records – page 1 of 6.