PTEN and IGFBP-3 Correlation in Ovarian Carcinoma Invasion

Ovarian Cancer Clinical Trial

Official title:

Correlation of PTEN and IGFBP-3 in the Invasion of Ovarian Endometrioid Carcinoma

Clinical Trial Details — Status: Withdrawn

Administrative data

• NCT number: NCT00173407
• Other study ID #: 9461700640
• Status: Withdrawn
• Phase: N/A
• First received: September 12, 2005
• Last updated: December 26, 2012
• Start date: January 2006
• Est. completion date: October 2012

Study information

• Verified date: December 2012
• Source: National Taiwan University Hospital
• Contact: n/a
• Is FDA regulated: No
• Health authority: Taiwan: Department of Health
• Study type: Interventional

Clinical Trial Summary

We have identified insulin-like growth factor binding protein (IGFBP)-3 as an invasion suppressor gene in ovarian endometrioid carcinoma, and showed association with lower cancer migration, invasion and metastasis. Recently, a novel model of ovarian EC formation from endometriosis was reported, and PTEN was found to be a major protein involved. Inactivation of PTEN has been reported in some ovarian EC tumors and methylation was suggested as one of the major epigenetic changes. This tumorigenesis model has lots of similarity to our established invasion model. Therefore, we plan to study the important of PTEN expression in ovarian EC and if inactivation of PTEN and IFGBP-3 is through methylation. Furthermore, by studying the signal transduction pathways using PTEN and IGFBP-3 transfection, we plan to study the mutual interaction between PTEN and IGFBP-3 on the suppression of tumor invasion in ovarian EC.

Description:

We have successfully established an ovarian cancer cell line (OVTW-59), which was derived from an ovarian endometrioid carcinoma (EC), and have also established an ovarian EC invasion model. By using cDNA microarray and quantitative reverse-transcriptase polymerase chain reaction, we identified insulin-like growth factor binding protein (IGFBP)-3 as an invasion suppressor gene, which were associated with lower cancer migration, invasion and metastasis. Clinically, lower IGFBP-3 was found associated with significantly higher tumor grade, advanced stage and poor survival in patients with EC tumors. Furthermore, we have proved IGFBP-3 expression correlated with lower Erk activation, but with no effect on the activation of Akt. All these two signal transduction proteins have crucial roles in cancer invasion. Recently, a novel model of ovarian EC formation from endometriosis was reported, and PTEN was found to be a major protein involved. Inactivation of PTEN has been reported in some ovarian EC tumors and methylation was suggested as one of the major epigenetic changes. This tumorigenesis model has lots of similarity to our established invasion model. Therefore, we plan to study the important of PTEN expression in ovarian EC and if inactivation of PTEN and IFGBP-3 is through methylation. Furthermore, by studying the signal transduction pathways using PTEN and IGFBP-3 transfection, we plan to study the mutual interaction between PTEN and IGFBP-3 on the suppression of tumor invasion in ovarian EC.

Recruitment information / eligibility

• Status: Withdrawn
• Enrollment: 0
• Est. completion date: October 2012
• Est. primary completion date: October 2012
• Accepts healthy volunteers: No
• Gender: Female
• Age group: 21 Years to 80 Years

Eligibility

Inclusion Criteria:

Clinical diagnosis of ovarian endometrioid carcinoma

Exclusion Criteria:

other types of ovarian epithelial carcinoma

Study Design

Endpoint Classification: Bio-equivalence Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Diagnostic

Related Conditions & MeSH terms

• Carcinoma, Endometrioid
• Ovarian Cancer

Intervention

Procedure:
• immunohistochemical, methylation, gene transfection

Locations

Country	Name	City	State
Taiwan	National Taiwan University Hospital	Taipei

Sponsors (1)

Lead Sponsor	Collaborator
National Taiwan University Hospital

Country where clinical trial is conducted

Taiwan, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	migration
Primary	invasion
Primary	metastasis
Secondary	Immunohistochemical staining
Secondary	methylation
Secondary	signal tranduction