Evidence map›Paper›PMID 25900027›Full record

Trial reportBMC cancer2015

The impact of FGFR1 and FRS2α expression on sorafenib treatment in metastatic renal cell carcinoma.

Thai H Ho, Xian-De Liu, Yanqing Huang, Carla L Warneke, Marcella M Johnson, Anh Hoang, Pheroze Tamboli, Fen Wang, Eric Jonasch

Registry-linked trialOpen access · goldAbstract readClinical Trial, Phase IIRandomized Controlled Trial
In one paragraph

Trial report in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00126594 (A Phase II Clinical Trial to Evaluate the Efficacy of BAY 43-9006 With or Without Low Dose Interferon in Metastatic Renal Cell Carcinoma), which is not on this map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT00126594 phase2completednot on this map

A Phase II Clinical Trial to Evaluate the Efficacy of BAY 43-9006 With or Without Low Dose Interferon in Metastatic Renal Cell Carcinoma

TypeinterventionalSponsorNational Cancer Institute (NCI)Ran2005 to 2013Enrolled80ConditionsClear Cell Renal Cell Carcinoma, Recurrent Renal Cell Carcinoma, Stage IV Renal Cell CancerArmsSorafenib Tosylate, Recombinant Interferon Alfa-2b, Laboratory Biomarker Analysis
3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Phosphoinositides in the kidney.Journal of lipid research · 2019
    Review
  9. Article
  10. Review
  11. Review
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Thai H HoDivision of Hematology and Medical Oncology, Mayo Clinic, Scottsdale, USA. ho.thai@mayo.edu.
Xian-De LiuDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA. XLiu10@mdanderson.org.
Yanqing HuangCenter for Cancer and Stem Cell Biology, Texas A&M Institute of Biosciences and Technology, Houston, USA. yhuang@ibt.tamhsc.edu.
Carla L WarnekeDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, USA. cwarneke@mdanderson.org.
Marcella M JohnsonDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, USA. mmjohnso@mdanderson.org.
Anh HoangDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA. anhoang@mdanderson.org.
Pheroze TamboliDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, USA. ptamboli@mdanderson.org.
Fen WangCenter for Cancer and Stem Cell Biology, Texas A&M Institute of Biosciences and Technology, Houston, USA. fwang@ibt.tamhsc.edu.
Eric JonaschDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, USA. ejonasch@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USTexas A&M Health Science Center · USMayo Clinic in Arizona · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Paul Calabresi Program in Clinical/Translational Research at Mayo ClinicK12CA090628 · NCI · MAYO CLINIC ROCHESTER · PI WEROHA, SARAVUT · 2001 to 2025
$19.7M
NCI NIH HHS K12 CA090628NCI NIH HHS K12CA90628
6 · The paper itself

Abstract

backgroundAngiogenesis plays a role in tumor growth and is partly mediated by factors in both the fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) pathways. Durable clinical responses with VEGF tyrosine kinase inhibitors (TKIs) may be limited by intrinsic tumor resistance. We hypothesized that FGF signaling may impact clinical responses to sorafenib.

methodsNephrectomy material was available from 40 patients with metastatic renal cell carcinoma (RCC) enrolled in a phase II clinical trial of sorafenib ± interferon (ClinicalTrials.gov Identifier NCT00126594). Fibroblast growth factor receptor 1 (FGFR1) and fibroblast growth factor receptor substrate 2 alpha (FRS2α) expression was assessed by in situ hybridization and immunofluorescence, respectively. The relationship between fibroblast growth factor pathway marker levels and progression-free survival (PFS) was analyzed using Kaplan-Meier and Cox proportional hazards regression methods.

resultsUnivariate analysis indicated that more intense FGFR1 staining was associated with shorter PFS (log-rank P = 0.0452), but FRS2α staining was not significantly associated with PFS (log-rank P = 0.2610). Multivariate Cox proportional hazards regression models were constructed for FGFR1 and FRS2α individually, adjusting for baseline Eastern Cooperative Oncology Group performance status, treatment arm and anemia status. When adjusted for each of these variables, the highest intensity level of FGFR1 (level 3 or 4) had increased progression risk relative to the lowest intensity level of FGFR1 (level 1) (P = 0.0115). The highest intensity level of FRS2α (level 3 or 4) had increased progression risk relative to the lowest intensity level of FRS2α (level 1) (P = 0.0126).

conclusionsIncreased expression of FGFR1 and FRS2α was associated with decreased PFS among patients with metastatic RCC treated with sorafenib. The results suggest that FGF pathway activation may impact intrinsic resistance to VEGF receptor inhibition.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAgedAged, 80 and overAntineoplastic AgentsCarcinoma, Renal CellFemaleHumansMaleMembrane ProteinsMiddle AgedNiacinamidePhenylurea CompoundsProspective StudiesReceptor, Fibroblast Growth Factor, Type 1SorafenibAdaptor Proteins, Signal TransducingAntineoplastic AgentsFGFR1 protein, humanFRS2 protein, humanMembrane ProteinsNiacinamidePhenylurea CompoundsReceptor, Fibroblast Growth Factor, Type 1Sorafenib

Identifiers

PMID25900027
PMCPMC4406182
OpenAlexW2107798417

What OpenQuestion holds

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LicenceCC BY
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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.