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Clinical and Molecular Characteristics of Post-Colonoscopy Colorectal Cancer: A Population-based Study.

https://arctichealth.org/en/permalink/ahliterature283032
Source
Gastroenterology. 2016 Nov;151(5):870-878.e3
Publication Type
Article
Date
Nov-2016
Author
Elena M Stoffel
Rune Erichsen
Trine Frøslev
Lars Pedersen
Mogens Vyberg
Erika Koeppe
Seth D Crockett
Stanley R Hamilton
Henrik T Sørensen
John A Baron
Source
Gastroenterology. 2016 Nov;151(5):870-878.e3
Date
Nov-2016
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - diagnosis - epidemiology - genetics - pathology
Adenoma - diagnosis - epidemiology - genetics - pathology
Adult
Aged
Aged, 80 and over
Colonoscopy
Colorectal Neoplasms - diagnosis - epidemiology - genetics - pathology
Cross-Sectional Studies
DNA Mismatch Repair
DNA Repair-Deficiency Disorders - diagnosis - epidemiology
Denmark - epidemiology
Female
Humans
Incidence
Logistic Models
Male
Middle Aged
Registries
Time Factors
Abstract
Colonoscopy provides incomplete protection from colorectal cancer (CRC), but determinants of post-colonoscopy CRC are not well understood. We compared clinical features and molecular characteristics of CRCs diagnosed at different time intervals after a previous colonoscopy.
We performed a population-based, cross-sectional study of incident CRC cases in Denmark (2007-2011), categorized as post-colonoscopy or detected during diagnostic colonoscopy (in patients with no prior colonoscopy). We compared prevalence of proximal location and DNA mismatch repair deficiency (dMMR) in CRC tumors, relative to time since previous colonoscopy, using logistic regression and cubic splines to assess temporal variation.
Of 10,365 incident CRCs, 725 occurred after colonoscopy examinations (7.0%). These were more often located in the proximal colon (odds ratio [OR], 2.34; 95% confidence interval [CI], 1.90-2.89) and were more likely to have dMMR (OR, 1.26; 95% CI, 1.00-1.59), but were less likely to be metastatic at presentation (OR, 0.65; 95% CI, 0.48-0.89) compared with CRCs diagnosed in patients with no prior colonoscopy. The highest proportions of proximal and/or dMMR tumors were observed in CRCs diagnosed 3-6 years after colonoscopy, but these features were still more frequent among cancers diagnosed up to 10 years after colonoscopy. The relative excess of dMMR tumors was most pronounced in distal cancers. In an analysis of 85 cases detected after colonoscopy, we found BRAF mutations in 23% of tumors and that 7% of cases had features of Lynch syndrome. Colonoscopy exams were incomplete in a higher proportion of cases diagnosed within
Notes
Cites: Am J Gastroenterol. 2012 Sep;107(9):1315-29; quiz 1314, 133022710576
Cites: Am J Clin Pathol. 2014 Apr;141(4):559-7224619758
Cites: Dig Dis Sci. 2010 Aug;55(8):2352-620300843
Cites: Gastroenterology. 2015 Sep;149(3):783-813.e2026226576
Cites: JAMA Intern Med. 2016 Jul 1;176(7):894-90227214731
Cites: Cancer. 2012 Jun 15;118(12):3044-5221989586
Cites: Dig Dis Sci. 2014 Sep;59(9):2255-6324705641
Cites: Gastroenterology. 2006 Dec;131(6):1700-517087932
Cites: Am J Gastroenterol. 2010 Dec;105(12):2588-9620877348
Cites: Ann Intern Med. 2009 Jan 6;150(1):1-819075198
Cites: Mod Pathol. 2013 Oct;26(10):1401-1223599155
Cites: Ugeskr Laeger. 2008 Jun 16;170(25):2232-418565311
Cites: Nature. 2012 Jul 18;487(7407):330-722810696
Cites: Gastroenterology. 2010 Mar;138(3):870-619909750
Cites: Am J Gastroenterol. 2014 Sep;109(9):1375-8924957158
Cites: J Mol Diagn. 2013 Mar;15(2):220-623273605
Cites: Ugeskr Laeger. 2007 Feb 5;169(6):514-717303033
Cites: Fam Cancer. 2010 Jun;9(2):155-6620012372
Cites: N Engl J Med. 1993 Dec 30;329(27):1977-818247072
