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Histopathology. 2005 Dec;47(6):560-4.

Demonstration of EGFR gene copy loss in colorectal carcinomas by fluorescence in situ hybridization (FISH): a surrogate marker for sensitivity to specific anti-EGFR therapy?

Author information

1
Department of Pathology, Ullevaal University Hospital, Oslo, Norway. torill.sauer@medisin.uio.no

Abstract

AIMS:

To investigate EGFR gene copy number heterogeneity in colorectal carcinomas compared with copy number of chromosome 7 and immunohistochemical expression of the EGFR protein.

METHODS AND RESULTS:

Fluorescence in situ hybridization of the EGFR gene and CEP7 was carried out on paraffin-embedded material from 48 rectal carcinomas combined with immunohistochemical detection of EGFR with a polymer detection kit. EGFR gene copy number had a range of 1.4-7.3 with a mean of 2.5. CEP7 copy number had a range of 1.5-6.1 with a mean of 2.5. The EGFR gene/CEP7 ratio ranged from 0.4 to 1.5 with a mean of 0.96. Most cases had a balanced EGFR gene/CEP7 ratio (37 cases = 77%). Copy gain was found in seven cases (15%) with a ratio of up to 1.5, consistent with gain of one EGFR gene copy in one chromosome. Copy loss was found in four cases (8%). All cases with EGFR gene copy loss were immunohistochemically positive.

CONCLUSIONS:

Demonstration of EGFR gene copy loss might be a surrogate marker for EGFR mutation/deletion and could be used in a routine setting in pathology departments. Further studies are needed to determine whether this may be used to select patients that might benefit from specific anti-EGFR therapy.

[Indexed for MEDLINE]

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