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Background  Although preliminary reports suggest that  ALK  gene amplification may occur in inflammatory breast cancer (IBC), data are limited. We performed a comprehensive investigation of the status of  ALK  gene in IBC.    Methods  We used core biopsy (CB) samples from 30 IBC patients for immunohistochemistry (IHC), 25 of these samples for fluorescence in situ hybridization (FISH) of  ALK  gene rearrangement, 8 for chromosome 2 aneusomy, and 20 microdissected frozen CBs for array comparative genomic hybridization (CGH) and mRNA analysis.    Results  All 30 samples were negative for ALK protein expression by IHC. FISH analysis showed no  EML4-ALK  gene rearrangement in any samples, although 16 of the 25 samples (64%) contained 3 to 4 extra copies of the  ALK  gene, and chromosome 2 aneusomy was found in 7 of 8 samples that had extra copies of the  ALK  gene. Only 3 of the 20 samples showed evidence of mild  ALK  gene amplification by array CGH. mRNA analysis revealed that mRNA expression of  ALK  was not significantly higher in these samples compared with samples that showed no evidence of  ALK  gene amplification in CGH analysis, nor was mRNA expression of  ALK  significantly different in tumor compared with 5 normal breast samples ( P  > 0.05,  t  test).    Conclusion  Our comprehensive evaluation suggests that  ALK  gene rearrangement did not occur in the IBC patients studied. The significance of our finding of mildly increased copy numbers of the  ALK  gene resulting from chromosome 2 aneusomy rather than mild amplification of the  ALK  gene requires further investigation.

Status of the anaplastic lymphoma kinase (ALK) gene in inflammatory breast carcinoma