Targeting the mitochondria in acute myeloid leukemia
Appl. cancer res
;
37: 1-7, 2017. ilus
Article
in English
| LILACS, Inca
| ID: biblio-915434
ABSTRACT
Acute myeloid leukemia (AML) is a clonal hematologic neoplasm characterized by heterogeneity of genetic abnormalities found at diagnosis. These abnormalities serve to classify patients by risk group into low, intermediate, and high risk. It also provides specific targets for the development of new combinational therapies. However, because of the heterogeneity of genetic abnormalities, targeted therapy is not always possible. Altered mitochondrial metabolism is a common feature in cancer cells, a phenomenon first described by Otto Warburg. In AML patients, the discovery of mutations in the isocitrate dehydrogenase gene provided for the first time a link between altered mitochondrial metabolism and AML. This raised the possibility of testing drugs known as mitocans for new combinational therapeutic approaches. Mitocans are a diverse group of anti-cancer compounds that target mitochondria. They disrupt energy production leading to enhanced generation of reactive oxygen species along with the activation of the intrinsic pathway of apoptosis. The present review discusses the different types of mitocans and their mechanism of action along with preclinical and clinical studies in AML (AU)
Full text:
Available
Index:
LILACS (Americas)
Main subject:
Leukemia, Myeloid, Acute
/
Genetic Heterogeneity
/
Hematologic Neoplasms
/
Mitochondria
Limits:
Adult
/
Aged
/
Female
/
Humans
/
Male
Language:
English
Journal:
Appl. cancer res
Journal subject:
Neoplasms
Year:
2017
Type:
Article
Affiliation country:
Brazil
Institution/Affiliation country:
University of São Paulo, Medical School of Ribeirão Preto/BR
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