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FGFR2 Amplification in Colorectal Adenocarcinoma

2017-08-29 13:59:38

Cold Spring Harbor Laboratory Press; August 29, 2017 doi:10.1101/mcs.a001495

Jamal H Carter MD, Catherine E Cottrell PhD, Samantha N McNulty PhD, Katinka A Vigh-Conrad PhD, Stephen Lamp, Jonathan W Heusel MD, Eric J Duncavage MD



Abstract


FGFR2 is recurrently amplified in 5% of gastric cancers and 1-4% of breast cancers; however, this
molecular alteration has never been reported in a primary colorectal cancer specimen. Preclinical studies
indicate that several FGFR tyrosine-kinase inhibitors (TKI), such as AZD4547, have in vitro activity
against the FGFR2-amplified colorectal cell line, NCI-H716. The efficacy of these inhibitors is currently
under investigation in clinical trials for breast and gastric cancer. Thus, better characterizing colorectal
tumors for FGFR2 amplification could identify a subset of patients who may benefit from FGFR TKI
therapies. Here, we describe a novel FGFR2 amplification identified by clinical next-generation
sequencing (NGS) in a primary colorectal cancer. Further characterization of the tumor by
immunohistochemistry showed neuroendocrine differentiation, similar to the reported properties of the
NCI-H716 cell line. These findings demonstrate that the spectrum of potentially clinically actionable mutations detected by targeted clinical sequencing panels is not just limited to single nucleotide
polymorphisms and insertions/deletions, but also copy number alterations.





Empire Genomic's Control 10 and
Custom FISH probes were used in this publication.

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