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Antiangiogenic Factors in Gastric Cancer

This study has been completed.
Information provided by (Responsible Party):
Jun Ho Lee, National Cancer Center, Korea Identifier:
First received: August 13, 2008
Last updated: October 16, 2012
Last verified: October 2012
Endogenous antiangiogenic factors are related with gastric cancer progression.

Gastric Cancer

Study Type: Observational
Study Design: Observational Model: Cohort
Time Perspective: Prospective
Official Title: The Role of Endogenous Antiangiogenic Factors in Gastric Cancer Progression

Resource links provided by NLM:

Further study details as provided by Jun Ho Lee, National Cancer Center, Korea:

Primary Outcome Measures:
  • Relationship between antiangiogenic factor and tumor, node, metastasis [ Time Frame: One year ]

Secondary Outcome Measures:
  • Overall survival, treatment failure [ Time Frame: 5 years ]

Biospecimen Retention:   Samples Without DNA
Serum for protein assay using ELISA

Enrollment: 240
Study Start Date: April 2006
Study Completion Date: January 2012
Primary Completion Date: July 2008 (Final data collection date for primary outcome measure)
Detailed Description:
Gastric cancers have been known to secrete the proangiogenic cytokine VEGF in vitro and in vivo. Tumor VEGF expression is correlated with the severity of disease in patients with gastric cancer and some authors have suggested using circulating VEGF as a prognostic factor or tumor marker.In addition to producing proangiogenic cytokines, recent data demonstrate that tumors can produce antiangiogenic cytokine as well. It has been suggested that, in humans, the generation of antiangiogenic compounds in the presence of a primary tumor suppresses the growth of distant metastases. This phenomenon has been demonstrated in mice and in patients with clear cell renal cancer, breast cancer, and colorectal cancer. However, the presence of endogenous antiangiogenic cytokines in patients with gastric cancer has not been reported.

Ages Eligible for Study:   20 Years to 80 Years   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes
Sampling Method:   Non-Probability Sample
Study Population
Eligible patients will undergo subtotal or total gastrectomy with D2 lymph node dissection

Inclusion Criteria:

  • Histologic diagnosis of gastric adenocarcinoma
  • No other forms of cancer therapy, such as chemotherapy or radiotherapy for at least 3 weeks before the enrollment in study
  • Performance status of 0, 1, 2 on the ECOG criteria
  • ASA class I, II
  • Patient compliance that allow adequate follow up
  • Informed consent from patient or patient's relative.

Exclusion Criteria:

  • Second primary malignancy
  • EMR (Endoscopic mucosal resection) indication
  • Laparoscopic gastrectomy
  • Radiologic or clinical evidence of metastasis
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its identifier: NCT00735566

Korea, Republic of
National Cancer Center
Goyang-si, Geonggi-do, Korea, Republic of, 410-0769
Sponsors and Collaborators
National Cancer Center, Korea
Principal Investigator: Jun Ho Lee, M.D., Ph.D Gastric Cancer Branch, National Cancer Center
  More Information

Responsible Party: Jun Ho Lee, Staff Surgeon, National Cancer Center, Korea Identifier: NCT00735566     History of Changes
Other Study ID Numbers: NCCCTS 04-105
Study First Received: August 13, 2008
Last Updated: October 16, 2012

Keywords provided by Jun Ho Lee, National Cancer Center, Korea:
gastric cancer
antiangiogenic factors
TNM stage

Additional relevant MeSH terms:
Stomach Neoplasms
Gastrointestinal Neoplasms
Digestive System Neoplasms
Neoplasms by Site
Digestive System Diseases
Gastrointestinal Diseases
Stomach Diseases
Angiogenesis Inhibitors
Angiogenesis Modulating Agents
Growth Substances
Physiological Effects of Drugs
Growth Inhibitors
Antineoplastic Agents processed this record on June 23, 2017