Evidence map›Paper›PMID 27255663›Full record

ArticleScientific reports2016

IGF1R as a Key Target in High Risk, Metastatic Medulloblastoma.

Matthew N Svalina, Ken Kikuchi, Jinu Abraham, Sangeet Lal, Monika A Davare, Teagan P Settelmeyer, Michael C Young, Jennifer L Peckham, Yoon-Jae Cho, Joel E Michalek and 14 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

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  17. The molecular biology of medulloblastoma metastasis.Brain pathology (Zurich, Switzerland) · 2020
    Review
  18. Review
  19. Article
  20. IGF-1R inhibitor PQ401 inhibits osteosarcoma cell proliferation, migration and colony formation.International journal of clinical and experimental pathology · 2019
    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

24 authors at 6 institutions in 1 country.

Matthew N SvalinaChildren's Cancer Therapy Development Institute, Beaverton, OR USA.
Ken KikuchiDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Jinu AbrahamDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Sangeet LalDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Monika A DavareDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Teagan P SettelmeyerChildren's Cancer Therapy Development Institute, Beaverton, OR USA.
Michael C YoungChildren's Cancer Therapy Development Institute, Beaverton, OR USA.
Jennifer L PeckhamDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Yoon-Jae ChoDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Joel E MichalekDepartment of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, TX 78229 USA.
Brian S HernandezDepartment of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio, TX 78229 USA.
Noah E BerlowChildren's Cancer Therapy Development Institute, Beaverton, OR USA.
Melanie JacksonDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Daniel J GuillaumeDivision of Pediatric Neurosurgery, Department of Neurological Surgery, Oregon Health &Science University, Portland, OR 97239 USA.
Nathan R SeldenDivision of Pediatric Neurosurgery, Department of Neurological Surgery, Oregon Health &Science University, Portland, OR 97239 USA.
Darell D BignerPediatric Brain Tumor Foundation Institute at Duke, Duke University Medical Center, Durham, NC 27705 USA.
Kellie J NazemiDepartment of Pediatrics, Oregon Health &Science University, Portland, OR 97239 USA.
Sarah C GreenDepartment of Pathology, Oregon Health &Science University, Portland, OR 97239 USA.
Christopher L CorlessDepartment of Pathology, Oregon Health &Science University, Portland, OR 97239 USA.
Sakir GultekinDepartment of Pathology, Oregon Health &Science University, Portland, OR 97239 USA.
Atiya MansoorDepartment of Pathology, Oregon Health &Science University, Portland, OR 97239 USA.
Brian P RubinDepartments of Anatomic Pathology and Molecular Genetics, Taussig Cancer Center and Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195 USA.
Randall WoltjerDepartment of Pathology, Oregon Health &Science University, Portland, OR 97239 USA.
Charles KellerChildren's Cancer Therapy Development Institute, Beaverton, OR USA.
Oregon Health & Science University · USChildren's Cancer Therapy Development Institute · USNeurological Surgery · USThe University of Texas Health Science Center at San Antonio · USCleveland Clinic · USDuke University Hospital · US

Funding

Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
NCI NIH HHS P30 CA069533
6 · The paper itself

Abstract

Risk or presence of metastasis in medulloblastoma causes substantial treatment-related morbidity and overall mortality. Through the comparison of cytokines and growth factors in the cerebrospinal fluid (CSF) of metastatic medulloblastoma patients with factors also in conditioned media of metastatic MYC amplified medulloblastoma or leptomeningeal cells, we were led to explore the bioactivity of IGF1 in medulloblastoma by elevated CSF levels of IGF1, IGF-sequestering IGFBP3, IGFBP3-cleaving proteases (MMP and tPA), and protease modulators (TIMP1 and PAI-1). IGF1 led not only to receptor phosphorylation but also accelerated migration/adhesion in MYC amplified medulloblastoma cells in the context of appropriate matrix or meningothelial cells. Clinical correlation suggests a peri-/sub-meningothelial source of IGF-liberating proteases that could facilitate leptomeningeal metastasis. In parallel, studies of key factors responsible for cell autonomous growth in MYC amplified medulloblastoma prioritized IGF1R inhibitors. Together, our studies identify IGF1R as a high value target for clinical trials in high risk medulloblastoma.

Indexed as

AdolescentAntineoplastic AgentsBiomarkers, TumorCase-Control StudiesCell AdhesionCell Line, TumorCell MovementCell ProliferationCerebellar NeoplasmsChildDrug Screening Assays, AntitumorFemaleGene ExpressionHumansInhibitory Concentration 50Insulin-Like Growth Factor Binding Protein 3Antineoplastic AgentsBiomarkers, TumorIGF1 protein, humanIGF1R protein, humanIGFBP3 protein, humanInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IMatrix Metalloproteinase 9MMP9 protein, humanPlasminogen Activator Inhibitor 1Receptor, IGF Type 1Receptors, SomatomedinSERPINE1 protein, humanTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID27255663
PMCPMC4891740
OpenAlexW2460096751

What OpenQuestion holds

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Registered trials

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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.