ArticleOncogene2001
Activation of the IGF-IR system contributes to malignant growth of human and mouse medulloblastomas.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
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.
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Who cites it
36 citing papers in PubMed, 80 citations in OpenAlex.
- Mapping naturally presented T cell antigens in medulloblastoma based on integrative multi-omics.Nature communications · 2025Article
- Article
- Transcriptional repressor REST drives lineage stage-specific chromatin compaction atScience signaling · 2019Article
- Luteolin reduces migration of human glioblastoma cell lines via inhibition of the p-IGF-1R/PI3K/AKT/mTOR signaling pathway.Oncology letters · 2017Article
- Aryl hydrocarbon receptor deletion in cerebellar granule neuron precursors impairs neurogenesis.Developmental neurobiology · 2016Article
- Estrogen Receptor-β Up-Regulates IGF1R Expression and Activity to Inhibit Apoptosis and Increase Growth of Medulloblastoma.Endocrinology · 2015Article
- Sorafenib and DE605, a novel c-Met inhibitor, synergistically suppress hepatocellular carcinoma.Oncotarget · 2015Article
- A Phase I Study of Cixutumumab (IMC-A12) in Combination with Temsirolimus (CCI-779) in Children with Recurrent Solid Tumors: A Children's Oncology Group Phase I Consortium Report.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Article
- DJ-1 is activated in medulloblastoma and is associated with cell proliferation and differentiation.World journal of surgical oncology · 2014Article
- Pediatric patients with refractory central nervous system tumors: experiences of a clinical trial combining bevacizumab and temsirolimus.Anticancer research · 2014Article
- PID1 (NYGGF4), a new growth-inhibitory gene in embryonal brain tumors and gliomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Novel agents targeting the IGF-1R/PI3K pathway impair cell proliferation and survival in subsets of medulloblastoma and neuroblastoma.PloS one · 2012Article
- A polymeric nanoparticle formulation of curcumin inhibits growth, clonogenicity and stem-like fraction in malignant brain tumors.Cancer biology & therapy · 2011Article
- ROS accumulation and IGF-IR inhibition contribute to fenofibrate/PPARalpha -mediated inhibition of glioma cell motility in vitro.Molecular cancer · 2010Article
- Developmental and oncogenic effects of insulin-like growth factor-I in Ptc1+/- mouse cerebellum.Molecular cancer · 2010Article
- IGF-IR-dependent expression of Survivin is required for T-antigen-mediated protection from apoptosis and proliferation of neural progenitors.Cell death and differentiation · 2010Article
- Tuberous sclerosis complex suppression in cerebellar development and medulloblastoma: separate regulation of mammalian target of rapamycin activity and p27 Kip1 localization.Cancer research · 2009Article
- Expression and function of the insulin receptor substrate proteins in cancer.Cell communication and signaling : CCS · 2009Article
- Estrogen receptor beta-mediated nuclear interaction between IRS-1 and Rad51 inhibits homologous recombination directed DNA repair in medulloblastoma.Journal of cellular physiology · 2009Article
- IGF-IR in neuroprotection and brain tumors.Frontiers in bioscience (Landmark edition) · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Insulin-like growth factor I receptor (IGF-IR) has been implicated in the normal and malignant growth of many cell types including cells from the central nervous system. In the cerebellar cortex IGF-IR mRNA is found in granular cells and IGF-I stimulation is mitogenic and protects cells from low-potassium-induced apoptosis. Since primitive neuroectodermal tumors/medulloblastomas (PNETs/medulloblastomas) are suspected to originate from the external cerebellar granular layer, it is reasonable to postulate that IGF-IR and/or its signaling molecules may contribute to the transformation of these poorly differentiated cells. To study activation of the IGF-IR system in medulloblastomas, we have utilized an antibody (anti-pY1316) that specifically recognizes the phosphorylated (active) form of the IGF-IR. Medulloblastoma biopsy specimens were positive when examined immunohistochemically with anti-Y1316 antibody. Further analysis of the IGF-IR system was performed in three human (Daoy, TE-671, D283 Med) and four mouse (BsB8, BsB13, Bs-1b, Bs-1c) medulloblastoma cell lines. All the murine cell lines examined express IGF-IR and PI3-kinase at relatively normal levels, and grossly overexpress IRS-1, when compared with normal mouse cerebellum. Within 15 min following IGF-I stimulation both mouse and human cell lines phosphorylate the beta subunit of the IGF-IR, IRS-1, Akt, and MAP kinases. They respond with cell proliferation when stimulated solely with IGF-I and are strongly inhibited when challenged with a dominant negative mutant of the IGF-IR (486/STOP), or with antisense oligonucleotides against the IGF-IR mRNA.
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What OpenQuestion holds
Registered trials
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.