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

NCT01195506 | Unknown

• 1 other identifier: 99025
• Study Type: observational
• Target: 40
• Locations: 1 country
• Sites: 1

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.

Conditions

Acute Myeloid Leukemia

Keywords

We Will Collect the Bone Marrow Specimens From AML Patients

Eligibility Criteria

• Age: 18 Years - 60 Years
• Sex: all
• Healthy Volunteers: No
• Age Groups: Adult (18-64)
• Sampling Method: Probability Sample

Study Population

patients who were diagnosed acute myeloid leukemia

You may qualify if:

• patients who were diagnosed acute myeloid leukemia

You may not qualify if:

• patients who were diagnosed other type leukemia

Sponsors & Collaborators

• Taipei Medical University WanFang Hospital: lead

Study Sites (1)

Taipei Medical University - WanFang Hospital

Taipei, Taiwan

Location

MeSH Terms

Conditions

Leukemia, Myeloid, Acute

Condition Hierarchy (Ancestors)

Leukemia, Myeloid; Leukemia; Neoplasms by Histologic Type; Neoplasms; Hematologic Diseases; Hemic and Lymphatic Diseases

Study Officials

• Ming-Hsien Chien

  Taipei Medical University

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: observational
• Observational Model: CASE ONLY
• Time Perspective: RETROSPECTIVE
• Sponsor Type: OTHER

Study Record Dates

• First Submitted: September 3, 2010
• First Posted: September 6, 2010
• Study Start: September 1, 2010
• Last Updated: October 6, 2010

Record last verified: 2010-10

Locations

TW (1)