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

Acute Myeloid Leukemia Clinical Trial

Official title:

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

Clinical Trial Details — Status: Active, not recruiting

Administrative data

• NCT number: NCT01195506
• Other study ID #: 99025
• Status: Active, not recruiting
• Phase: N/A
• First received: September 3, 2010
• Last updated: October 5, 2010
• Start date: September 2010

Study information

• Verified date: October 2010
• Source: Taipei Medical University WanFang Hospital
• Contact: n/a
• Is FDA regulated: No
• Health authority: Taiwan: Department of Health
• Study type: Observational

Clinical Trial 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.

Recruitment information / eligibility

• Status: Active, not recruiting
• Enrollment: 40
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years to 60 Years

Eligibility

Inclusion Criteria:

• patients who were diagnosed acute myeloid leukemia

Exclusion Criteria:

• patients who were diagnosed other type leukemia

Study Design

Observational Model: Case-Only, Time Perspective: Retrospective

Related Conditions & MeSH terms

• Acute Myeloid Leukemia
• Leukemia
• Leukemia, Myeloid
• Leukemia, Myeloid, Acute

Locations

Country	Name	City	State
Taiwan	Taipei Medical University - WanFang Hospital	Taipei

Sponsors (1)

Lead Sponsor	Collaborator
Taipei Medical University WanFang Hospital

Country where clinical trial is conducted

Taiwan,