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Activation of Notch signaling in human colon adenocarcinoma.

https://arctichealth.org/en/permalink/ahliterature154123
Source
Int J Oncol. 2008 Dec;33(6):1223-9
Publication Type
Article
Date
Dec-2008
Author
Michael Reedijk
Silvia Odorcic
Hui Zhang
Runjan Chetty
Carsten Tennert
Brendan C Dickson
Gina Lockwood
Steven Gallinger
Sean E Egan
Author Affiliation
Program in Developmental Biology and Stem Cell Research, The Hospital for Sick Children, MaRS East Tower, Ontario M5G 1L7, Canada.
Source
Int J Oncol. 2008 Dec;33(6):1223-9
Date
Dec-2008
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - genetics - mortality - pathology
Basic Helix-Loop-Helix Transcription Factors - genetics
Calcium-Binding Proteins - genetics
Cell Differentiation
Colonic Neoplasms - genetics - mortality - pathology
Gene Expression Regulation, Neoplastic
Germany
Glycosyltransferases - genetics
Homeodomain Proteins - genetics
Humans
In Situ Hybridization
Intercellular Signaling Peptides and Proteins - genetics
Kaplan-Meier Estimate
Membrane Proteins - genetics
Ontario
Prognosis
RNA, Messenger - analysis
Receptor, Notch1 - genetics
Receptors, Notch - genetics
Registries
Signal Transduction - genetics
Abstract
Notch and Wnt signaling function together to regulate colonic progenitor cell division and differentiation. Studies in mice have also shown that Notch signaling is required for adenoma formation in response to elevated Wnt-pathway signaling that occurs in the APCMin mouse model of human adenomatous polyposis coli. We therefore used in situ hybridization to analyze expression of Notch ligands, receptors and fringe genes, as well as the Notch target gene, HES1, in human colorectal cancer (CRC). In a small cohort of tumors, JAGGED ligands, NOTCH1, LFNG and HES1 were expressed at levels similar to, or higher than, levels observed in the crypt. To explore the possibility that Notch signaling may play a quantitative role in human CRC we next analyzed HES1 mRNA expression in 130 tumors, each associated with outcome data. The vast majority of these tumors expressed HES1, although at varying levels. Absolute expression levels did not correlate with patient survival. These results establish that JAG ligands and NOTCH1, as well as Notch receptor activation are consistent features of human CRC and support the notion that many of these tumors, like the APCMin mouse, may respond to anti-Notch therapeutic regimes.
Notes
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PubMed ID
19020755 View in PubMed
Less detail

Agreement between proxy- and case-reported information obtained using the self- administered Ontario Familial Colon Cancer Registry epidemiologic questionnaire.

https://arctichealth.org/en/permalink/ahliterature185270
Source
Chronic Dis Can. 2003;24(1):1-8
Publication Type
Article
Date
2003
Author
Victoria Nadalin
Michelle Cotterchio
Gail McKeown-Eyssen
Steven Gallinger
Author Affiliation
Division of Preventive Oncology, Research Unit, Cancer Care Ontario, Toronto, Ontario, Canada.
Source
Chronic Dis Can. 2003;24(1):1-8
Date
2003
Language
English
Publication Type
Article
Keywords
Case-Control Studies
Colonic Neoplasms - epidemiology - genetics
Data Collection - standards
Female
Humans
Male
Ontario - epidemiology
Proxy
Questionnaires
Rectal Neoplasms - epidemiology - genetics
Registries
Abstract
Case-control studies of fatal cancers often rely on proxy respondents. Therefore, it is important to determine the completeness and accuracy of proxy-reported information. We evaluated proxy reports using the Ontario Familial Colon Cancer Registry epidemiology questionnaire. A proxy questionnaire was completed by spouses or relatives identified by a sample of participating cases. Item non-response and percentage agreement (between case and proxy reports) were assessed. More than 30% of proxies were unable to report on physical activity, gynecological surgery, alcohol intake, weight 20 years ago, and oral contraceptive use. Proxy reports of medical history and bowel screening varied, the percentage missing ranging from 5% for diabetes to 44% for familial polyposis in the case of medical history, and from 4% for colonoscopy to 27% for hemoccult tests in the case of screening. Agreement between case and proxy report was good to excellent for colonic screening, most medical history, and for reproductive, medication and vitamin use variables (74% to 100%). It is useful to collect proxy information on such variables as medical history, parity, colonic screening and vitamin use, whereas oral contraceptive use and previous weight are not well reported.
PubMed ID
12757630 View in PubMed
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Allergies are associated with reduced pancreas cancer risk: A population-based case-control study in Ontario, Canada.

