Novel targetable FGFR2 and FGFR3 alterations in glioblastoma associate with aggressive phenotype and distinct gene expression programs

Table 1 FGFR glioblastoma patients: clinical-histologic-molecular correlations

Sex/age	Race/smoker	Cancer history	Location	Size (cm)	Res	RT/TMZ/Avastin	Survival (months	Histology	MGMT	TMB	FGFR alteration
F48	W No	No	R Temp	4 × 2	2×	None	2.5	HG-Embryonal HG-LM Rhabdoid LG-DI	neg	2.1	FGFR2↑ FGFR2-TACC2↑
M60	W No	No	L Frontal	4 × 3.4	2×	RT/TMZ/A	20	RMF FGFR3	neg	0.8	FGFR3-TACC3; FRS2↑
F62	W No	BrCa^a	R Par	3.5 × 3	2×	RT/TMZ	7.3	RMF FGFR3	neg	5.8	FGFR3 CTdup; FRS2↑
F72	W No	BrCa^b	R Temp	6.8 × 4.5	1×	RT/TMZ/A	23	RMF FGFR3	low	5.8	FGFR3-TACC3
F75	W No	No^b	R Temp	7.4 × 3.8	LITT	None^c	2	RMF FGFR3	high	3.2	FGFR3-TLN1

F female, M male, W white, BrCa breast cancer, R right, L left, Temp temporal, Par parietal, Res surgical resection, LITT laser interstitial thermal therapy, RT radiotherapy, TMZ temozolomide, HG high grade, LM leptomeningeal, LG low grade, DI diffusely infiltrating astrocytoma, RMF FGFR3 recurrent morphologic features of FGFR3 glioblastoma, MGMT methylguanyl methyl transferase promoter methylation, TMB tumor mutation burden, ↑ amplification
^aSurgically resected breast cancer
^bHistory of Hashimoto thyroiditis and arteriosclerosis (myocardial infarction and stroke)
^cTMZ not tolerated

ISSN: 2051-5960