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Acute Myelocytic Leukemia, Acute Lymphocytic Leukemia

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Trial Information

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

Inclusion Criteria:

- acute leukemia

Exclusion Criteria:

- nil

Type of Study:


Study Design:

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

Principal Investigator

Liang-In Lin, PhD

Investigator Role:

Principal Investigator

Investigator Affiliation:

Department of Clinical Laboratory Sciences and Medical Biotechnology, National Taiwan University


Taiwan: Department of Health

Study ID:




Start Date:

February 2003

Completion Date:

July 2004

Related Keywords:

  • Acute Myelocytic Leukemia
  • Acute Lymphocytic Leukemia
  • Leukemia
  • Leukemia, Lymphoid
  • Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • Leukemia, Myeloid, Acute
  • Leukemia, Myeloid