Linked Life Data

17425506

Source:http://linkedlifedata.com/resource/pubmed/id/17425506

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2007-4-11
pubmed:abstractText
The linear sequence of genetic alterations illustrated in the Vogelstein model provides a readily understandable illustration of the fundamental principles underlying colorectal tumorigenesis. However, it is now clear that colorectal cancer is a multi-pathway disease. In this review, the concept that inactivation of the tumor suppressor gene APC serves to initiate virtually all colorectal cancers is shown to be an oversimplification. APC inactivation may have important tumorigenic pathogenic effects beyond the mere initiation of precancerous adenomas. Furthermore, the early evolution of colorectal neoplasia must sometimes occur by mechanisms other than inactivation of APC or related alterations that would drive dysregulated Wnt pathway signaling. Oncogenic mutations implicating both BRAF and KRAS are highlighted as alternative initiating steps that synergize with DNA methylation and occur within the context of serrated polyps. CRC comprises subgroups with particular clinical, pathological, and molecular features.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0893-9675
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
273-87
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Colorectal cancer: a multipathway disease.
pubmed:affiliation
Department of Pathology, McGill University, Duff Medical Building, 3775 University Street, Montreal, Quebec H3A 2B4, Canada. jeremy.jass@mcgill.ca
pubmed:publicationType
Journal Article, Review