Leukemia Clinical Trial
Official title:
Metabolic Pathways in T-Cell Acute Lymphoblastic Leukemia (T-ALL)
RATIONALE: Studying samples of blood, tissue, and bone marrow from patients with cancer in
the laboratory may help doctors identify learn more about biomarkers related to cancer. It
may also help doctors to find better ways to treat cancer.
PURPOSE: This research studies samples from patients with T-cell acute lymphoblastic
leukemia (T-ALL).
OBJECTIVES:
- Determine the metabolic status and regulation of primary T-cell acute lymphoblastic
leukemia (T-ALL) relative to control resting peripheral T cells.
- Establish the effects of metabolic inhibition on metabolic stress pathways and
apoptosis.
- Determine how metabolic inhibition interacts with chemotherapy or targeted therapy
drugs to kill T-ALL cells.
OUTLINE: T-ALL samples cultured alone or with gamma secretase inhibitors (GSI) or PI3K
inhibitors are analyzed for metabolic characteristics including glucose transporter 1
(Glut1) expression, mitochondrial mass, phospho-flow for 5' adenosine
monophosphate-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), and mammalian
target of rapamycin (mTOR) by flow cytometry. T-ALL samples and normal CD4+ T cells
(control) are also exposed to ± 2-deoxyglucose or ± the glutaminolysis inhibitor media and
analyzed for metabolic stress responses over time in particular, AMPK activation, autophagy
(immunofluorescence for LC3-II processing), and BCL2-associated X protein (Bak) and Bax
activation to indicate apoptosis. These cells (T-ALL and control) are then cultured with
cyclophosphamide, dexamethasone, or the B-cell CLL/lymphoma 2 (Bcl-2) inhibitor, ABT-737, to
determine cell death over time.
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Observational Model: Case-Only, Time Perspective: Retrospective
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