ReviewCancer letters2008
Receptor "hijacking" by malignant glioma cells: a tactic for tumor progression.
Review in Cancer letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled 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.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Systematic review of protein biomarkers of invasive behavior in glioblastoma.Molecular neurobiology · 2014Pooled it
- TheNeural regeneration research · 2020Review
- SIRT1 in the Development and Treatment of Hepatocellular Carcinoma.Frontiers in nutrition · 2019Review
- Article
- Expression and Functions of Formyl Peptide Receptor 1 in Drug-Resistant Bladder Cancer.Technology in cancer research & treatment · 2018Article
- The urokinase receptor-derived cyclic peptide [SRSRY] suppresses neovascularization and intravasation of osteosarcoma and chondrosarcoma cells.Oncotarget · 2016Article
- Article
- Microarray expression profiling identifies genes, including cytokines, and biofunctions, as diapedesis, associated with a brain metastasis from a papillary thyroid carcinoma.American journal of cancer research · 2016Article
- Annexin A1 in primary tumors promotes melanoma dissemination.Clinical & experimental metastasis · 2014Article
- The role of chemoattractant receptors in shaping the tumor microenvironment.BioMed research international · 2014Review
- The leukocyte chemotactic receptor FPR1 is functionally expressed on human lens epithelial cells.The Journal of biological chemistry · 2012Article
- Chemoattractant receptors as pharmacological targets for elimination of glioma stem-like cells.International immunopharmacology · 2011Review
- Annexin 1 released by necrotic human glioblastoma cells stimulates tumor cell growth through the formyl peptide receptor 1.The American journal of pathology · 2011Article
- HCV peptide (C5A), an amphipathic α-helical peptide of hepatitis virus C, is an activator of N-formyl peptide receptor in human phagocytes.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- The G-protein-coupled formylpeptide receptor FPR confers a more invasive phenotype on human glioblastoma cells.British journal of cancer · 2010Article
- Use of FDA approved methamphetamine to allow adjunctive use of methylnaltrexone to mediate core anti-growth factor signaling effects in glioblastoma.Journal of neuro-oncology · 2009Review
- Regulation of the leucocyte chemoattractant receptor FPR in glioblastoma cells by cell differentiation.Carcinogenesis · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
Gliomas are the most common and deadly tumors in the central nervous system (CNS). In the course of studying the role of chemoattractant receptors in tumor growth and metastasis, we discovered that highly malignant human glioblastoma and anaplastic astrocytoma specimens were stained positively for the formylpeptide receptor (FPR), which is normally expressed in myeloid cells and accounts for their chemotaxis and activation induced by bacterial peptides. Screening of human glioma cell lines revealed that FPR was expressed selectively in glioma cell lines with a more highly malignant phenotype. FPR expressed in glioblastoma cell lines mediates cell chemotaxis, proliferation and production of an angiogenic factor, vascular endothelial growth factor (VEGF), in response to agonists released by necrotic tumor cells. Furthermore, FPR in glioblastoma cells activates the receptor for epidermal growth factor (EGFR) by increasing the phosphorylation of a selected tyrosine residue in the intracellular tail of EGFR. Thus, FPR hijacked by human glioblastoma cells exploits the function of EGFR to promote rapid tumor progression.
Indexed as
Identifiers
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.