Esterase D and gamma 1 actin level might predict results of induction therapy in patients with acute myeloid leukemia without and with maturation

نویسندگان

  • Maciej Kaźmierczak
  • Magdalena Luczak
  • Krzysztof Lewandowski
  • Luiza Handschuh
  • Anna Czyż
  • Małgorzata Jarmuż
  • Michał Gniot
  • Michał Michalak
  • Marek Figlerowicz
  • Mieczysław Komarnicki
چکیده

Development of modern proteomic methods in recent years has opened also new perspectives in the identification of new biomarkers which ensure more effective diagnosis, treatment monitoring and prediction of therapeutic outcome. We evaluated usefulness of comparative proteomics (MALDI-TOF) in two subtypes of acute myeloid leukemia (AML), M1 and M2, according to FAB classification. The bone marrow or blood cell proteomes were examined in 33 newly diagnosed patients before "3 + 7" induction therapy, after treatment and when the disease relapsed. We found that bone marrow and peripheral mononuclear cells from healthy volunteers revealed a number of quantitative and qualitative differences between the two proteomes, reflecting differences in the maturational status of normal cells. Such differences were not detected in our AML M1/M2 patients. Additionally, we found 9 proteins, which are potential biomarkers differentiating between the AML patients and healthy volunteers. Using comparative proteomics, we found that annexin I, glutathione transferase omega, esterase D and gamma 1 actin had prognostic significance. Applying statistical methods, we detected two proteins which might allow to predict results of induction therapy in AML M1/M2. One of them was esterase D, the higher concentration of which was associated with higher complete remission rate, and the other was gamma 1 actin, the higher concentration of which was related to resistance. In the article, we also discussed the role of these two proteins in the biology of AML, and we suggested potential usefulness of modification in induction therapy reflecting the presence of proteins.

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عنوان ژورنال:

دوره 30  شماره 

صفحات  -

تاریخ انتشار 2013