Linked Life Data

19662600

Source:http://linkedlifedata.com/resource/pubmed/id/19662600

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-8-7
pubmed:abstractText
The authors review the antineoplastic effect of mammalian target of rapamycin (mTOR) inhibitors and their biological basis. mTOR is an intracellular serine/threonine kinase that is a central controller of cell growth and proliferation. mTOR integrates signals from sources such as nutrients and growth factors. mTOR regulation can affect angiogenesis, cell growth, nutrient uptake and utilization, and metabolism. Growth factors such as insulin growth factor, epidermal growth factor, platelet-derived growth factor and vascular endothelial growth factor bind to and activate receptors located on the cell surface. Receptors activate intracellular signaling cascades phosphatidylinositol 3 kinase-serine-threonine kinase-mTOR (PI3K-AKT-mTOR) leading to protein synthesis. Activation of the mTOR pathway is linked to increased protein synthesis by modulating elements that are important in cellular processes, including growth, proliferation, angiogenesis and nutrient uptake. Many growth factor receptors and signaling pathway components are deregulated in cancer. Deregulations in mTOR-linked pathways increase the risk of developing cancer or have been identified in many human cancers. Deregulations include overexpression of growth factors, overexpression or mutations of growth factor receptors, loss of tumor suppressor genes, and gain-of-function mutations in mTOR-linked pathways. These deregulations permit the survival, growth, proliferation and migration of cancer cells and promote tumor angiogenesis. Targeting them has been a successful anticancer strategy. Targeting mTOR as well as these deregulated pathways could provide enhanced anticancer activity. The efficacy of mTOR inhibitors in preventing several types of cancers in transplanted patients or in recovering cancers developed in transplant patients has been documented in both trials and single reports.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1121-8428
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
457-62
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:articleTitle
Antineoplastic effect of proliferation signal inhibitors: from biology to clinical application.
pubmed:affiliation
Renal Unit, Careggi University Hospital, Florence, Italy. salvadorim@aou-careggi.toscana.it
pubmed:publicationType
Journal Article, Review