FGFR2 amplification in colorectal adenocarcinoma.
Cold Spring Harb Mol Case Stud
; 3(6)2017 Nov.
Article
en En
| MEDLINE
| ID: mdl-28835367
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 (TKIs), 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 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 limited to only single-nucleotide polymorphisms and insertions/deletions but also to copy-number alterations.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Poliposis Adenomatosa del Colon
/
Receptor Tipo 2 de Factor de Crecimiento de Fibroblastos
Tipo de estudio:
Prognostic_studies
Límite:
Female
/
Humans
/
Middle aged
Idioma:
En
Revista:
Cold Spring Harb Mol Case Stud
Año:
2017
Tipo del documento:
Article
País de afiliación:
Estados Unidos