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Paper · 23744832

Parallel RNA interference screens identify EGFR activation as an escape mechanism in FGFR3-mutant cancer.

Herrera-Abreu MT and 6 others. Cancer Discov, 2013. Cited by 108 papers, by iCite.

11 sourcespapers-2026-11-12-0.1.0

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ConductScience Library. Parallel RNA interference screens identify EGFR activation as an escape mechanism in FGFR3-mutant cancer. Papers, record 23744832. Release papers-2026-11-12-0.1.0, 12 Nov 2026. https://conductscience.org/library/papers/23744832

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Paper

PubMed's record of the paper, with iCite's citation figures. No abstract is shown.

Title
Parallel RNA interference screens identify EGFR activation as an escape mechanism in FGFR3-mutant cancer.
PubMed
Journal
Cancer Discov
PubMed
Year
2013
PubMed
Publication types
Journal Article, Research Support, Non-U.S. Gov't
PubMed
Citations, by iCite
108
iCite
Relative citation ratio, by iCite
2.58
iCite
Revised in PubMed
2025-05-29
PubMed

Authors7

The authors in the order PubMed's record lists them, with the ORCID iDs it states.

OrderAuthorForenameKindORCID iD
1Herrera-Abreu MTMaria Teresa
2Pearson AAlex
3Campbell JJames
4Shnyder SDSteve D
5Knowles MAMargaret A
6Ashworth AAlan
7Turner NCNicholas C

Source PubMed

Topics20

NLM's MeSH indexing of the paper, its major topics first.

MeSH termMajor
ErbB ReceptorsMajor topic
NeoplasmsMajor topic
Receptor, Fibroblast Growth Factor, Type 3Major topic
Animals
Cell Line, Tumor
Dasatinib
Gefitinib
Heterografts
High-Throughput Screening Assays
Humans
MAP Kinase Signaling System
Mice
Neoplasm Transplantation
Protein Kinase Inhibitors
Pyrimidines
Quinazolines
RNA Interference
RNA, Small Interfering
Signal Transduction
Thiazoles

Source PubMed

Grants5

Each grant PubMed's record writes, matched to the NIH project NIH's grant and paper links name for this paper, and each of those links the record does not write.

Grant, as the record writes itAgencyCountryNIH projectStated by
BREAST CANCER NOW RESEARCH CENTREBreast Cancer NowUnited KingdomPubMed
A11847Cancer Research UKUnited KingdomPubMed
C30746/A10038Cancer Research UKUnited KingdomPubMed
C347/A11847Cancer Research UKUnited KingdomPubMed
16642Cancer Research UKUnited KingdomPubMed

Source PubMed

Trials0

The trials whose ClinicalTrials.gov record lists the paper, and the trial numbers the paper's PubMed record names.

None in this release.

Comments and corrections0

PubMed's comments and corrections, NLM's own indexing: retractions first, then expressions of concern, errata and updates, and comments last.

None in this release.

References43

The papers the reference list in PubMed's record names, those in our copy of PubMed, in the list's order.

OrderPMIDTitleJournalYearIn PapersSource
121,984,977Functional viability profiles of breast cancer.Cancer Discov2011https://conductscience.org/library/papers/21984977PubMed
218,552,176Drug-sensitive FGFR2 mutations in endometrial carcinoma.Proc Natl Acad Sci U S A2008https://conductscience.org/library/papers/18552176PubMed
38,845,844Missense FGFR3 mutations create cysteine residues in thanatophoric dwarfism type I (TD1).Hum Mol Genet1996https://conductscience.org/library/papers/8845844PubMed
419,381,019Antibody-based targeting of FGFR3 in bladder carcinoma and t(4;14)-positive multiple myeloma in mice.J Clin Invest2009https://conductscience.org/library/papers/19381019PubMed
511,056,689Characterization of fibroblast growth factor receptor 2 overexpression in the human breast cancer cell line SUM-52PE.Breast Cancer Res2000https://conductscience.org/library/papers/11056689PubMed
623,558,953Identification of targetable FGFR gene fusions in diverse cancers.Cancer Discov2013https://conductscience.org/library/papers/23558953PubMed
719,843,843Distinct microRNA alterations characterize high- and low-grade bladder cancer.Cancer Res2009https://conductscience.org/library/papers/19843843PubMed
823,298,836The tumorigenic FGFR3-TACC3 gene fusion escapes miR-99a regulation in glioblastoma.J Clin Invest2013https://conductscience.org/library/papers/23298836PubMed
920,179,196FGFR1 amplification drives endocrine therapy resistance and is a therapeutic target in breast cancer.Cancer Res2010https://conductscience.org/library/papers/20179196PubMed
1021,215,704AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity.Cancer Cell2011https://conductscience.org/library/papers/21215704PubMed

Cited by71

The papers in our copy of PubMed whose reference list names this one, newest first. iCite, which reads more sources, counts 108 citations.

