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Effects of cytarabine and various anthracyclins on platelet activation: Characterization of in vitro effects and their possible clinical relevance in acute myelogenous leukemia
Author(s) -
Foss Brynjar,
Ulvestad Elling,
Hervig Tor,
Bruserud Øystein
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.1566
Subject(s) - cytarabine , daunorubicin , platelet , leukemia , mitoxantrone , pharmacology , in vivo , acute leukemia , idarubicin , immunology , medicine , doxorubicin , cancer research , chemistry , chemotherapy , biology , microbiology and biotechnology
Previous in vitro studies have demonstrated that normal platelets and platelet‐released mediators can alter in vitro characteristics of human acute myelogenous leukemia (AML) blasts. To further investigate whether platelets can be expected to adhere to and thereby affect AML blasts through their release of soluble mediators into a common microenvironment, we investigated (i) the effects on platelet activation by cytotoxic drugs commonly used in AML therapy; (ii) the occurrence of circulating activated platelets in acute leukemia patients; and (iii) the in vivo and in vitro adherence of platelets to AML blasts. The anthracyclins daunorubicin and idarubicin increased the expression of activation‐associated membrane molecules (GPIIb/IIIa, CD62P, CD63) by normal platelets, daunorubicin then having the strongest effect. In contrast, cytarabine, epirubicin, doxorubicin and mitoxantrone had no significant effects. Although AML patients did not show increased levels of activated platelets in the circulation, adhesion of platelets to AML blasts was demonstrated both in vivo and in vitro . These results suggest that platelets and AML blasts may locate to common in vivo microenvironments, and platelet‐derived soluble mediators may thereby affect the functional characteristics of the leukemia cells. © 2002 Wiley‐Liss, Inc.

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