Oncotarget

Research Papers:

Antitumoral effect of Ocoxin on acute myeloid leukemia

Elena Díaz-Rodríguez, Susana Hernández-García, Eduardo Sanz and Atanasio Pandiella _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2016; 7:6231-6242. https://doi.org/10.18632/oncotarget.6862

Metrics: PDF 2103 views  |   HTML 1713 views  |   ?  


Abstract

Elena Díaz-Rodríguez1, Susana Hernández-García1, Eduardo Sanz2, Atanasio Pandiella1

1Instituto de Biología Molecular y Celular del Cáncer CSIC-Universidad de Salamanca, Salamanca, Spain

2Catalysis, S.L., Madrid, Spain

Correspondence to:

Atanasio Pandiella, e-mail: [email protected]

Keywords: acute myeloid leukemia, antioxidants, cell cycle, p27

Received: November 19, 2015     Accepted: December 22, 2015     Published: January 09, 2016

ABSTRACT

Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy whose incidence is growing in developed countries. In the relapse setting, very limited therapeutic options are available and in most cases only palliative care can be offered to patients. The effect of a composite formulation that contains several antioxidants, Ocoxin Oral solution (OOS), was tested in this condition. When analyzed in vitro, OOS exhibited anti-AML action that was both time and dose dependent. In vivo OOS induced a ralentization of tumor growth that was due to a decrease in cell proliferation. Such effect could, at least partially, be due to an increase in the cell cycle inhibitor p27, although other cell cycle proteins seemed to be altered. Besides, OOS induced an immunomodulatory effect through the induction of IL6. When tested in combination with other therapeutic agents normally used in the treatment of AML patients, OOS demonstrated a higher antiproliferative action, suggesting that it may be used in combination with those standard of care treatments to potentiate their antiproliferative action in the AML clinic.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 6862