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dc.creatorLiu, Jian-Miao
dc.creatorBignon, Jerome
dc.creatorIlić, Vesna
dc.creatorBriscoe, Cecilia
dc.creatorLallemand, Jean-Yves
dc.creatorRiches, Andrew
dc.creatorWdzieczak-Bakala, Joanna
dc.date.accessioned2021-04-20T12:10:56Z
dc.date.available2021-04-20T12:10:56Z
dc.date.issued2006
dc.identifier.issn1042-8194
dc.identifier.urihttp://rimi.imi.bg.ac.rs/handle/123456789/142
dc.description.abstractEvidence from clinical and laboratory studies suggests that angiogenesis is important in the progression of solid tumours and hematologic malignancies. We have shown that the naturally occurring tetrapeptide Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a potent angiogenic factor normally present at nanomolar concentrations in the blood. A murine leukemia model was used to assess whether there was a correlation between levels of endogenous AcSDKP and the development of disease. Levels of AcSDKP in the plasma and bone marrow (BM) cells from mice bearing an acute myeloid leukemia (AML) were five- to ten-fold greater than those in non-leukemic mice. Furthermore, a strong correlation between the concentration of endogenous AcSDKP and the progression of AML was demonstrated. These results are consistent with the marked increase in BM vascularity observed in leukemic mice. The physiologic relevance of these findings awaits further studies and the contribution of AcSDKP to the pathogenesis of leukemia is under investigation.en
dc.publisherTaylor & Francis Ltd, Abingdon
dc.rightsrestrictedAccess
dc.sourceLeukemia & Lymphoma
dc.subjectAcSDKPen
dc.subjectleukemiaen
dc.subjectangiogenesisen
dc.subjectdiagnosticen
dc.titleEvidence for an association of high levels of endogenous Acetyl-Ser-Asp-Lys-Pro, a potent mediator of angiogenesis, with acute myeloid leukemia developmenten
dc.typearticle
dc.rights.licenseARR
dc.citation.epage1920
dc.citation.issue9
dc.citation.other47(9): 1915-1920
dc.citation.rankM23
dc.citation.spage1915
dc.citation.volume47
dc.identifier.doi10.1080/10428190600688131
dc.identifier.pmid17065006
dc.identifier.scopus2-s2.0-33750451989
dc.identifier.wos000241600200032
dc.type.versionpublishedVersion


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