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Cell-based evaluation of changes in coagulation activity induced by antineoplastic drugs for the treatment of acute myeloid leukemia.

Abstract Idarubicin (IDR), cytarabine (AraC), and tamibarotene (Am80) are effective for treatment of acute myeloid leukemia (AML). In acute leukemia, the incidence of venous thromboembolism or disseminated intravascular coagulation is associated with induction chemotherapy. Procoagulant effects of IDR, AraC, and Am80 were investigated in a vascular endothelial cell line EAhy926 and AML cell lines HL60 (AML M2), NB4 (AML M3, APL), and U937 (AML M5), focusing on tissue factor (TF), phosphatidylserine (PS), and thrombomodulin (TM). IDR induced procoagulant activity on the surface of vascular endothelial and AML cell lines. Expression of TF antigen, TM antigen, and PS were induced by IDR on the surface of each cell line, whereas expression of TF and TM mRNAs were unchanged. Conversely, Am80 decreased TF exposure and procoagulant activity, and increased TM exposure on NB4 cells. In NB4 cells, we observed downregulation of TF mRNA and upregulation of TM mRNA. These data suggest IDR may induce procoagulant activity in vessels by apoptosis through PS exposure and/or TF expression on vascular endothelial and AML cell lines. Am80 may suppress blood coagulation through downregulation of TF expression and induction of TM expression. Our methods could be useful to investigate changes in procoagulant activity induced by antineoplastic drugs.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 28406995
OWN - NLM
STAT- MEDLINE
DA  - 20170413
DCOM- 20170420
LR  - 20170420
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - Cell-based evaluation of changes in coagulation activity induced by
      antineoplastic drugs for the treatment of acute myeloid leukemia.
PG  - e0175765
LID - 10.1371/journal.pone.0175765 [doi]
AB  - Idarubicin (IDR), cytarabine (AraC), and tamibarotene (Am80) are effective for
      treatment of acute myeloid leukemia (AML). In acute leukemia, the incidence of
      venous thromboembolism or disseminated intravascular coagulation is associated
      with induction chemotherapy. Procoagulant effects of IDR, AraC, and Am80 were
      investigated in a vascular endothelial cell line EAhy926 and AML cell lines HL60 
      (AML M2), NB4 (AML M3, APL), and U937 (AML M5), focusing on tissue factor (TF),
      phosphatidylserine (PS), and thrombomodulin (TM). IDR induced procoagulant
      activity on the surface of vascular endothelial and AML cell lines. Expression of
      TF antigen, TM antigen, and PS were induced by IDR on the surface of each cell
      line, whereas expression of TF and TM mRNAs were unchanged. Conversely, Am80
      decreased TF exposure and procoagulant activity, and increased TM exposure on NB4
      cells. In NB4 cells, we observed downregulation of TF mRNA and upregulation of TM
      mRNA. These data suggest IDR may induce procoagulant activity in vessels by
      apoptosis through PS exposure and/or TF expression on vascular endothelial and
      AML cell lines. Am80 may suppress blood coagulation through downregulation of TF 
      expression and induction of TM expression. Our methods could be useful to
      investigate changes in procoagulant activity induced by antineoplastic drugs.
FAU - Tsunaka, Misae
AU  - Tsunaka M
AD  - Laboratory Molecular Genetics of Hematology, Field of Applied Laboratory Science,
      Graduate School of Health Care Sciences, Tokyo Medical and Dental University,
      Tokyo, Japan.
FAU - Shinki, Haruka
AU  - Shinki H
AD  - Laboratory Molecular Genetics of Hematology, Field of Applied Laboratory Science,
      Graduate School of Health Care Sciences, Tokyo Medical and Dental University,
      Tokyo, Japan.
FAU - Koyama, Takatoshi
AU  - Koyama T
AUID- ORCID: http://orcid.org/0000-0002-1640-0039
AD  - Laboratory Molecular Genetics of Hematology, Field of Applied Laboratory Science,
      Graduate School of Health Care Sciences, Tokyo Medical and Dental University,
      Tokyo, Japan.
LA  - eng
PT  - Journal Article
DEP - 20170413
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Benzoates)
RN  - 0 (Phosphatidylserines)
RN  - 0 (Tetrahydronaphthalenes)
RN  - 0 (Thrombomodulin)
RN  - 04079A1RDZ (Cytarabine)
RN  - 08V52GZ3H9 (tamibarotene)
RN  - 9035-58-9 (Thromboplastin)
RN  - ZRP63D75JW (Idarubicin)
SB  - IM
MH  - Antineoplastic Agents/*adverse effects/pharmacology
MH  - Benzoates/adverse effects/pharmacology
MH  - Cell Line, Tumor
MH  - Cytarabine/adverse effects/pharmacology
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - HL-60 Cells
MH  - Humans
MH  - Idarubicin/adverse effects/pharmacology
MH  - Leukemia, Myeloid, Acute/drug therapy/genetics/*metabolism
MH  - Phosphatidylserines/*metabolism
MH  - Tetrahydronaphthalenes/adverse effects/pharmacology
MH  - Thrombomodulin/genetics/*metabolism
MH  - Thromboplastin/genetics/*metabolism
EDAT- 2017/04/14 06:00
MHDA- 2017/04/21 06:00
CRDT- 2017/04/14 06:00
PHST- 2017/01/03 [received]
PHST- 2017/03/30 [accepted]
AID - 10.1371/journal.pone.0175765 [doi]
AID - PONE-D-17-00289 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 13;12(4):e0175765. doi: 10.1371/journal.pone.0175765.
      eCollection 2017.

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