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Clinical Trial Details — Status: Recruiting

Administrative data

NCT number NCT00155844
Other study ID # 9200200606
Secondary ID
Status Recruiting
Phase N/A
First received September 9, 2005
Last updated September 9, 2005
Start date February 2003
Est. completion date July 2004

Study information

Verified date January 2003
Source National Taiwan University Hospital
Contact Liang-In Lin, PhD
Phone 886-2-23810611
Email lilin@ha.mc.ntu.edu.tw
Is FDA regulated No
Health authority Taiwan: Department of Health
Study type Observational

Clinical Trial Summary

Bone marrow consists of a complex hematopoietic cellular component.When the blood progenitor cells differentiate to mature cells, they will exit unassisted to peripheral blood. On the other hand, the immature cells trapped by marrow-blood barrier. However, malignant transformation of the hematopoietic progenitor cells in AML and CML results in a blockade of their ability to terminally differentiate, causing a rapid accumulation of immature cells.Chemokines have been shown to direct the movement of cells between intravascular and extravascular compartments.The CXC chemokine CXCL12, the ligand of CXCR4, activates distinct signaling pathways that may mediate cell migration.In the preliminary research, we analyze the CXCR4 expression and the chemotactic response of CXCL12 and peripheral plasma in six leukemia cell lines (HL-60, HL-CZ, K562, U937, Raji and Jurkat) and found that three categories among them could be suggested: one is CXCR4 (-) and CXCL12 response (-), such as HL-CZ and K562 cells; the other is CXCR4 (+) and CXCL12 response (-), such as HL-60 and Raji cells; the rest is CXCR4 (+) and CXCL12 response (+), such as Jurkat and U937 cells. These results make us wonder that the leukemic cells could egress to PB from BM is due to destruction of homing process or the activation of mobilization process through CXCR4-CXCL12 axis dysfunction. Therefore,we will focus on evaluating the mechanism of CXCR4-CXCL12 axis dysfunction in the various leukemic cell lines and primary leukemic cells.


Description:

Bone marrow consists of a complex hematopoietic cellular component that continuously goes through self-replication and/or differentiation processes. When the blood progenitor cells differentiate to mature cells, they will exit unassisted to peripheral blood. On the other hand, the immature cells trapped by marrow-blood barrier. However, malignant transformation of the hematopoietic progenitor cells in AML and CML results in a blockade of their ability to terminally differentiate, causing a rapid accumulation of immature cells.Chemokines have been shown to direct the movement of cells between intravascular and extravascular compartments.The CXC chemokine CXCL12, the ligand of CXCR4, activates distinct signaling pathways that may mediate cell migration. Recent reports demonstrated that the migration of HPC after transplantation from PB to BM via concentration gradients created by CXCL12, produced by marrow stromal cells, has been proposed as integral to the homing process. The mirror image of homing is mobilization of HPC from the BM to PB, which in a clinical setting is induced by administration of various stimuli including hematopoietic growth factors. The CXCR4-CXCL12 axis is reported to be very important in retaining the immature cells in the appropriate bone marrow compartment. In the preliminary research, we analyze the CXCR4 expression and the chemotactic response of CXCL12 and peripheral plasma in six leukemia cell lines (HL-60, HL-CZ, K562, U937, Raji and Jurkat) by flow cytometry and two-chamber migration assay, respectively. Three categories among them could be suggested: one is CXCR4 (-) and CXCL12 response (-), such as HL-CZ and K562 cells; the other is CXCR4 (+) and CXCL12 response (-), such as HL-60 and Raji cells; the rest is CXCR4 (+) and CXCL12 response (+), such as Jurkat and U937 cells. These results make us wonder that the leukemic cells could egress to PB from BM is due to destruction of homing process or the activation of mobilization process through CXCR4-CXCL12 axis dysfunction. Therefore,we will focus on evaluating the mechanism of CXCR4-CXCL12 axis dysfunction in the various leukemic cell lines and primary leukemic cells from several aspects: 1). Evaluate the CXCR4 expression and the CXCL12 response of leukemic cells from patients with acute leukemia;2). Study on the molecular mechanism for the blockade of CXCR4-CXCL12 signaling in CXCR4 (+) and SDF response (-) cells;3). Evaluate the marrow plasma and peripheral plasma to find out plasma factors that interfering the migration behavior of leukemic CXCR4 (+) but CXCL12 response (-) cells


Recruitment information / eligibility

Status Recruiting
Enrollment 30
Est. completion date July 2004
Est. primary completion date
Accepts healthy volunteers Accepts Healthy Volunteers
Gender Both
Age group N/A and older
Eligibility Inclusion Criteria:

- acute leukemia

Exclusion Criteria:

Study Design

Observational Model: Case Control, Primary Purpose: Screening, Time Perspective: Cross-Sectional


Related Conditions & MeSH terms


Locations

Country Name City State
Taiwan Liang-In Lin Taipei

Sponsors (1)

Lead Sponsor Collaborator
National Taiwan University Hospital

Country where clinical trial is conducted

Taiwan, 

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