Linked Life Data

16442709

Source:http://linkedlifedata.com/resource/pubmed/id/16442709

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-8-8
pubmed:abstractText
The spleen tyrosine kinase Syk was long thought to be a hematopoietic cell-specific signaling molecule. Recent evidence demonstrated that it is also expressed by many non-hematopoietic cell types and that it plays a negative role in cancer. A significant drop in its expression was first observed during breast cancer progression, but an anomalous Syk expression has now also been evidenced in many other tumor types. Mechanistic studies using Syk re-expression demonstrated its suppressive function in tumorigenesis and metastasis formation, which is surprising for a tyrosine kinase. Loss of Syk expression is regulated, albeit not exclusively, by its promoter hypermethylation. The molecular mechanism of its tumor-suppressive function remains largely unknown; the identification of its activators and effectors in non-hematopoietic cells will be a challenge for the years to come. An increasing number of clinical studies reveal a correlation between reduced Syk expression and an increased risk for metastasis formation, and assign Syk as a potential new prognostic marker in different tumor types.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0304-3835
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
241
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
159-73
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
The Syk tyrosine kinase: a new negative regulator in tumor growth and progression.
pubmed:affiliation
CNRS UMR 5539, Université Montpellier 2, 34095 Montpellier, France. coopman@univ-montp2.fr
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural