Studying Samples From Patients With T-Cell Acute Lymphoblastic Leukemia

This study has been completed.
Sponsor:
Collaborator:
National Cancer Institute (NCI)
Information provided by (Responsible Party):
Children's Oncology Group
ClinicalTrials.gov Identifier:
NCT01581528
First received: April 19, 2012
Last updated: May 17, 2016
Last verified: May 2016

April 19, 2012
May 17, 2016
April 2012
May 2016   (final data collection date for primary outcome measure)
  • Metabolic status of primary T-ALL [ Designated as safety issue: No ]
  • Effects of metabolic inhibition on metabolic stress pathways and apoptosis [ Designated as safety issue: No ]
  • Metabolic inhibition interaction with chemotherapy or targeted drugs [ Designated as safety issue: No ]
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).

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.

Observational
Observational Model: Case-Only
Time Perspective: Retrospective
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Non-Probability Sample
patients diagnosed with T-ALL
Leukemia
  • 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.
 
Completed
15
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May 2016   (final data collection date for primary outcome measure)

DISEASE CHARACTERISTICS:

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

PATIENT CHARACTERISTICS:

  • Not specified

PRIOR CONCURRENT THERAPY:

  • Not specified
Both
Child, Adult, Senior
Yes
Contact information is only displayed when the study is recruiting subjects
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NCT01581528
AALL12B5, COG-AALL12B5, AALL12B5, NCI-2012-00728
No
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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

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP