Gastric CancerNCT02002416
Prognostic Value and Clinical Pathology of c-MET Expression and Amplification in Gastric Carcinoma
An observational study of Gastric Cancer, run by Sun Yat-sen University at 1 site in China.
Trial 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 protec¬tion from apoptosis. Read more about this study
- Who is it for?
- Ages 18 to 70 years
- Conditions the study is for
- Gastric Cancer
- How many people
- 200 participants
- Where
- 1 siteChina
- Study dates
- Jan 2006to Dec 2014
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 70 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: 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. 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). In order to compare c-Met expression and amplification between early and advanced stage, we will match 100 early stage (stage I and stage II) patients. MET IHC will employ the Dako MET IHC assay and supplied assay protocol and pathology scoring guideline.
Who may be able to join
- 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
- 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
Who cannot join
- Older than 70 years old or younger than 18 years old
- without paraffin-embedded tissue
- without information of follow-up
Trial locations and contacts
1 site in 1 country.
About this study
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
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.
Read more
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
Read the 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.
- Conditions
- Gastric Cancer
- Keywords
- C-met expression, gastric cancer, overall survival
- Medical subject headings
- Stomach Neoplasms
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Metastatic gastric cancer patients | 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. | |
| Early stage gastric cancer | Selected 100 cases of eligible gastric cancer patients with previously early stage gastric cancer |
What is being measured
The primary outcome is the main question the study is designed to answer.
Overall survival
From the diagnosis to the time of last follow up or death
Measured: 2 years
Secondary outcomes (1)
Positive rate of C-met
The positive rate of c-met in the primary and metastastic diseases and in different stage diseases patients
Measured: 8%
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted5 Dec 2013 (estimated)
- Study startJan 2006
- Primary completionDec 2014 (estimated)
- Study completionDec 2014 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Gastric CancerStudies of the same condition, open and under way.
- More trials run by Sun Yat-sen UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Retrospective
- Enrolment
- 200 participants (actual)
Sponsor and investigators
- Lead sponsor
- Sun Yat-sen University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Ruihua Xu, Sun Yat-sen University
- Investigators
- Rui-hua Xu, MD, PhD, Principal investigator, Sun Yat-sen University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02002416
- Sponsor's protocol ID
- C-met in gastric cancer
- Other IDs
- Amgen
- Status last verified
- Nov 2013
- First submitted
- 20 Nov 2013
- Last updated
- 5 Dec 2013
- Results posted
- No
- Data monitoring committee
- No
Study at a glance
From the registry record, last updated by the sponsor on 5 Dec 2013. Recruitment status is as the sponsor reported it: confirm with the study team.
- 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
- ClinicalTrials.gov ID
- NCT02002416
- Acronym / sponsor ID
- C-met in gastric cancer
- Conditions
- Gastric Cancer
- Keywords
- C-met expression, gastric cancer, overall survival
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 200 participants (actual)
- Lead sponsor
- Sun Yat-sen UniversityUniversity, hospital or other
- Study start
- Jan 2006
- Primary completion
- Dec 2014 (estimated)
- Study completion
- Dec 2014 (estimated)
- First posted
- 5 Dec 2013 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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
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.
Study design
- Observational model
- Case-control
- Time perspective
- Retrospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Metastatic gastric cancer patients | – | –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. |
| Early stage gastric cancer | – | –Selected 100 cases of eligible gastric cancer patients with previously early stage gastric cancer |
Who may qualify
- Ages
- 18 to 70 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- 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. 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). In order to compare c-Met expression and amplification between early and advanced stage, we will match 100 early stage (stage I and stage II) patients. MET IHC will employ the Dako MET IHC assay and supplied assay protocol and pathology scoring guideline.
Key inclusion criteria (2 listed)
- 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
- 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
Key exclusion criteria (3 listed)
- Older than 70 years old or younger than 18 years old
- without paraffin-embedded tissue
- without information of follow-up
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Overall survival
Time frame: 2 years
From the diagnosis to the time of last follow up or death
1 secondary outcome
Positive rate of C-met
Time frame: 8%
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 5 Dec 2013.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Rui-hua Xu, MD, PhD principal investigator
Sun Yat-sen University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Gastric Cancer, run by Sun Yat-sen University at 1 site in China.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 5 Dec 2013. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in China. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Overall survival (time frame: 2 years). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 5 Dec 2013.