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Oncogene expression in carotid body tumors
D G Wang1, A A Barros D'Sa, C F Johnston
1Division of Metabolism and Endocrinology, School of Clinical Medicine, The Queen's University of Belfast, United Kingdom.
Cancer
|June 15, 1996
Summary
The study found abnormal expression of oncogenes c-myc, bcl-2, and c-jun in carotid body tumors. This abnormal expression may play a role in the development of these rare neoplasms.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Carotid body tumors have suggested genetic and environmental etiologies.
- Sporadic tumors at sea level lack a known developmental mechanism.
- Familial occurrence and high-altitude prevalence hint at underlying factors.
Purpose of the Study:
- Investigate the molecular basis of carotid body tumor development.
- Examine the expression of key oncogenes in tumor samples.
- Identify potential contributors to tumor genesis.
Main Methods:
- Clinical and pathological review of 13 carotid body tumors.
- Immunohistochemical analysis for oncoproteins: c-myc, bcl-2, c-erbB-2, c-erbB-3, c-jun, and PCNA.
- Follow-up of patients for up to 17 years.
Main Results:
- c-myc was detected in all tumors; bcl-2 in 11/13; c-jun in 5/13.
- Over 10% of tumor cells showed c-myc positivity in 12 cases.
- c-erbB-2 and c-erbB-3 showed limited positivity.
Conclusions:
- Abnormal expression of c-myc, bcl-2, and c-jun oncogenes is observed in carotid body tumors.
- These oncogenes may be involved in the genesis of carotid body tumors.
- Further research into these molecular pathways is warranted.