Evidence map›Paper›PMID 24166906›Full record

Trial reportClinical cancer research : an official journal of the American Association for Cancer Research2013

Comprehensive biomarker analysis and final efficacy results of sorafenib in the BATTLE trial.

George R Blumenschein, Pierre Saintigny, Suyu Liu, Edward S Kim, Anne S Tsao, Roy S Herbst, Christine Alden, J Jack Lee, Ximing Tang, David J Stewart and 17 more

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
5.0field-weighted citation impact, top 4% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Guideline
  4. Article
  5. Emerging Targets in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2024
    Review
  6. Lung Cancer: New Directions in Senior Patients Assessment.Geriatrics (Basel, Switzerland) · 2024
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Current therapy of KRAS-mutant lung cancer.Cancer metastasis reviews · 2020
    Review
  16. Article
  17. TargetingInternational journal of molecular sciences · 2020
    Review
  18. De novo lipogenesis represents a therapeutic target in mutant Kras non-small cell lung cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  19. Review
  20. 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

27 authors at 11 institutions in 3 countries.

George R BlumenscheinAuthors' Affiliations: Departments of Thoracic/Head and Neck Medical Oncology, Biostatistics and Applied Mathematics, Translational Molecular Pathology, Diagnostic Imaging, Diagnostic Radiology, and Bioinformatics and Computational Biology; Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston; The Hamon Center for Therapeutic Oncology Research and Departments of Internal Medicine and Pharmacology, The University of Texas Southwestern Medical Center, Dallas, Texas; Solid Tumor Oncology and Investigational Therapeutics, Levine Cancer Institute, Charlotte, North Carolina; Medical Oncology, Yale Cancer Center, New Haven, Connecticut; Division of Medical Oncology, University of Ottawa, Ottawa, Ontario; Department of Oncology and Diagnostic Sciences, University of Maryland Dental School, Baltimore, Maryland; UC San Diego Moores Cancer Center, La Jolla, California; and Centre de Recherche en Cancérologie de Lyon, UMR INSERM 1052-CNRS 5286, Centre Léon Bérard, Lyon, France.
Pierre Saintigny
Suyu Liu
Edward S Kim
Anne S Tsao
Roy S Herbst
Christine Alden
J Jack Lee
Ximing Tang
David J Stewart
Merrill S Kies
Frank V Fossella
Hai T Tran
L Mao
Marshall E Hicks
Jeremy Erasmus
Sanjay Gupta
Luc Girard
Michael Peyton
Lixia Diao
Jing Wang
Suzanne E Davis
John D Minna
Ignacio Wistuba
Waun K Hong
John V Heymach
Scott M Lippman
Moores Cancer CenterYale Cancer Center · USThe University of Texas MD Anderson Cancer Center · USUniversity of California, San Diego · USInserm · FRUniversity of Maryland, Baltimore · USUniversity of Ottawa · CACentre de Recherche en Cancérologie de Lyon · FRCentre National de la Recherche Scientifique · FRLevine Cancer Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NCI NIH HHS P30 CA023100NCI NIH HHS P50 CA070907
6 · The paper itself

Abstract

purposeTo report the clinical efficacy of sorafenib and to evaluate biomarkers associated with sorafenib clinical benefit in the BATTLE (Biomarker-Integrated Approaches of Targeted Therapy for Lung Cancer Elimination) program. PATIENTS AND

methodsPatients with previously treated non-small cell lung cancer (NSCLC) received sorafenib until progression or unacceptable toxicity. Eight-week disease control rate (DCR), progression-free survival (PFS), and overall survival (OS) were assessed. Prespecified biomarkers included K-RAS, EGFR, and B-RAF mutations, and EGFR gene copy number. Gene expression profiles from NSCLC cell lines and patient tumor biopsies with wild-type EGFR were used to develop a sorafenib sensitivity signature (SSS).

resultsA total of 105 patients were eligible and randomized to receive sorafenib. Among 98 patients evaluable for eight-week DCR, the observed DCR was 58.2%. The median PFS and OS were 2.83 [95% confidence interval (CI), 2.04-3.58] and 8.48 months (95% CI, 5.78-10.97), respectively. Eight-week DCR was higher in patients with wild-type EGFR than patients with EGFR mutation (P = 0.012), and in patients with EGFR gene copy number gain (FISH-positive) versus patients FISH-negative (P = 0.048). In wild-type EGFR tumors, the SSS was associated with improved PFS (median PFS 3.61 months in high SSS vs. 1.84 months in low SSS; P = 0.026) but not with eight-week DCR. Increased expression of fibroblast growth factor-1, NF-κB, and hypoxia pathways were identified potential drivers of sorafenib resistance.

conclusionSorafenib demonstrates clinical activity in NSCLC, especially with wild-type EGFR. SSS was associated with improved PFS. These data identify subgroups that may derive clinical benefit from sorafenib and merit investigation in future trials.

Indexed as

AgedBiomarkers, TumorCarcinoma, Non-Small-Cell LungDisease-Free SurvivalErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm StagingNiacinamidePhenylurea CompoundsSorafenibBiomarkers, TumorEGFR protein, humanErbB ReceptorsNiacinamidePhenylurea CompoundsSorafenib

Identifiers

PMID24166906
PMCPMC3905243
OpenAlexW2122327814

What OpenQuestion holds

Textmetadata
LicenceTDM
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Registered trials

None linked

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.