Background: Among the combinations of coamplified genes, Myc and ERBB2 or EGFR have attracted much attention for their relevance to cytogenetics, carcinogenesis and cancer therapy.
Materials and methods: Gene amplification of Myc, ERBB2 and EGFR were examined on 97 formalin-fixed and paraffin-embedded gallbladder carcinomas, by fluorescence in situ hybridization (FISH).
Results: FISH revealed three tumors had Myc amplification. By dual color FISH, one of these three tumors had two populations of tumor cells with the coexistence of amplified Myc and ERBB2, and Myc and EGFR. The second tumor had a high level of amplification of Myc without amplification of ERBB2 or EGFR. The third tumor had a low level of coamplification of Myc and ERBB2. A case of polysomy 8 also demonstrated amplification of ERBB2 and EGFR.
Conclusion: The present study shows that genomic instability due to Myc amplification may cause specific amplification of EGFR and/or ERBB2.