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FGFR3S249C mutation promotes chemoresistance by activating Akt signaling in bladder cancer cells.

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Exp Ther Med2019PMID 31316618PMC6601368stubpubmedProvenance
Source
PubMed
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-CIVIC-20260908-000001
Published

Abstract

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Linked entities

Linked entities (4)

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Validated 4

Curated evidence

Evidence citing this paper (1)

civicProvenance
Source
CIViC — Clinical Interpretation of Variants in Cancer
Dataset
CIViC evidence items
Version
civic-2026-09-08
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Evidence
expert curation
License
CC0 1.0
PMID
31316618
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–1 of 1 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
FGFR3 S249C1
CisplatinTransitional Cell CarcinomaPredictiveDSupports Resistance3accepted
EID8642

Bladder cancer cell line 97-7 expressing endogenous FGFR3 S249C (IC50 44.6ug/ml) was resistant to cisplatin compared to two FGFR3 wild-type cell lines, 5637 (IC50 2.07ug/ml) and T24 (IC50 1.58ug/ml) a… (full text at CIViC)

PMID 31316618 · Xie et al., 2019 · Open in CIViC

civic