ReviewJournal of neuro-oncology1997
Signal transduction pathways and their relevance in human astrocytomas.
Review in Journal of neuro-oncology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 76 citations in OpenAlex.
- mTOR-Rictor-EGFR axis in oncogenesis and diagnosis of glioblastoma multiforme.Molecular biology reports · 2021Review
- Overexpression of EP300-interacting inhibitor of differentiation 3 predicts poor prognosis in patients with glioblastoma multiforme.International journal of clinical and experimental pathology · 2020Article
- Autophagic and Apoptotic Pathways as Targets for Chemotherapy in Glioblastoma.International journal of molecular sciences · 2018Review
- Overview of Transgenic Glioblastoma and Oligoastrocytoma CNS Models and Their Utility in Drug Discovery.Current protocols in pharmacology · 2016Review
- Current Understanding on EGFR and Wnt/β-Catenin Signaling in Glioma and Their Possible Crosstalk.Genes & cancer · 2013Review
- Differential transformation capacity of neuro-glial progenitors during development.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- PKC signaling in glioblastoma.Cancer biology & therapy · 2013Review
- The potential origin of glioblastoma initiating cells.Frontiers in bioscience (Scholar edition) · 2012Review
- Efficacy of the HSP90 inhibitor 17-AAG in human glioma cell lines and tumorigenic glioma stem cells.Neuro-oncology · 2009Article
- GO Explorer: A gene-ontology tool to aid in the interpretation of shotgun proteomics data.Proteome science · 2009Article
- Phorbol 12-myristate 13-acetate and serum synergize to promote rapamycin-insensitive cell proliferation via protein kinase C-eta.Oncogene · 2007Article
- Mechanisms of angiogenesis in gliomas.Journal of neuro-oncology · 2006Review
- Article
- Overexpression of c-MYC promotes an undifferentiated phenotype in cultured astrocytes and allows elevated Ras and Akt signaling to induce gliomas from GFAP-expressing cells in mice.Neuron glia biology · 2004Article
- Biological mechanisms of glioma invasion and potential therapeutic targets.Journal of neuro-oncology · 2001Review
- Radiotherapy for brain tumors.Current oncology reports · 2000Review
- Protein kinase C zeta isoform is critical for proliferation in human glioblastoma cell lines.Journal of neuro-oncology · 2000Article
- Mitogenic signaling via endogenous kappa-opioid receptors in C6 glioma cells: evidence for the involvement of protein kinase C and the mitogen-activated protein kinase signaling cascade.Journal of neurochemistry · 2000Article
- No complementation between TP53 or RB-1 and v-src in astrocytomas of GFAP-v-src transgenic mice.Brain pathology (Zurich, Switzerland) · 1999Article
- Growth factors in glioma angiogenesis: FGFs, PDGF, EGF, and TGFs.Journal of neuro-oncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrations in a number of signal transduction pathways have been identified as playing a key role in the molecular pathogenesis of astrocytomas and their progression to high grade glioblastoma multiforme (GBM). GBMs are characterized by overexpression of the Platelet Derived Growth Factor Receptors (PDGFR) and their ligands (PDGF), as well as the Epidermal Growth Factor Receptor (EGF-R). These receptors activate the Ras pathway, a key cellular signal transduction pathway, culminating in the activation of a wide range of Ras-dependent cellular events. GBMs have also been found to either overexpression or lose expression of various Protein Kinase C (PKC) isoforms. Major strides are being made in developing pharmacological agents which specifically inhibit these growth factor receptors and intracellular signal transduction pathways. Elucidating the role of these pathways in GBMs is thus of major clinical importance, as these novel molecularly-targeted agents may prove of use in the clinical management of GBMs in the future.
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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.