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Studying Samples From Patients With T-Cell Acute Lymphoblastic Leukemia

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ClinicalTrials.gov Identifier: NCT01581528
Recruitment Status : Completed
First Posted : April 20, 2012
Last Update Posted : May 18, 2016
Information provided by (Responsible Party):

April 19, 2012
April 20, 2012
May 18, 2016
April 2012
May 2016   (Final data collection date for primary outcome measure)
  • Metabolic status of primary T-ALL
  • Effects of metabolic inhibition on metabolic stress pathways and apoptosis
  • Metabolic inhibition interaction with chemotherapy or targeted drugs
Same as current
Complete list of historical versions of study NCT01581528 on ClinicalTrials.gov Archive Site
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Studying Samples From Patients With T-Cell Acute Lymphoblastic Leukemia
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).


  • 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.

Observational Model: Case-Only
Time Perspective: Retrospective
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Non-Probability Sample
patients diagnosed with T-ALL
  • Genetic: gene expression analysis
  • Other: cell culture procedure
  • Other: flow cytometry
  • Other: laboratory biomarker analysis
  • Other: metabolic assessment
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
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May 2016   (Final data collection date for primary outcome measure)


  • Sample from patients diagnosed with T-ALL
  • Samples from independent healthy donors obtained through the Gulf Coast Regional Blood Center (controls)


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Sexes Eligible for Study: All
Child, Adult, Senior
Contact information is only displayed when the study is recruiting subjects
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COG-AALL12B5 ( Other Identifier: clinicaltrials.gov )
AALL12B5 ( Other Identifier: Children's Oncology Group )
NCI-2012-00728 ( Registry Identifier: CTRP (Clinical Trial Reporting Program) )
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Children's Oncology Group
Children's Oncology Group
National Cancer Institute (NCI)
Principal Investigator: Jeffrey C. Rathmell, PhD Duke Cancer Institute
Children's Oncology Group
May 2016