https://arctichealth.org/en/permalink/ahliterature162881
Source
Int J Cancer. 2007 Nov 15;121(10):2241-5
Publication Type
Article
Date
Nov-15-2007
Author
Ayelet Eppel
Michelle Cotterchio
Steven Gallinger
Author Affiliation
Familial Gastrointestinal Cancer Registry, Digestive Diseases Clinical Research Centre, Joseph and Wolf Lebovic Centre, Mount Sinai Hospital, Toronto, Ontario, Canada. aeppel@mtsinai.on.ca
Source
Int J Cancer. 2007 Nov 15;121(10):2241-5
Date
Nov-15-2007
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Distribution
Aged
Case-Control Studies
Child
Female
Humans
Hypersensitivity - epidemiology
Male
Middle Aged
Ontario
Pancreatic Neoplasms - epidemiology
Risk factors
Abstract
Pancreatic adenocarcinoma is one of the deadliest cancers with mortality rates almost equaling incidence rates. Each year, approximately 3,500 Canadians are diagnosed with this disease. Although somewhat inconsistent, epidemiological studies have found that allergies are associated with a reduced pancreas cancer risk while there appears to be no association with asthma. These associations were evaluated in a population-based case-control study conducted in Ontario. Incident cases of pancreatic adenocarcinoma, identified through the Ontario Cancer Registry (OCR), and diagnosed April 1, 2003 to June 1, 2006, were recruited by the Ontario Pancreas Cancer Study (OPCS). Controls were recruited from the Ontario Familial Colorectal Cancer Registry (OFCCR). Data on 276 cases and 378 controls were available for the current study. Multivariable logistic regression analysis was used to obtain age-adjusted odds ratio (AOR) estimates. Ever having allergies or hayfever was associated with reduced pancreas cancer risk (OR = 0.43, 95% confidence interval (CI): 0.29-0.63). There was no association observed between a history of asthma and pancreas cancer risk. Findings are of great importance to understanding the biological mechanisms involved in pancreas cancer development.
PubMed ID
17582608 View in PubMed
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Assessing the management of hepatic colorectal cancer metastases: is treatment consistent in Ontario?

https://arctichealth.org/en/permalink/ahliterature124578
Source
HPB (Oxford). 2012 Jun;14(6):409-13
Publication Type
Article
Date
Jun-2012
Author
Lakhbir Sandhu
Adrian Fox
Cindy Nhan
Heidi Barnett
Robin S McLeod
Steven Gallinger
Carol-Anne Moulton
Author Affiliation
Department of Surgery, Division of General Surgery, University of Toronto Cancer Care Ontario, Toronto, ON, Canada. lakho.sandhu@utoronto.ca
Source
HPB (Oxford). 2012 Jun;14(6):409-13
Date
Jun-2012
Language
English
Publication Type
Article
Keywords
Catheter Ablation - statistics & numerical data
Chemotherapy, Adjuvant
Colorectal Neoplasms - epidemiology - pathology
Embolization, Therapeutic - statistics & numerical data
Guideline Adherence - statistics & numerical data
Health Care Surveys
Hepatectomy - statistics & numerical data
Humans
Internet
Liver Neoplasms - epidemiology - secondary - therapy
Lung Neoplasms - secondary - therapy
Neoadjuvant Therapy - statistics & numerical data
Ontario - epidemiology
Physician's Practice Patterns - statistics & numerical data
Pneumonectomy - statistics & numerical data
Practice Guidelines as Topic
Questionnaires
Treatment Outcome
Abstract
Advances in surgical techniques and chemotherapeutic options have expanded indications for surgery in patients with metastatic colorectal cancer. This study aimed to examine how hepatopancreatobiliary (HPB) surgeons approach the management of patients with hepatic colorectal cancer metastases (HCCM).
A web-based survey utilizing 10 clinical scenarios was distributed by e-mail to 37 HPB surgeons in Ontario, Canada. The study region has a population of approximately 13 million people and a universal, single-payer health care system. Descriptive analyses were used to tabulate results.
Twenty-two (59%) surgeons responded to the survey. The majority (19/22, 86%) of respondents favoured neoadjuvant chemotherapy for patients with multiple synchronous and unilobar metastases; only nine of 22 (41%) respondents favoured neoadjuvant chemotherapy for patients with a single synchronous metastasis. In the setting of residual resectable disease following downstaging chemotherapy, 77% (17/22) of surgeons advocated hepatic resection with either radiofrequency ablation (RFA) or wedge resection of the 'ghost' lesions. Over 80% of surgeons would perform a liver and pulmonary resection in a patient with hepatic and multiple unilobar lung metastases. None would offer liver resection to patients with multiple retroperitoneal node involvement, although 55% (12/22) would do so if a single retroperitoneal node was involved. Preoperative portal vein embolization was favoured over RFA in patients with a small metastasis and inadequate functional hepatic volume.
Notable heterogeneity was observed among Ontario's HPB surgeons in approaches to HCCM.
Notes
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PubMed ID
22568418 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 between colonic screening, subject characteristics, and stage of colorectal cancer.

https://arctichealth.org/en/permalink/ahliterature172016
Source
Am J Gastroenterol. 2005 Nov;100(11):2531-9
Publication Type
Article
Date
Nov-2005
Author
Laura Fazio
Michelle Cotterchio
Michael Manno
John McLaughlin
Steven Gallinger
Author Affiliation
Department of Public Health Sciences, University of Toronto, Toronto, Ontario, Canada.
Source
Am J Gastroenterol. 2005 Nov;100(11):2531-9
Date
Nov-2005
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Body mass index
Colonic Neoplasms - diagnosis - genetics - pathology
Colonoscopy
Ethnic Groups
Female
Food Habits
Humans
Lymph Nodes - pathology
Male
Mass Screening - methods
Middle Aged
Neoplasm Metastasis
Neoplasm Staging
Ontario
Population Surveillance
Rectal Neoplasms - diagnosis - genetics - pathology
Registries
Retrospective Studies
Risk factors
Rural Health
Abstract
Colorectal cancer remains a significant cause of mortality and morbidity in North America. Colorectal cancer survival is highly dependent on stage at diagnosis, therefore it is important to identify factors related to stage. This study evaluated the association between subject factors (e.g., colonic screening, family history) and stage of colorectal cancer at diagnosis.
Population-based colorectal cancer cases recruited by the Ontario Familial Colon Cancer Registry between 1997 and 1999 were staged according to the tumor-nodal-metastasis (TNM) staging system and classified as early (TNM I/II) or late (TNM III/IV) stage. Epidemiologic information and stage was available for 768 cases. Multivariate logistic regression was used to obtain odds ratios (OR) estimates.
Having had screening endoscopy reduced the risk of late stage diagnosis (OR = 0.46, 95% CI 0.22-0.98). Being older (>45 yr) was associated with a reduced risk of late stage cancer (OR = 0.36, 95% CI 0.18-0.74), as was having a first degree relative with colorectal cancer (OR =0.66, 95% CI 0.46-0.95). Rural residence (OR = 1.48, 95% CI 1.01-2.17) and non-white ethnicity (OR = 3.34, 95% CI 1.20-9.36) were associated with an increased risk of late stage cancer.
Several factors are independently associated with late stage colorectal cancer. Colorectal cancer screening awareness and education programs need to consider targeting persons most likely to present with late stage colorectal cancer.
PubMed ID
16279911 View in PubMed
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Association between subject factors and colorectal cancer screening participation in Ontario, Canada.