Cites: Am J Gastroenterol. 2013 Aug;108(8):1332-4023774154
Cites: Ann Intern Med. 2011 Jan 4;154(1):22-3021200035
Cites: Cancer Prev Res (Phila). 2012 Feb;5(2):320-722086678
Cites: Adv Anat Pathol. 2009 Nov;16(6):405-1719851131
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):42-521775350
Cites: N Engl J Med. 2010 May 13;362(19):1795-80320463339
Cites: Gastroenterology. 2009 Mar;136(3):832-4119171141
Cites: Clin Gastroenterol Hepatol. 2013 Jul;11(7):768-7323376796
Cites: J Clin Epidemiol. 2009 May;62(5):511-7.e119135859
Cites: Clin Epidemiol. 2010 Aug 09;2:51-620865103
Cites: Science. 2003 Jul 11;301(5630):16312855788
Cites: Clin Gastroenterol Hepatol. 2010 Feb;8(2):174-8219835992
Cites: Gastroenterology. 2011 Aug;141(2):411-221708155
Cites: Am J Gastroenterol. 2010 May;105(5):1189-9520010923
Cites: Gut. 2014 Jun;63(6):957-6323744612
Cites: J Clin Oncol. 2009 Oct 1;27(28):4793-719720893
Cites: N Engl J Med. 2013 Sep 19;369(12):1095-10524047059
Cites: Gut. 2012 Nov;61(11):1576-8222200840
Cites: N Engl J Med. 2014 Apr 3;370(14):1298-30624693890
Cites: Scand J Public Health. 2011 Jul;39(7 Suppl):30-321775347
Cites: Ann Intern Med. 2012 Aug 21;157(4):225-3222910933
Cites: Gastroenterology. 2014 Apr;146(4):950-6024417818
Comment In: Transl Gastroenterol Hepatol. 2017 Feb 15;2:928275741
PubMed ID
27443823 View in PubMed
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Colorectal cancer risks in relatives of young-onset cases: is risk the same across all first-degree relatives?

https://arctichealth.org/en/permalink/ahliterature161866
Source
Clin Gastroenterol Hepatol. 2007 Oct;5(10):1195-8
Publication Type
Article
Date
Oct-2007
Author
Lisa A Boardman
Bruce W Morlan
Kari G Rabe
Gloria M Petersen
Noralane M Lindor
Sandra K Nigon
Julia Goldberg
Steven Gallinger
Author Affiliation
Division of Gastroenterology, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Source
Clin Gastroenterol Hepatol. 2007 Oct;5(10):1195-8
Date
Oct-2007
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Colorectal Neoplasms - diagnosis - epidemiology - genetics
DNA Mismatch Repair
DNA, Neoplasm - analysis
Electrophoresis, Gel, Two-Dimensional
Family
Female
Genetic Predisposition to Disease
Humans
Inheritance Patterns - genetics
Male
Middle Aged
Minnesota - epidemiology
Mutation
Ontario - epidemiology
Polymerase Chain Reaction
Prognosis
Retrospective Studies
Risk factors
SEER Program
Siblings
Abstract
During the last 15 years, several single-gene mendelian disorders have been discovered that might account for some of the familial aggregation detected in large population studies of colorectal cancer (CRC). Mutations in DNA mismatch repair (MMR) genes cause hereditary nonpolyposis colorectal cancer-Lynch syndrome, the most common of the recognized CRC-predisposition syndromes, in which one major feature is a young age for cancer onset. However, for young-onset microsatellite stable (MSS) CRC, the familial risk for CRC is unknown.
Patients with CRC who were
Notes
Cites: Am J Hum Genet. 2001 Oct;69(4):780-9011524701
Cites: J Clin Oncol. 2002 Feb 15;20(4):1043-811844828
Cites: Ann Intern Med. 1993 May 15;118(10):785-908470852
Cites: J Natl Cancer Inst. 1994 Nov 2;86(21):1618-267932826
Cites: Cancer Res. 1997 Nov 1;57(21):4787-949354440
Cites: Cancer Res. 1998 Apr 15;58(8):1713-89563488
Cites: Cancer Res. 1998 Nov 15;58(22):5248-579823339
Cites: Int J Cancer. 2005 Jul 10;115(5):835-815704173
Cites: J Natl Cancer Inst. 2005 Nov 2;97(21):1556-716264169
Cites: J Natl Cancer Inst. 2005 Nov 2;97(21):1575-916264177
Cites: Fam Cancer. 2006;5(3):221-616998667
PubMed ID
17702662 View in PubMed
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Family history of colorectal cancer in a Sweden county.