PMIDTitleJournalYearIn PapersSource
42,177,363FGFR3 oncogenic activation drives oxidative metabolic reprogramming in bladder cancer: a systems metabolomics approach.Commun Biol2026https://conductscience.org/library/papers/42177363PubMed
41,870,032Blocking SHP2 benefits FGFR2 inhibitor and overcomes its resistance in FGFR2-amplified gastric cancer.Elife2026https://conductscience.org/library/papers/41870032PubMed
41,514,604FGFR Aberrations in Solid Tumors: Mechanistic Insights and Clinical Translation of Targeted Therapies.Cancers (Basel)2025https://conductscience.org/library/papers/41514604PubMed
39,161,208FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies.Cancer Commun (Lond)2024https://conductscience.org/library/papers/39161208PubMed
39,082,679A Tetravalent Bispecific Antibody Selectively Inhibits Diverse FGFR3 Oncogenic Variants.Cancer Res2024https://conductscience.org/library/papers/39082679PubMed
39,031,286The roles of FGFR3 and c-MYC in urothelial bladder cancer.Discov Oncol2024https://conductscience.org/library/papers/39031286PubMed
38,831,455Targeting FGFR for cancer therapy.J Hematol Oncol2024https://conductscience.org/library/papers/38831455PubMed
38,598,298TGFβ overcomes FGF-induced transinhibition of EGFR in lens cells to enable fibrotic secondary cataract.Mol Biol Cell2024https://conductscience.org/library/papers/38598298PubMed
38,424,198FGFR-targeted therapeutics: clinical activity, mechanisms of resistance and new directions.Nat Rev Clin Oncol2024https://conductscience.org/library/papers/38424198PubMed
38,378,518Resistance of HNSCC cell models to pan-FGFR inhibition depends on the EMT phenotype associating with clinical outcome.Mol Cancer2024https://conductscience.org/library/papers/38378518PubMed

1 to 10 of 71

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Genes27

The genes the Gene search release ties to the paper: Swiss-Prot's references first, then PubTator's text mining.

Drugs0

The drugs whose trials, in the Pipelines release, list the paper.

None in this release.

Data0

The data bank entries PubMed's record names. Trial numbers are under Trials.

None in this release.

Data dates

The date of each source this release read.

PubMed
2026-11-06
PubMed
iCite
2026-11-05
iCite
PMC's ID file
2026-11-05
PMC's ID file
NIH RePORTER's grant and paper links
2026-11-01
NIH RePORTER's grant and paper links
Trials
2026-11-12
Gene search
2026-11-11
Pipelines
2026-09-18

Sources 11

  • ChEMBL, through Open TargetsCC BY-SA 3.0
  • ClinicalTrials.govNo license stated
  • HGNCCC0
  • iCiteCC BY 4.0
  • NCBI GenePublic domain (US government)
  • NIH RePORTER's grant and paper linksPublic domain
  • Open TargetsCC0 1.0
  • PMC's ID filePublic domain (US government)
  • PubMedNLM's terms
  • PubTator 3Public domain
  • UniProtCC BY 4.0
Each source's terms
  • ChEMBL, through Open TargetsCC BY-SA 3.0, for the parts from ChEMBL. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
  • ClinicalTrials.govnone stated
  • HGNCCC0: https://www.genenames.org/about/license/
  • iCiteCC BY 4.0
  • NCBI GeneNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
  • NIH RePORTER's grant and paper linksPublic domain (NIH RePORTER)
  • Open TargetsCC0 1.0. Open Targets asks that users cite its latest paper: Buniello et al. 2025, Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery, Nucleic Acids Research 53(D1):D1467, PMID 39657122. Read on 8 Nov 2026 at https://platform-docs.opentargets.org/licence
  • PMC's ID fileNone named for the file. NCBI says information created by or for the US government on its site is in the public domain, and asks that NLM be acknowledged: https://www.ncbi.nlm.nih.gov/home/about/policies/
  • PubMedNLM's terms
  • PubTator 3Public domain
  • UniProtCC BY 4.0. UniProt's licence file: "All databases and documents in the UniProt FTP directory may be copied and redistributed freely, without advance permission, provided that this copyright statement is reproduced with each copy." UniProt asks that users cite its latest paper: The UniProt Consortium, UniProt: the Universal Protein Knowledgebase in 2025, Nucleic Acids Research 53:D609-D617, https://doi.org/10.1093/nar/gkae1010. Read on 9 Nov 2026 at https://www.uniprot.org/help/license

ClinicalTrials.gov's data carry an international copyright outside the United States: https://clinicaltrials.gov/about-site/terms-conditions.

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