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

Sponsor
Taipei Medical University WanFang Hospital (Other)
Overall Status
Unknown status
CT.gov ID
NCT01195506
Collaborator
(none)
40
1

Study Details

Study Description

Brief Summary

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.

Condition or Disease Intervention/Treatment Phase

    Study Design

    Study Type:
    Observational
    Anticipated Enrollment :
    40 participants
    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)
    Study Start Date :
    Sep 1, 2010

    Outcome Measures

    Primary Outcome Measures

      Eligibility Criteria

      Criteria

      Ages Eligible for Study:
      18 Years to 60 Years
      Sexes Eligible for Study:
      All
      Accepts Healthy Volunteers:
      No
      Inclusion Criteria:
      • patients who were diagnosed acute myeloid leukemia
      Exclusion Criteria:
      • patients who were diagnosed other type leukemia

      Contacts and Locations

      Locations

      Site City State Country Postal Code
      1 Taipei Medical University - WanFang Hospital Taipei Taiwan

      Sponsors and Collaborators

      • Taipei Medical University WanFang Hospital

      Investigators

      • Principal Investigator: Ming-Hsien Chien, Taipei Medical University

      Study Documents (Full-Text)

      None provided.

      More Information

      Publications

      None provided.
      Responsible Party:
      , ,
      ClinicalTrials.gov Identifier:
      NCT01195506
      Other Study ID Numbers:
      • 99025
      First Posted:
      Sep 6, 2010
      Last Update Posted:
      Oct 6, 2010
      Last Verified:
      Oct 1, 2010

      Study Results

      No Results Posted as of Oct 6, 2010