Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-5-24
pubmed:abstractText
Cancer cells can contribute to activation of the clotting system by their capacity to produce and release procoagulant/fibrinolytic substances and inflammatory cytokines, and by their interaction with host cells (endothelial, monocytes, platelets, and neutrophils). Moreover, anticancer drugs (chemotherapy/hormone therapy) may greatly affect the risk of thromboembolic complications in cancer patients by similar mechanisms, eg, through the release of procoagulants by tumor cells, through endothelial damage, or stimulation of tissue factor production by host cells. The interactions between cancer/metastatic processes and thrombosis have been reviewed here from the pathogenetic viewpoint. We hope that better knowledge of these pathogenetic pathways will lead to the development of more targeted strategies to prevent thromboembolism in cancer patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0925-5710
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
137-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Pathogenesis of thrombosis in patients with malignancy.
pubmed:affiliation
Hematology Division, Ospedali Riuniti, Bergamo, Italy.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't