Evidence map›Paper›PMID 28282575›Full record

ArticleInternational immunopharmacology2017

Sorafenib combined with HER-2 targeted vaccination can promote effective T cell immunity in vivo.

Melek M E Sunay, Jeremy B Foote, James M Leatherman, Justin P Edwards, Todd D Armstrong, Christopher J Nirschl, Jessica Hicks, Leisha A Emens

Open access · greenAbstract read
In one paragraph

Article in International immunopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  19. Combined Antitumor Effects of Sorafenib and GPC3-CAR T Cells in Mouse Models of Hepatocellular Carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
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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

8 authors at 2 institutions in 1 country.

Melek M E SunayJohns Hopkins University School of Medicine, Department of Oncology, Baltimore, MD 21287, USA; Johns Hopkins University School of Medicine, Graduate Program in Pathobiology, Baltimore, MD 21287, USA.
Jeremy B FooteJohns Hopkins University School of Medicine, Department of Oncology, Baltimore, MD 21287, USA; Department of Molecular and Comparative Pathobiology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
James M LeathermanJohns Hopkins University School of Medicine, Department of Oncology, Baltimore, MD 21287, USA.
Justin P EdwardsJohns Hopkins University School of Medicine, Department of Oncology, Baltimore, MD 21287, USA.
Todd D ArmstrongJohns Hopkins University School of Medicine, Department of Oncology, Baltimore, MD 21287, USA.
Christopher J NirschlJohns Hopkins University School of Medicine, Department of Oncology, Baltimore, MD 21287, USA.
Jessica HicksDepartment of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Leisha A EmensJohns Hopkins University School of Medicine, Department of Oncology, Baltimore, MD 21287, USA; Johns Hopkins University School of Medicine, Graduate Program in Pathobiology, Baltimore, MD 21287, USA. Electronic address: emensle@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI WILLIAM George NELSON · 1985 to 2026
$208.6M
VACCINES--A NEW PARADIGM FOR BREAST CANCERP50CA088843 · NCI · JOHNS HOPKINS UNIVERSITY · PI DAVIDSON, NANCY ELLEN · 2000 to 2010
$27.8M
Training Veterinarians for Careers in Biomedical ResearchT32OD011089 · OD · JOHNS HOPKINS UNIVERSITY · PI JOSEPH L MANKOWSKI · 2012 to 2026
$6.7M
NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA088843NIH HHS T32 OD011089
6 · The paper itself

Abstract

The tumor microenvironment (TME) is established and maintained through complex interactions between tumor cells and host stromal elements. Therefore, therapies that target multiple cellular components of the tumor may be most effective. Sorafenib, a multi-kinase inhibitor, alters signaling pathways in both tumor cells and host stromal cells. Thus, we explored the potential immune-modulating effects of sorafenib in a murine HER-2-(neu) overexpressing breast tumor model alone and in combination with a HER-2 targeted granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting vaccine (3T3neuGM). In vitro, sorafenib inhibited the growth of HER-2 overexpressing NT2.5 tumor cells, inducing apoptosis. Sorafenib also interfered with ERK MAPK, p38 MAPK, and STAT3 signaling, as well as cyclin D expression, but did not affect HER-2 or AKT signaling. In vivo, single agent sorafenib disrupted the tumor-associated vasculature and induced tumor cell apoptosis, effectively inducing the regression of established NT2.5 tumors in immune competent FVB/N mice. Immune depletion studies demonstrated that both CD4

Indexed as

AnimalsApoptosisBreast NeoplasmsCancer VaccinesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell Growth ProcessesCell Line, TumorCell MovementCombined Modality TherapyErb-b2 Receptor Tyrosine KinasesExtracellular Signal-Regulated MAP KinasesFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansImmunity, CellularCancer VaccinesErb-b2 Receptor Tyrosine KinasesExtracellular Signal-Regulated MAP KinasesGranulocyte-Macrophage Colony-Stimulating FactorNiacinamidePhenylurea CompoundsSorafenibBreast cancerImmunityImmunotherapySorafenibVaccine

Identifiers

PMID28282575
PMCPMC5811992
OpenAlexW2591744083

What OpenQuestion holds

Textmetadata
LicenceTDM
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.