Linked Life Data

18407736

Source:http://linkedlifedata.com/resource/pubmed/id/18407736

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-4-14
pubmed:abstractText
The mechanisms that underlie the initiation of human cancer are poorly understood. Here, we describe the development of hereditary diffuse gastric cancer and argue that it arises from the disruption of the regenerative processes that are inherent to all epithelial tissues. This model supports the cancer stem cell hypothesis, in which tumors contain a subpopulation of cells with the key stem cell characteristics of capacity for self renewal, differentiation and limitless replication. We argue that epigenetic modifications induced by common environmental and physiological pressures are able to initiate this disruption. The carcinogenic effects of these modifications are potentially reversible through the use of epigenetic therapies such as DNA demethylating agents and histone deacetylation inhibitors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1744-8301
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
229-39
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Hereditary diffuse gastric cancer and lost cell polarity: a short path to cancer.
pubmed:affiliation
University of Otago, Cancer Genetics Laboratory, Department of Biochemistry, Dunedin, New Zealand. bostjan.humar@otago.ac.nz
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't