Risk Factors and Incidence of Colorectal Cancer According to Major Molecular Subtypes.
Adiposity
Age Factors
Body Mass Index
Cohort Studies
Colorectal Neoplasms
/ epidemiology
CpG Islands
DNA Methylation
Diet
Female
Follow-Up Studies
Genes, ras
Humans
Incidence
Life Style
Male
Microsatellite Instability
Middle Aged
Mutation
Phenotype
Proportional Hazards Models
Proto-Oncogene Proteins B-raf
/ genetics
Risk Factors
Sex Factors
Smoking
United States
/ epidemiology
Journal
JNCI cancer spectrum
ISSN: 2515-5091
Titre abrégé: JNCI Cancer Spectr
Pays: England
ID NLM: 101721827
Informations de publication
Date de publication:
02 2021
02 2021
Historique:
received:
11
06
2020
revised:
28
08
2020
accepted:
09
09
2020
entrez:
14
1
2021
pubmed:
15
1
2021
medline:
15
1
2021
Statut:
epublish
Résumé
Colorectal cancer (CRC) is a heterogeneous disease that can develop via 3 major pathways: conventional, serrated, and alternate. We aimed to examine whether the risk factor profiles differ according to pathway-related molecular subtypes. We examined the association of 24 risk factors with 4 CRC molecular subtypes based on a combinatorial status of microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and We documented 1175 CRC patients with molecular subtype data: subtype 1 (n = 498; conventional pathway; non-MSI-high, CIMP-low or negative, Risk factor profiles may differ for CRC arising from different molecular pathways.
Sections du résumé
Background
Colorectal cancer (CRC) is a heterogeneous disease that can develop via 3 major pathways: conventional, serrated, and alternate. We aimed to examine whether the risk factor profiles differ according to pathway-related molecular subtypes.
Methods
We examined the association of 24 risk factors with 4 CRC molecular subtypes based on a combinatorial status of microsatellite instability (MSI), CpG island methylator phenotype (CIMP), and
Results
We documented 1175 CRC patients with molecular subtype data: subtype 1 (n = 498; conventional pathway; non-MSI-high, CIMP-low or negative,
Conclusions
Risk factor profiles may differ for CRC arising from different molecular pathways.
Identifiants
pubmed: 33442661
doi: 10.1093/jncics/pkaa089
pii: pkaa089
pmc: PMC7791624
doi:
Substances chimiques
Proto-Oncogene Proteins B-raf
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Subventions
Organisme : NIDDK NIH HHS
ID : K24 DK098311
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA137178
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA230873
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA087969
Pays : United States
Organisme : NCI NIH HHS
ID : R03 CA197879
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA202704
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA151993
Pays : United States
Organisme : NCI NIH HHS
ID : R00 CA215314
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA197735
Pays : United States
Organisme : NCI NIH HHS
ID : K07 CA188126
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA167552
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA167552
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA186107
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA055075
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA127003
Pays : United States
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press.
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