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Gene amplification is an important mechanism for activating oncogenes in malignant tumors. Although amplification of  HER2 ,  C-MYC ,  CCND1  and  FGFR1  has been reported in breast cancers, their role in the progression of  in situ  to invasive breast carcinoma is unclear. To investigate this question we compared the amplification frequencies of these genes in pure ductal carcinoma  in situ  (DCIS), DCIS associated with invasive carcinoma, and invasive carcinoma.    Methods  We performed fluorescence  in situ  hybridization of the selected genes on tissue microarrays composed of 179 pure DCIS and 438 invasive carcinomas. Two hundred and sixteen of the latter had DCIS components, and in those cases we compared gene amplification in the intraductal and invasive components of each carcinoma.    Results  The rate of amplification of  FGFR1  was higher in invasive carcinomas than in the pure DCIS, but the opposite was true for  HER2  amplification. These findings applied consistently to high-grade tumors, but not to low/intermediate-grade tumors. The amplification status of  HER2 ,  C-MYC ,  CCND1  and  FGFR1  was generally similar in the matched invasive and DCIS components of the same tumors. However,  FGFR1  amplification was more common in the invasive components than in the DCIS components. In survival analyses,  FGFR1  amplification was found to be an independent prognostic factor for poor disease-free survival for all patients with invasive carcinoma and for the hormone receptor-positive subgroup.    Conclusion  Amplification of  HER2 ,  C-MYC  and  CCND1  seems to play a role in the early development of breast cancer, but not in its progression. However, the increased frequency of  FGFR1  amplification in invasive carcinomas compared with pure DCIS and in the invasive components of individual tumors, and its association with decreased disease-free survival, suggests a role for  FGFR1  amplification in the progression of breast cancer including  in situ -to-invasive transition, as well as initiation.

FGFR1 is amplified during the progression of in situto invasive breast carcinoma