https://arctichealth.org/en/permalink/ahliterature18145
Source
Fam Cancer. 2003;2(2):87-93
Publication Type
Article
Date
2003
Author
Louise Olsson
Annika Lindblom
Author Affiliation
Department of Surgery, Central Hospital, Västerås, Uppsala University, Sweden, olsson@ltvastmanland.se
Source
Fam Cancer. 2003;2(2):87-93
Date
2003
Language
English
Publication Type
Article
Keywords
Adenomatous Polyposis Coli - diagnosis - epidemiology - genetics
Adolescent
Adult
Age Distribution
Age of Onset
Aged
Aged, 80 and over
Child
Child, Preschool
Colorectal Neoplasms - diagnosis - epidemiology - genetics
Colorectal Neoplasms, Hereditary Nonpolyposis - diagnosis - epidemiology - genetics
Family Health
Female
Genetic Predisposition to Disease
Humans
Infant
Infant, Newborn
Male
Mass Screening
Middle Aged
Pedigree
Questionnaires
Sweden - epidemiology
Abstract
Hereditary nonpolyposis colorectal cancer (HNPCC) and familial adenomatosis polyposis (FAP) are well-known high-risk cancer syndromes. Hereditary colorectal cancer (HCRC) with at least three relatives with colorectal cancer and a dominant pattern of inheritance but with no specifications for age at onset and two close relatives with colorectal cancer (TCR) are other forms of familial clustering known to carry an increased risk of the disease. The frequency of the total burden of familial colorectal cancer is not well known. We therefore investigated the family history of 400/411 (97%) eligible patients with recently diagnosed colorectal cancer in Västmanland county, Sweden, during a 3-year period. Records or death certificates confirmed the diagnoses of relatives. Five patients (1.2%, 95% CI 0.15-2.2) were diagnosed as having HNPCC, eight (1.9%, 95% CI 0.6-3.2) as having HCRC and thirty-four (8.3%, 95% CI 5.6-11.0) were identified as having TCR. In total, 47 patients (11.4%, 95% CI 8.3-14.5) were found to have a contributing familial background. The implication is thus that every ninth patient with colorectal cancer represents a highly or intermediately increased risk of the disease among relatives. We conclude that the low frequency of individuals identified by family history alone makes the establishment of surveillance programs feasible.
PubMed ID
14574157 View in PubMed
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A population-based audit for diagnosing colorectal cancer.

https://arctichealth.org/en/permalink/ahliterature17876
Source
Scand J Gastroenterol. 2004 Feb;39(2):158-63
Publication Type
Article
Date
Feb-2004
Author
L. Olsson
L. Lööf
A. Ekbom
Author Affiliation
Dept. of Surgery and Center for Clinical Research, Central Hospital, Uppsala University, Västerås, Sweden. louise.olsson@ltvastmanland.se
Source
Scand J Gastroenterol. 2004 Feb;39(2):158-63
Date
Feb-2004
Language
English
Publication Type
Article
Keywords
Barium Sulfate - diagnostic use
Colonoscopy
Colorectal Neoplasms - diagnosis - epidemiology - genetics
Diagnosis, Differential
Enema
Humans
Medical History Taking
Occult Blood
Primary Health Care
Risk assessment
Sweden - epidemiology
Abstract
BACKGROUND: Knowledge of the diagnostic work-up of colorectal cancer is a prerequisite to improve its quality. Family history is one of few known risk factors of the disease and it is therefore important to investigate to what extent this factor is used in routine management. METHODS: Copies of records from all health-care suppliers visited during diagnostic work-up were requested for 227/235 (97%) patients with recently diagnosed colorectal cancer in the county of Västmanland during 1998-99. A first consultation was identified and records and all diagnostic measures related to the initial consultation were scrutinized. A family history of colorectal cancer was known for 179 patients. RESULTS: Most of the patients, 107 (66%) colon and 57 (86%) rectal cancer patients, had consulted with a general practitioner. The median diagnostic work-up time was 42 days (IQ 12-110) for colon and 23 days (IQ 0-49) for rectal cancer. A double-contrast barium enema was the most commonly used diagnostic method for colon cancer. Family history was documented at the first consultation in 2/179 (1%) cases. In patients with right-sided cancer, median diagnostic work-up time was 53 days in patients with a positive result of faecal occult blood test (FOBT) as compared with 448 in patients with a negative result (P
PubMed ID
15000278 View in PubMed
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Search for familial clustering of multiple myeloma with any cancer.

