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PTEN and IGFBP-3 Correlation in Ovarian Carcinoma Invasion

NCT ID: NCT00173407

Last Updated: 2012-12-27

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

WITHDRAWN

Clinical Phase

NA

Study Classification

INTERVENTIONAL

Study Start Date

2006-01-31

Study Completion Date

2012-10-31

Brief Summary

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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.

Detailed Description

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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.

Conditions

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Ovarian Cancer

Keywords

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Ovarian endometrioid carcinoma invasion IGFBP-3 transfection signal transduction PTEN methylation

Study Design

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Allocation Method

NA

Intervention Model

SINGLE_GROUP

Primary Study Purpose

DIAGNOSTIC

Blinding Strategy

NONE

Interventions

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immunohistochemical, methylation, gene transfection

Intervention Type PROCEDURE

Eligibility Criteria

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Inclusion Criteria

Clinical diagnosis of ovarian endometrioid carcinoma

Exclusion Criteria

other types of ovarian epithelial carcinoma
Minimum Eligible Age

21 Years

Maximum Eligible Age

80 Years

Eligible Sex

FEMALE

Accepts Healthy Volunteers

No

Sponsors

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National Taiwan University Hospital

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Torng Pao-Ling, MD, PhD

Role: PRINCIPAL_INVESTIGATOR

Department of Obstetric and Gynecology, National Taiwan University Hospital

Locations

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National Taiwan University Hospital

Taipei, , Taiwan

Site Status

Countries

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Taiwan

Other Identifiers

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9461700640

Identifier Type: -

Identifier Source: org_study_id