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Study the Novel Functions and Molecular Mechanisms of Vascular Endothelial Growth Factor-C (VEGF-C) in Acute Myeloid Leukemia (AML)

The recruitment status of this study is unknown. The completion date has passed and the status has not been verified in more than two years.
Verified October 2010 by Taipei Medical University WanFang Hospital.
Recruitment status was:  Active, not recruiting
Information provided by:
Taipei Medical University WanFang Hospital Identifier:
First received: September 3, 2010
Last updated: October 5, 2010
Last verified: October 2010
Vascular endothelial growth factor (VEGF)-C is recognized as a tumor lymphangiogenic factor based on the effects of activated VEGFR3 on lymphatic endothelial cells. VEGFR3 has been proposed as a specific marker for lymphatic endothelial cells. Recent studies indicated that VEGFR3 also expressed in a variety of human malignancies, including lung, colon rectal, or head and neck cancer. Moreover, VEGF-C/VEGFR3 axis was demonstrated in regulating angiogenesis, cell invasion, and metastasis in several solid tumors. The promotion of cell mobility in response to VEGF-C was required the involvement of adhesion molecule contactin-1. In addition to solid tumors, it has been reported that the VEGF-C/VEGFR3 axis is activated in subsets of leukemia patients. Until now, it has been demonstrated that higher endogenous VEGFC levels of acute myelogenous leukemia (AML) cells are related to decreased in vitro and in vivo responsiveness to chemotherapy; an effect that may result from inhibition of apoptosis by increasing Bcl-2/Bax ratios by the VEGF-C/VEGFR3 pathway. Thus, a functional VEGF-C/VEGFR3 system may exist in leukemia. However, the detail information concerning the role of VEGF-C/VEGFR3 in non-solid tumors is still lacking. Bone marrow neoangiogenesis plays a crucial pathogenic and possible prognostic role in AML. The VEGF-C/VEGFR3 axis has been proven in the regulation of solid tumors angiogenesis. In the investigators preliminary study, the investigators found VEGF-C may play a critical role in angiogenesis regulation of leukemic cells by upregulating cyclooxygenase-2 (COX-2). Furthermore, the investigators found that the upregulation of COX-2 also correlate with the VEGF-C-induced proliferation in leukemic cells and this phenomenon might further regulate the chemoresistance of VEGF-C. In this study, the investigators will investigate the extent of angiogenesis and chemoresistance induced by VEGF-C in leukemic cells. This study will provide evidences on the subject of the novel role of VEGF-C in leukemia. With progress in molecular biology of VEGF-C, its value as a therapeutic target is highly promising.

Acute Myeloid Leukemia

Study Type: Observational
Study Design: Observational Model: Case-Only
Time Perspective: Retrospective
Official Title: Study the Novel Functions and Molecular Mechanisms of Vascular Endothelial Growth Factor-C (VEGF-C) in Acute Myeloid Leukemia (AML)

Resource links provided by NLM:

Further study details as provided by Taipei Medical University WanFang Hospital:

Estimated Enrollment: 40
Study Start Date: September 2010

Ages Eligible for Study:   18 Years to 60 Years   (Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population
patients who were diagnosed acute myeloid leukemia

Inclusion Criteria:

  • patients who were diagnosed acute myeloid leukemia

Exclusion Criteria:

  • patients who were diagnosed other type leukemia
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Please refer to this study by its identifier: NCT01195506

Taipei Medical University - WanFang Hospital
Taipei, Taiwan
Sponsors and Collaborators
Taipei Medical University WanFang Hospital
Principal Investigator: Ming-Hsien Chien Taipei Medical University
  More Information

Responsible Party: Ming-Hsien Chien/stem cell research center, Taipei Medical University Identifier: NCT01195506     History of Changes
Other Study ID Numbers: 99025
Study First Received: September 3, 2010
Last Updated: October 5, 2010

Keywords provided by Taipei Medical University WanFang Hospital:
We Will Collect the Bone Marrow Specimens From AML Patients

Additional relevant MeSH terms:
Leukemia, Myeloid
Leukemia, Myeloid, Acute
Neoplasms by Histologic Type
Endothelial Growth Factors
Growth Substances
Physiological Effects of Drugs
Mitosis Modulators
Molecular Mechanisms of Pharmacological Action processed this record on May 25, 2017