https://arctichealth.org/en/permalink/ahliterature274662
Source
Leukemia. 2016 Mar;30(3):627-32
Publication Type
Article
Date
Mar-2016
Author
C. Frank
M. Fallah
T. Chen
E K Mai
J. Sundquist
A. Försti
K. Hemminki
Source
Leukemia. 2016 Mar;30(3):627-32
Date
Mar-2016
Language
English
Publication Type
Article
Keywords
Aged
Breast Neoplasms - diagnosis - epidemiology - genetics - pathology
Cluster analysis
Colorectal Neoplasms - diagnosis - epidemiology - genetics - pathology
Family
Female
Genetic Association Studies
Genetic Predisposition to Disease
Humans
Lymphoma, Non-Hodgkin - diagnosis - epidemiology - genetics - pathology
Male
Middle Aged
Multiple Myeloma - diagnosis - epidemiology - genetics - pathology
Plasma Cells - metabolism - pathology
Prostatic Neoplasms - diagnosis - epidemiology - genetics - pathology
Registries
Risk factors
Sweden - epidemiology
Waldenstrom Macroglobulinemia - diagnosis - epidemiology - genetics - pathology
Abstract
Multiple myeloma (MM) is a disease of immunoglobulin-producing plasma cells, which reside mainly in the bone marrow. Family members of MM patients are at a risk of MM, but whether other malignancies are in excess in family members is not established and is the aim of this study. MM patients (24 137) were identified from the Swedish Cancer Registry from years 1958 to 2012. Relative risks (RRs) were calculated for MM defined by any cancer diagnosed in first-degree relatives and compared with individuals whose relatives had no cancer. MM was reliably associated with relative's colorectal, breast and prostate cancers, non-thyroid endocrine tumors, leukemia and cancer of unknown primary; in addition, MM was associated with subsites of bone and connective tissue tumors and of non-Hodgkin lymphoma, including lymphoplasmacytic lymphoma/Waldenstr?m macroglobulinema (RR 3.47). MM showed a strong association (RR 1.91) in colorectal cancer families, possibly as part of an unidentified syndrome. All the associations of MM with discordant cancers are novel suggesting that MM shares genetic susceptibility with many cancers. The associations of MM bone and connective tissue tumors were supported by at least two independent results. Whether the results signal bone-related biology shared by MM and these tumors deserves further study.
PubMed ID
26449663 View in PubMed
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Very high incidence of familial colorectal cancer in Newfoundland: a comparison with Ontario and 13 other population-based studies.

https://arctichealth.org/en/permalink/ahliterature167042
Source
Fam Cancer. 2007;6(1):53-62
Publication Type
Article
Date
2007
Author
R C Green
J S Green
S K Buehler
J D Robb
D. Daftary
S. Gallinger
J R McLaughlin
P S Parfrey
H B Younghusband
Author Affiliation
Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada. rcgreen@mun.ca
Source
Fam Cancer. 2007;6(1):53-62
Date
2007
Language
English
Publication Type
Article
Keywords
Adenomatous Polyposis Coli - epidemiology - genetics
Age of Onset
Colonoscopy
Colorectal Neoplasms - diagnosis - epidemiology - genetics - surgery
Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology - genetics
Family Characteristics
Female
Genes, APC - physiology
Genetic Predisposition to Disease
Germ-Line Mutation - genetics
Humans
Incidence
Male
MutS Homolog 2 Protein - genetics
Neoplasms, Second Primary - epidemiology - genetics
Newfoundland and Labrador - epidemiology
Ontario - epidemiology
Pedigree
Population Surveillance
Precancerous Conditions - diagnosis - epidemiology - surgery
Registries
Risk Assessment - statistics & numerical data
Abstract
Newfoundland has the highest rate of colorectal cancer (CRC) of any Canadian province. In order to investigate the factors, especially genetic components, responsible for CRC we established the Newfoundland Colorectal Cancer Registry. In a 5-year period we examined every case of CRC diagnosed under the age of 75 years and obtained consent from 730 cases. Careful analysis of family history was used to assign a familial cancer risk, based on established criteria. We observed that 3.7% of CRC cases came from families meeting the Amsterdam II criteria and a further 0.9% of cases involved familial adenomatous polyposis (FAP). An additional 43% of cases met one or more of the revised Bethesda criteria and 31% of all cases had a first-degree relative affected with CRC. We compared the Newfoundland data with data from the province of Ontario, where the same recruitment and risk-assessment criteria were used. In all categories, the indicators of familial risk were significantly higher in Newfoundland. These data were also compared to results published from 13 other population-based studies worldwide. In every category the proportion of Newfoundland cases meeting the criteria was higher than in any other population. The mean differences were: 3.5-fold greater for FAP, 2.8-fold higher for Amsterdam criteria, 2.0-fold higher for Bethesda criteria and 1.9-fold higher for the number of affected first-degree relatives. We conclude that the high incidence of CRC in Newfoundland may be attributable to genetic, or at least familial, factors. In the high-risk families we provide evidence for the involvement of founder mutations in the APC and MSH2 genes.
PubMed ID
17039269 View in PubMed
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6 records – page 1 of 1.