Evidence map›Paper›PMID 25879388›Full record

ArticleOncotarget2015

Knockdown of EphB1 receptor decreases medulloblastoma cell growth and migration and increases cellular radiosensitization.

Shilpa Bhatia, Nimrah A Baig, Olga Timofeeva, Elena B Pasquale, Kellen Hirsch, Tobey J MacDonald, Anatoly Dritschilo, Yi Chien Lee, Mark Henkemeyer, Brian Rood and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  10. The role of EphA7 in different tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
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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

16 authors at 8 institutions in 2 countries.

Shilpa BhatiaDepartment of Radiation Oncology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
Nimrah A BaigDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Olga TimofeevaDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Elena B PasqualeSanford-Burnham Medical Research Institute, La Jolla, CA, USA.
Kellen HirschDepartment of Radiation Oncology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
Tobey J MacDonaldDepartment of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
Anatoly DritschiloDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Yi Chien LeeDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Mark HenkemeyerDepartment of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Brian RoodChildren's National Medical Center, Washington DC, USA.
Mira JungDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Xiao-Jing WangDepartment of Pathology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
Marcel KoolDivision of Pediatric Neurooncology, German Cancer Research Center DKFZ, Heidelberg, Germany.
Olga RodriguezDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Chris AlbaneseDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA.
Sana D KaramDepartment of Radiation Oncology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
Georgetown University · USUniversity of Colorado Denver · USGeorgetown University Medical Center · USChildren's National · USEmory University · USGerman Cancer Research Center · DESanford Burnham Prebys Medical Discovery Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI MARCUS S NOEL · 1990 to 2026
$71.5M
Targeting Eph receptors in cancerP01CA138390 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI PASQUALE, ELENA B · 2010 to 2014
$7.3M
Bidirectional Tyrosine Kinase Signal TransductionR01MH066332 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI HENKEMEYER, MARK J · 2002 to 2018
$6.1M
NCI NIH HHS P01 CA138390NCI NIH HHS P01CA138390NCI NIH HHS P30 CA051008NCI NIH HHS P30 CA51008NIMH NIH HHS R01 MH066332
6 · The paper itself

Abstract

The expression of members of the Eph family of receptor tyrosine kinases and their ephrin ligands is frequently dysregulated in medulloblastomas. We assessed the expression and functional role of EphB1 in medulloblastoma cell lines and engineered mouse models. mRNA and protein expression profiling showed expression of EphB1 receptor in the human medulloblastoma cell lines DAOY and UW228. EphB1 downregulation reduced cell growth and viability, decreased the expression of important cell cycle regulators, and increased the percentage of cells in G1 phase of the cell cycle. It also modulated the expression of proliferation, and cell survival markers. In addition, EphB1 knockdown in DAOY cells resulted in significant decrease in migration, which correlated with decreased β1-integrin expression and levels of phosphorylated Src. Furthermore, EphB1 knockdown enhanced cellular radiosensitization of medulloblastoma cells in culture and in a genetically engineered mouse medulloblastoma model. Using genetically engineered mouse models, we established that genetic loss of EphB1 resulted in a significant delay in tumor recurrence following irradiation compared to EphB1-expressing control tumors. Taken together, our findings establish that EphB1 plays a key role in medulloblastoma cell growth, viability, migration, and radiation sensitivity, making EphB1 a promising therapeutic target.

Indexed as

AnimalsCell Cycle ProteinsCell Line, TumorCell MovementCerebellar NeoplasmsDisease-Free SurvivalG1 PhaseHumansIntegrin beta1MedulloblastomaMiceMice, KnockoutMice, Mutant StrainsMice, TransgenicNeoplasm ProteinsNeoplasm TransplantationCell Cycle ProteinsIntegrin beta1Neoplasm ProteinsProto-Oncogene Proteins pp60(c-src)Receptor, EphB1RNA, Small InterferingATMcell cycleEphmedulloblastomaradiosensitization

Identifiers

PMID25879388
PMCPMC4496193
OpenAlexW2099273238

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.