Metabolic Mechanisms of Drug Resistance in Leukemia

Birgit Knoechel; Jon C Aster

doi:10.1016/j.cmet.2015.10.005

Metabolic Mechanisms of Drug Resistance in Leukemia

Cell Metab. 2015 Nov 3;22(5):759-60. doi: 10.1016/j.cmet.2015.10.005.

Authors

Birgit Knoechel¹, Jon C Aster²

Affiliations

¹ Department of Pediatric Oncology, Dana Farber Cancer Institute and Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA.
² Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA. Electronic address: jaster@partners.org.

PMID: 26536486
DOI: 10.1016/j.cmet.2015.10.005

Abstract

Tumor cells frequently undergo metabolic reprogramming, but it is unknown how these metabolic changes relate to drug resistance. A recent article now demonstrates that PI3K/AKT signaling causes a metabolic switch from glutaminolysis to aerobic glycolysis in Notch-dependent T cell acute lymphoblastic leukemia (T-ALL).

MeSH terms

Apoptosis / genetics
Drug Resistance, Neoplasm / genetics*
Glycolysis
Humans
Oncogene Protein v-akt / genetics
Oncogene Protein v-akt / metabolism
Phosphatidylinositol 3-Kinases / genetics
Phosphatidylinositol 3-Kinases / metabolism
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology
Receptors, Notch / genetics
Receptors, Notch / metabolism*
Signal Transduction / genetics

Substances

Receptors, Notch
Phosphatidylinositol 3-Kinases
Oncogene Protein v-akt

Grants and funding

K08 CA191091/CA/NCI NIH HHS/United States