Ignite Creation Date:
2024-05-06 @ 2:16 AM
Last Modification Date:
2024-10-26 @ 11:15 AM
Study NCT ID:
NCT02002416
Status:
UNKNOWN
Last Update Posted:
2013-12-05
First Post:
2013-11-20
Brief Title:
Prognostic Value and Clinical Pathology of c-MET Expression and Amplification in Gastric Carcinoma
Sponsor:
Sun Yat-sen University
Organization:
Sun Yat-sen University
Study Overview
Official Title:
Prognostic Value and Clinical Pathology of c-MET Expression and Amplification in Gastric Carcinoma the Comparison Between the Primary and Metastatic Lesions Early Stage and Advanced Stage
Status:
UNKNOWN
Status Verified Date:
2013-11
Last Known Status:
ACTIVE_NOT_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The MET oncogene encodes the receptor tyrosine kinase RTK for hepatocyte growth factor HGF and controls genetic programs leading to cell growth invasion and protection from apoptosis Although the definitive role of MET oncogene is yet to be determined in carcinogenesis of gastric cancer overexpression and amplification of c-Met has been demonstrated in gastric cancer cell lines In addition approximately 10-20 of gastric cancer tissues and up to 40 of the scirrhous histological subtype were shown to harbor increased MET gene copy numbers Importantly PHA-665752 a selective c-Met kinase inhibitor showed significant reduction of established tumor mass in mouse xenografts with GTL16 a gastric cancer cell line with 10-fold MET amplification Another pivotal study showed that gastric cancer cells with MET amplification were extremely sensitive to PHA-665752 and implicated a potential role of c-Met protein in developing theranostics in gastric cancer More and more data indicated that c-Met was an important prognostic factor in gastric cancer
Gastric cancer is a heterogeneous disease Does the expression and amplification of c-Met in the primary lesion differ from the metastatic disease Does the expression and amplification of c-Met in the early disease differ from advanced disease Till now there is no related report
Purposes
Compare the expression and amplification of c-Met between primary lesion and metastatic lesion together with clinical characteristic to explore the relationship of c-Met expression and metastatic pattern
Compare the expression and amplification of c-Met between early stage and metastatic stage and to explore the role of c-MET in the development of carcinoma
Gastric cancer is a heterogeneous disease Does the expression and amplification of c-Met in the primary lesion differ from the metastatic disease Does the expression and amplification of c-Met in the early disease differ from advanced disease Till now there is no related report
Purposes
Compare the expression and amplification of c-Met between primary lesion and metastatic lesion together with clinical characteristic to explore the relationship of c-Met expression and metastatic pattern
Compare the expression and amplification of c-Met between early stage and metastatic stage and to explore the role of c-MET in the development of carcinoma
Detailed Description:
We retrospectively collect the metastatic gastric cancer patients who received a surgical resection of both primary diseases and metastatic lesions during January 2006 and December 2012 Patients are collected based on the following criteria 1 pathology proven advanced gastric adenocarcinoma 2 the paraffin-embedded tissues of the primary and metastatic lesions were available 3 full information of follow-up There are 100 patients suitable for the analysis c-MET protein expression and amplification are assessed in paraffin-embedded tissues of the primary and metastatic diseases obtained from 100 patients by immunohistochemistry IHC and Fluorescence in situ hybridization FISH The clinical pathologic data of the patients are also collected for analysis including gender age Karnofsky performance score KPS chemotherapy regimens tumor locations Lauren classification histology subtypes metastatic sites
In order compare c-Met expression and amplification between early and advanced stage we will match 100 early stage stage I and stage II patients based on the following criteria 1 pathology proven gastric adenocarcinoma with radical resection 2 the paraffin-embedded tissues of the primary lesions is available 3 full information of follow-up MET IHC will employ the Dako MET IHC assay and supplied assay protocol and pathology scoring guideline
MET FISH will also employ the Dako MET FISH assay supplied assay protocol and pathology scoring guideline
In order compare c-Met expression and amplification between early and advanced stage we will match 100 early stage stage I and stage II patients based on the following criteria 1 pathology proven gastric adenocarcinoma with radical resection 2 the paraffin-embedded tissues of the primary lesions is available 3 full information of follow-up MET IHC will employ the Dako MET IHC assay and supplied assay protocol and pathology scoring guideline
MET FISH will also employ the Dako MET FISH assay supplied assay protocol and pathology scoring guideline
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| Amgen | OTHER_GRANT | Amgen | None |