Studying Samples From Patients With T-Cell Acute Lymphoblastic Leukemia

Leukemia Clinical Trial

Official title:

Metabolic Pathways in T-Cell Acute Lymphoblastic Leukemia (T-ALL)

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01581528
• Other study ID #: AALL12B5
• Secondary ID: COG-AALL12B5AALL
• Status: Completed
• Phase: N/A
• First received: April 19, 2012
• Last updated: May 17, 2016
• Start date: April 2012

Study information

• Verified date: May 2016
• Source: Children's Oncology Group
• Contact: n/a
• Is FDA regulated: No
• Health authority: United States: Federal Government
• Study type: Observational

Clinical Trial Summary

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).

Description:

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 15
• Est. primary completion date: May 2016
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Both
• Age group: N/A and older

Eligibility

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

Study Design

Observational Model: Case-Only, Time Perspective: Retrospective

Related Conditions & MeSH terms

• Leukemia
• Leukemia, Lymphoid
• Precursor Cell Lymphoblastic Leukemia-Lymphoma
• Precursor T-Cell Lymphoblastic Leukemia-Lymphoma

Intervention

Genetic:
• gene expression analysis

Other:
• cell culture procedure

• flow cytometry

• laboratory biomarker analysis

• metabolic assessment

Locations

Country	Name	City	State
n/a

Sponsors (2)

Lead Sponsor	Collaborator
Children's Oncology Group	National Cancer Institute (NCI)

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Metabolic status of primary T-ALL			No
Primary	Effects of metabolic inhibition on metabolic stress pathways and apoptosis			No
Primary	Metabolic inhibition interaction with chemotherapy or targeted drugs			No

External Links

•   Clinical trial summary from the National Cancer Institute's PDQ® database