https://arctichealth.org/en/permalink/ahliterature174775
Source
Cancer Detect Prev. 2005;29(3):221-6
Publication Type
Article
Date
2005
Author
Farah Ramji
Michelle Cotterchio
Michael Manno
Linda Rabeneck
Steven Gallinger
Author Affiliation
Department of Public Health Sciences, University of Toronto, Toronto, Ont., Canada.
Source
Cancer Detect Prev. 2005;29(3):221-6
Date
2005
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Colonoscopy - methods
Colorectal Neoplasms - diagnosis - epidemiology
Epidemiologic Studies
Female
Genetic Predisposition to Disease
Health Surveys
Humans
Male
Mass Screening - utilization
Middle Aged
Occult Blood
Odds Ratio
Ontario - epidemiology
Patient compliance
Pedigree
Prevalence
Risk factors
Sigmoidoscopy - utilization
Abstract
Colorectal cancer screening reduces colorectal cancer incidence and mortality. This population-based study was conducted to evaluate (i) the association between subject factors and colorectal screening participation and (ii) the lifetime prevalence of colorectal screening among the general population of Ontario, Canada. Population-based controls were recruited by the Ontario Familial Colorectal Cancer Registry during 1998-2000. The 1944 persons completed an epidemiologic questionnaire. Descriptive statistics were computed and step-wise multivariate logistic regression was used to estimate odds ratios and 95% confidence intervals. Overall, 23% of persons greater than 50 years of age reported ever having had colorectal cancer screening; 17% reported fecal occult blood test (FOBT), 6% sigmoidoscopy, and 4% colonoscopy. Family history of colorectal cancer, increased age, higher household income, and use of hormone replacement therapy (among women) were all significantly associated with ever having had colorectal cancer screening. The low prevalence of colorectal cancer screening among the target population suggests the need for an increased awareness of the public health importance of colorectal cancer screening.
PubMed ID
15896925 View in PubMed
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Cigarette smoking, genetic variants in carcinogen-metabolizing enzymes, and colorectal cancer risk.

https://arctichealth.org/en/permalink/ahliterature140152
Source
Am J Epidemiol. 2010 Nov 1;172(9):1000-14
Publication Type
Article
Date
Nov-1-2010
Author
Sean P Cleary
Michelle Cotterchio
Ellen Shi
Steven Gallinger
Patricia Harper
Author Affiliation
Cancer Care Ontario, Toronto, Ontario, Canada. sean.cleary@uhn.on.ca
Source
Am J Epidemiol. 2010 Nov 1;172(9):1000-14
Date
Nov-1-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Aryl Hydrocarbon Hydroxylases - genetics
Arylamine N-Acetyltransferase - genetics
Arylsulfotransferase - genetics
Biological Markers - blood
Case-Control Studies
Colorectal Neoplasms - enzymology - epidemiology - etiology - genetics
Confidence Intervals
Cytochrome P-450 CYP1A1 - genetics
Cytochrome P-450 CYP1A2 - genetics
Cytochrome P-450 CYP2E1 - genetics
Epoxide Hydrolases - genetics
Female
Genotype
Glutathione Transferase - genetics
Humans
Isoenzymes - genetics
Male
Medical Records
Middle Aged
Multivariate Analysis
Odds Ratio
Ontario - epidemiology
Polymorphism, Genetic
Questionnaires
Retrospective Studies
Risk
Smoking - adverse effects
Abstract
The risk of colorectal cancer associated with smoking is unclear and may be influenced by genetic variation in enzymes that metabolize cigarette carcinogens. The authors examined the colorectal cancer risk associated with smoking and 26 variants in carcinogen metabolism genes in 1,174 colorectal cancer cases and 1,293 population-based controls recruited in Canada by the Ontario Familial Colorectal Cancer Registry from 1997 to 2001. Adjusted odds ratios were calculated by multivariable logistic regression. Smoking for >27 years was associated with a statistically significant increased colorectal cancer risk (adjusted odds ratio (AOR) = 1.25, 95% confidence interval (CI): 1.02, 1.53) in all subjects. Colorectal cancer risk associated with smoking was higher in males for smoking status, duration, and intensity. The CYP1A1-3801-CC (AOR = 0.47, 95% CI: 0.23, 0.94) and CYP2C9-430-CT (AOR = 0.82, 95% CI: 0.68, 0.99) genotypes were associated with decreased risk, and the GSTM1-K173N-CG (AOR = 1.99, 95% CI: 1.21, 3.25) genotype was associated with an increased risk of colorectal cancer. Statistical interactions between smoking and genetic variants were assessed by comparing logistic regression models with and without a multiplicative interaction term. Significant interactions were observed between smoking status and SULT1A1-638 (P = 0.02), NAT2-857 (P = 0.01), and CYP1B1-4390 (P = 0.04) variants and between smoking duration and NAT1-1088 (P = 0.02), SULT1A1-638 (P = 0.04), and NAT1-acetylator (P = 0.03) status. These findings support the hypothesis that prolonged cigarette smoking is associated with increased risk of colorectal cancer and that this risk may be modified by variation in carcinogen metabolism genes.
Notes
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PubMed ID
20937634 View in PubMed
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Clinical and economic comparison of laparoscopic to open liver resections using a 2-to-1 matched pair analysis: an institutional experience.

https://arctichealth.org/en/permalink/ahliterature128531
Source
J Am Coll Surg. 2012 Feb;214(2):184-95
Publication Type
Article
Date
Feb-2012
Author
Faizal D Bhojani
Adrian Fox
Kristen Pitzul
Steven Gallinger
Alice Wei
Carol-Anne Moulton
Allan Okrainec
Sean P Cleary
Author Affiliation
Division of General Surgery, University Health Network, 200 Elizabeth Street, Toronto, Ontario, Canada.
Source
J Am Coll Surg. 2012 Feb;214(2):184-95
Date
Feb-2012
Language
English
Publication Type
Article
Keywords
Blood Loss, Surgical
Costs and Cost Analysis
Hepatectomy - adverse effects - economics - methods
Hospital Costs
Humans
Intention to Treat Analysis
Laparoscopy - economics
Length of Stay
Matched-Pair Analysis
Ontario
Operating Rooms - economics
Postoperative Complications - epidemiology
Abstract
Surgical resection of hepatic lesions is associated with intraoperative and postoperative morbidity and mortality. Our center has introduced a laparoscopic liver resection (LLR) program over the past 3 years. Our objective is to describe the initial clinical experience with LLR, including a detailed cost analysis.
We evaluated all LLRs from 2006 to 2010. Each was matched to 2 open cases for number of segments removed, patient age, and background liver histology. Model for End-Stage Liver Disease (MELD) and the Charlson comorbidity index were calculated retrospectively. Nonparametric statistical analysis was used to compare surgical and economic outcomes. Analyses were performed including and excluding converted cases.
Fifty-seven patients underwent attempted LLR. Demographic characteristics were similar between groups. Estimated blood loss was lower in the LLR vs the open liver resection (OLR) group, at 250 mL and 500 mL, respectively (p
PubMed ID
22192894 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
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PubMed ID
17702662 View in PubMed
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