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FGFR1 is amplified during the progression of in situ to invasive breast carcinoma

DOI: 10.1186/bcr3239

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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.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.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.Development of breast cancer depends on the accumulation of a variety of genetic alterations, including activation or amplification of oncogenes [1]. In breast cancer, the most prominent and frequent amplicons have been located at chromosomal positions 1q, 8p12, 8q24, 11q13, 12p13, 16p13, 7q12-21 and 20q13, and several target oncogenes have been identified [2-5]. The best characterized oncogene is HER2, located at 17q12-21, which is amplified in 15 to 20% of breast cancers [6,7]. Other oncogenes t


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