Studying Samples From Patients With T-Cell Acute Lymphoblastic Leukemia

The recruitment status of this study is unknown because the information has not been verified recently.
Verified April 2012 by National Cancer Institute (NCI).
Recruitment status was  Active, not recruiting
Sponsor:
Collaborator:
Information provided by:
National Cancer Institute (NCI)
ClinicalTrials.gov Identifier:
NCT01581528
First received: April 19, 2012
Last updated: April 21, 2012
Last verified: April 2012

April 19, 2012
April 21, 2012
April 2012
June 2012   (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
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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.
 
Active, not recruiting
15
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June 2012   (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
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Yes
Contact information is only displayed when the study is recruiting subjects
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NCT01581528
CDR0000732166, COG-AALL12B5
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Peter C. Adamson, Children's Oncology Group - Group Chair Office
Children's Oncology Group
National Cancer Institute (NCI)
Principal Investigator: Jeffrey C. Rathmell, PhD Duke Cancer Institute
National Cancer Institute (NCI)
April 2012

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