Clinical trial · Observational
Prognostic Value and Clinical Pathology of c-MET Expression and Amplification in Gastric Carcinoma
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
- Source
- ClinicalTrials.gov
- Retrieved
- Sep 8, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-CLINICALTRIALS-20260908-000001
Summary
Brief summary (as posted)
The MET oncogene encodes the receptor tyrosine kinase (RTK) for hepatocyte growth factor (HGF) and controls genetic programs leading to cell growth, invasion and protec¬tion 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-665,752, 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-665,752 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
Conditions
Conditions (1)
Free-text conditions as registered, with the CancerIndex entity they were reconciled to and the match type.
| Condition (as posted) | Mapped entity | Match | Confidence |
|---|---|---|---|
| Gastric Cancer | Malignant Gastric Neoplasm | CURATED_BROADER | 0.80 |
Interventions
Interventions (0)
Data not yet available
Design
Arms and outcomes
Arms (2)
- label
- Metastatic gastric cancer patients
- description
- Selecte 100 cases of eligible metastatic gastric cancer patients with primary and metastatic lesion (1:1). Use the immunohistochemistry (IHC) and Fluorescence in situ hybridization (FISH) to detect the status of C-met.
- label
- Early stage gastric cancer
- description
- Selected 100 cases of eligible gastric cancer patients with previously early stage gastric cancer
Primary outcomes (1)
- measure
- Overall survival
- timeFrame
- 2 years
- description
- From the diagnosis to the time of last follow up or death
Secondary outcomes (1)
- measure
- Positive rate of C-met
- timeFrame
Eligibility
Eligibility (as posted)
- Sex
- All
- Minimum age
- 18 Years
- Maximum age
- 70 Years
Show eligibility criteria text
Inclusion Criteria: 1. For metastatic gastric cancer patients (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 2. For early stage gastric cancer patients (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 Exclusion Criteria: 1. Older than 70 years old or younger than 18 years old 2. without paraffin-embedded tissue 3. without information of follow-up
References
Publications (0)
Data not yet available