Evidence map›Paper›PMID 28736761›Full record

ArticleCancer treatment and research communications2017

Phase II Study of Dovitinib in Patients Progressing on Anti-Vascular Endothelial Growth Factor Therapy.

Thomas J Semrad, Edward J Kim, Michael S Tanaka, Jacob Sands, Chris Roberts, Rebekah A Burich, Yu Li, David R Gandara, Primo Lara, Philip C Mack

Open access · greenAbstract read
In one paragraph

Article in Cancer treatment and research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  10. Anti-Angiogenic Therapy: Current Challenges and Future Perspectives.International journal of molecular sciences · 2021
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  14. Comprehensive review of targeted therapy for colorectal cancer.Signal transduction and targeted therapy · 2020
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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

10 authors at 4 institutions in 1 country.

Thomas J SemradDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
Edward J KimDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
Michael S TanakaDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
Jacob SandsLahey Clinic, Boston, MA.
Chris RobertsHTG Molecular Diagnostics, Inc., Tucson, AZ.
Rebekah A BurichDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
Yu LiDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
David R GandaraDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
Primo LaraDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
Philip C MackDivision of Hematology/Oncology, University of California, Davis Comprehensive Cancer Center, Sacramento, California.
UC Davis Comprehensive Cancer CenterUniversity of California, Davis · USHTG Molecular Diagnostics (United States) · USLahey Hospital and Medical Center · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
UC Davis Paul Calabresi K12 Clinical Oncology Research Career Development ProgramK12CA138464 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BIRKELAND, ANDREW CHARLES, LARA, PRIMO N. · 2011 to 2025
$11.4M
NCI NIH HHS K12 CA138464NCI NIH HHS L30 CA179414NCI NIH HHS P30 CA093373
6 · The paper itself

Abstract

backgroundPrior work identified the fibroblast growth factor (FGF) pathway as a mediator of resistance to anti-vascular endothelial growth factor (VEGF) therapy. We tested dovitinib, an inhibitor of both FGF and VEGF receptors, in patients progressing on anti-VEGF treatment.

methodsPatients with measurable advanced colorectal or non-small cell lung cancer with progression despite anti-VEGF treatment within 56 days, good performance status and adequate organ function were eligible. A research tumor biopsy was followed by treatment with dovitinib 500 mg on a 5-day on/2-day off schedule for 28-day cycles. The primary endpoint of tumor response was evaluated every 2 cycles. Secondary endpoints included toxicity and 8-week disease control rate. Intratumor mRNA expression of angiogenic mediators was analyzed using a next generation sequencing based expression array.

resultsTen patients treated previously with bevacizumab or ziv-aflibercept enrolled. The study closed with termination of dovitinib development. No responses were observed in 7 evaluable patients. The best response was stable disease in 1 patient. Common toxicities included gastrointestinal, metabolic, and biochemical derangements. All patients experienced at least one grade ≥ 3 treatment-related adverse event, most commonly fatigue, elevated GGT, and lymphopenia. Expression of multiple angiogenic mediators was common in tumors progressing on anti-VEGF therapy including high levels of FGFR1 and VEGFA.

conclusionsWe found no evidence for the activity of dovitinib in patients who had recently progressed on anti-VEGF therapy and toxicities were significant. In tumors progressing despite anti-VEGF therapy, a multitude of pro-angiogenic mediators are expressed, including members of the FGF pathway.

Indexed as

Angiogenesis InhibitorsDovitinibFibroblast Growth FactorsVascular Endothelial Growth Factors

Identifiers

PMID28736761
PMCPMC5519297
OpenAlexW2566593170

What OpenQuestion holds

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Read underepoch 390

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.