Linked Life Data

16861908

Source:http://linkedlifedata.com/resource/pubmed/id/16861908

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
16
pubmed:dateCreated
2006-9-13
pubmed:abstractText
Tumor dormancy, a complex and still poorly understood phenomenon observed both in experimental models and in patients, has been associated with insufficient angiogenic capacity. A defined event, termed "angiogenic switch" and characterized by an imbalance between pro- and anti-angiogenic factors, often marks interruption of the dormant state, thus triggering invasive tumor growth. In our current view, sustained angiogenesis is considered essential in promoting this transition. Recently, we demonstrated that co-administration of proliferation-arrested Kaposi's sarcoma cells or recombinant angiogenic factors interrupts dormancy of poorly angiogenic leukemia cells by providing a brief angiogenic burst. These findings indicate that even a transient angiogenic switch can prime progressive tumor growth and suggest that tumor angiogenesis is a process requiring a higher amount of angiogenic factors for its induction than maintenance. Here we discuss the implications of these observations on our view of tumor angiogenesis and on the therapeutic potential of angiogenesis inhibitors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1751-5
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Dormant tumors awaken by a short-term angiogenic burst: the spike hypothesis.
pubmed:affiliation
Istituto Oncologico Veneto, Padova, Italy. stefano.indraccolo@unipd.it
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't