Linked Life Data

19671741

Source:http://linkedlifedata.com/resource/pubmed/id/19671741

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2009-8-17
pubmed:abstractText
Increasing evidence indicates that adhesion signaling plays an important role in the tumor microenvironment, contributing to cancer progression, invasion, and metastasis. Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine kinase that regulates adhesion-dependent cell signaling and has been implicated in mediating steps in cancer progression and metastasis in many human cancers, including prostate. We have investigated the role of FAK in the appearance of adenocarcinoma (atypical epithelial hyperplasia of T antigen) and neuroendocrine carcinomas in the transgenic adenocarcinoma of mouse prostate (TRAMP) model using either Cre-mediated recombination to genetically ablate FAK expression or pharmacologic inhibition of FAK activity with the small-molecule inhibitor, PF-562,271. We provide evidence that loss of FAK or its inhibition with PF-562,271 does not alter the progression to adenocarcinoma. However, continued FAK expression (and activity) is essential for the androgen-independent formation of neuroendocrine carcinoma. These data indicate that integrin signaling through FAK is an important component of cancer progression in the TRAMP model and suggest that treatment modalities targeting FAK may be an appropriate strategy for patients with castrate-resistant cancer.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-11231059, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-11313859, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-11731413, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-12242727, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-12692788, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-12876277, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-14764858, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-15389779, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-15866427, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-15914540, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-17177290, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-17395594, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-17409287, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-18030362, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-18156212, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-18245520, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-18339875, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-18845837, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-19147981, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-7724580, http://linkedlifedata.com/resource/pubmed/commentcorrection/19671741-9916792
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1538-8514
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2470-7
pubmed:dateRevised
2011-5-4
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Differential requirement for focal adhesion kinase signaling in cancer progression in the transgenic adenocarcinoma of mouse prostate model.
pubmed:affiliation
Department of Microbiology, University of Virginia, Charlottesville, Virginia 22908, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural