Correction to: Use of an Integrated Pan-Cancer Oncology Enrichment Next-Generation Sequencing Assay to Measure Tumour Mutational Burden and Detect Clinically Actionable Variants

Pestinger, Valerie; Smith, Matthew; Sillo, Toju; Findlay, John M.; Laes, Jean-François; Martin, Gerald S.; Middleton, Gary; Taniere, Philippe; Beggs, Andrew D

doi:10.1007/s40291-020-00479-2

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“…Only gain was measured in the TSO 500 CNV files, and RNA translocation supporting reads > 4–12 is considered a translocation, subject to the quality of the sample. Filtered data exported from the TSO 500 pipeline [ 28 ] were annotated using the Ensembl Variant Effect Predictor (VEP) Annotation Engine [ 28 ] with information from databases, such as gnomAD genome and exome, 1000 genomes, dbSNP, COSMIC, RefSeq, ClinVar, and Ensembl. Genomic changes were categorized according to the 4-tier system proposed by the American Society of Clinical Oncology and the College of American Pathologists [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

Incidence of FGFR2 Amplification and FGFR2 Fusion in Patients with Metastatic Cancer Using Clinical Sequencing

Hyung

Han

Jung

et al. 2022

Journal of Oncology

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Aberrations in the fibroblast growth factor receptor2 (FGFR2) gene, including genetic alterations and chromosomal rearrangements, lead to the development and progression of cancer with poor prognosis. However, the mechanisms underlying the FGFR2 signaling pathway to facilitate the development of FGFR2-targeted therapies have not been fully explored. Here, we examined the clinicopathological features of FGFR2 amplification and fusion in gastrointestinal tract/genitourinary tract cancers. FGFR2 amplification and fusion were identified in approximately 1.5% and 1.1% of all cancer types in 1,373 patients, respectively, with both FGFR2 amplification and fusion occurring together at a rate of approximately 0.6%. Of all cancer types screened, gastric cancer (GC) was the most common cancer type with FGFR2 amplification (87.5% of all FGFR2 amplification case) or fusion (46.7% of all cases). In addition, FGFR2 alteration had poorer overall survival (OS, 13.7 months vs. 50.2 months, P = 0.0001 ) and progression-free survival (PFS, 5.6 months vs. 11.4 months, P = 0.0005 ) than did those without FGFR2 alteration, respectively. Taken together, our data underscore to screen solid cancer patients for FGFR2 aberrations in oncology clinic.

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Section: Methodsmentioning

confidence: 99%