Mutational analysis of PDGFR–RAS/MAPK pathway activation in childhood medulloblastoma
Aberrant signalling via platelet derived growth factor receptors (PDGFRs) and the RAS/MAPK pathway has been implicated in the development of medulloblastoma, the most common malignant brain tumour in childhood. To determine whether genetic mechanisms play a role in the activation of PDGFR–RAS/MAPK s...
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Published in | European journal of cancer (1990) Vol. 42; no. 5; pp. 646 - 649 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Oxford
Elsevier Ltd
01.03.2006
Elsevier |
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Abstract | Aberrant signalling via platelet derived growth factor receptors (PDGFRs) and the RAS/MAPK pathway has been implicated in the development of medulloblastoma, the most common malignant brain tumour in childhood. To determine whether genetic mechanisms play a role in the activation of PDGFR–RAS/MAPK signalling in medulloblastoma, we performed a direct sequence analysis of the established mutational “hotspots” of known targets of activating mutations within the pathway (
PDGFRA, NRAS, KRAS, HRAS and
BRAF) and
PDFRFB, in a cohort of 28 primary tumours. A synonymous sequence variation in
PDGFRA (CCG to CCA; PRO 567 PRO) was detected in two cases (∼7%), but not in 150 normal chromosomes assessed, suggesting that the
PDGFRA locus may be associated with medulloblastoma development in certain cases. No evidence for oncogenic mutations affecting
NRAS, KRAS, HRAS, BRAF or
PDFRFB was found in any case. These data demonstrate that activating mutations in established mutational hotspots within the PDGFR–RAS/MAPK pathway are rare events in medulloblastoma development, and suggest that alternative mechanisms are responsible for RAS/MAPK pathway activation in this disease. |
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AbstractList | Aberrant signalling via platelet derived growth factor receptors (PDGFRs) and the RAS/MAPK pathway has been implicated in the development of medulloblastoma, the most common malignant brain tumour in childhood. To determine whether genetic mechanisms play a role in the activation of PDGFR–RAS/MAPK signalling in medulloblastoma, we performed a direct sequence analysis of the established mutational “hotspots” of known targets of activating mutations within the pathway (
PDGFRA, NRAS, KRAS, HRAS and
BRAF) and
PDFRFB, in a cohort of 28 primary tumours. A synonymous sequence variation in
PDGFRA (CCG to CCA; PRO 567 PRO) was detected in two cases (∼7%), but not in 150 normal chromosomes assessed, suggesting that the
PDGFRA locus may be associated with medulloblastoma development in certain cases. No evidence for oncogenic mutations affecting
NRAS, KRAS, HRAS, BRAF or
PDFRFB was found in any case. These data demonstrate that activating mutations in established mutational hotspots within the PDGFR–RAS/MAPK pathway are rare events in medulloblastoma development, and suggest that alternative mechanisms are responsible for RAS/MAPK pathway activation in this disease. Aberrant signalling via platelet derived growth factor receptors (PDGFRs) and the RAS/MAPK pathway has been implicated in the development of medulloblastoma, the most common malignant brain tumour in childhood. To determine whether genetic mechanisms play a role in the activation of PDGFR-RAS/MAPK signalling in medulloblastoma, we performed a direct sequence analysis of the established mutational "hotspots" of known targets of activating mutations within the pathway (PDGFRA, NRAS, KRAS, HRAS and BRAF) and PDFRFB, in a cohort of 28 primary tumours. A synonymous sequence variation in PDGFRA (CCG to CCA; PRO 567 PRO) was detected in two cases (approximately 7%), but not in 150 normal chromosomes assessed, suggesting that the PDGFRA locus may be associated with medulloblastoma development in certain cases. No evidence for oncogenic mutations affecting NRAS, KRAS, HRAS, BRAF or PDFRFB was found in any case. These data demonstrate that activating mutations in established mutational hotspots within the PDGFR-RAS/MAPK pathway are rare events in medulloblastoma development, and suggest that alternative mechanisms are responsible for RAS/MAPK pathway activation in this disease. Aberrant signalling via platelet derived growth factor receptors (PDGFRs) and the RAS/MAPK pathway has been implicated in the development of medulloblastoma, the most common malignant brain tumour in childhood. To determine whether genetic mechanisms play a role in the activation of PDGFR-RAS/MAPK signalling in medulloblastoma, we performed a direct sequence analysis of the established mutational "hotspots" of known targets of activating mutations within the pathway (PDGFRA, NRAS, KRAS, HRAS and BRAF) and PDFRFB, in a cohort of 28 primary tumours. A synonymous sequence variation in PDGFRA (CCG to CCA; PRO 567 PRO) was detected in two cases ( similar to 7%), but not in 150 normal chromosomes assessed, suggesting that the PDGFRA locus may be associated with medulloblastoma development in certain cases. No evidence for oncogenic mutations affecting NRAS, KRAS, HRAS, BRAF or PDFRFB was found in any case. These data demonstrate that activating mutations in established mutational hotspots within the PDGFR-RAS/MAPK pathway are rare events in medulloblastoma development, and suggest that alternative mechanisms are responsible for RAS/MAPK pathway activation in this disease. |
Author | Gilbertson, Richard J. Langdon, Jaqueline A. Hollander, Andrew Hogg, Twala L. Clifford, Steven C. Hernan, Roberto Gajjar, Amar Fuller, Christine |
Author_xml | – sequence: 1 givenname: Richard J. surname: Gilbertson fullname: Gilbertson, Richard J. organization: Northern Institute for Cancer Research, University of Newcastle, The Medical School, Framlington Place, Newcastle-upon-Tyne, NE2 4HH, UK – sequence: 2 givenname: Jaqueline A. surname: Langdon fullname: Langdon, Jaqueline A. organization: Northern Institute for Cancer Research, University of Newcastle, The Medical School, Framlington Place, Newcastle-upon-Tyne, NE2 4HH, UK – sequence: 3 givenname: Andrew surname: Hollander fullname: Hollander, Andrew organization: Northern Institute for Cancer Research, University of Newcastle, The Medical School, Framlington Place, Newcastle-upon-Tyne, NE2 4HH, UK – sequence: 4 givenname: Roberto surname: Hernan fullname: Hernan, Roberto organization: Northern Institute for Cancer Research, University of Newcastle, The Medical School, Framlington Place, Newcastle-upon-Tyne, NE2 4HH, UK – sequence: 5 givenname: Twala L. surname: Hogg fullname: Hogg, Twala L. organization: Northern Institute for Cancer Research, University of Newcastle, The Medical School, Framlington Place, Newcastle-upon-Tyne, NE2 4HH, UK – sequence: 6 givenname: Amar surname: Gajjar fullname: Gajjar, Amar organization: Department of Hematology/Oncology, St. Jude Children’s Research Hospital, 332 N. Lauderdale Street, Memphis, TN 38105, USA – sequence: 7 givenname: Christine surname: Fuller fullname: Fuller, Christine organization: Department of Pathology, St. Jude Children’s Research Hospital, 332 N. Lauderdale Street, Memphis, TN 38105, USA – sequence: 8 givenname: Steven C. surname: Clifford fullname: Clifford, Steven C. email: s.c.clifford@ncl.ac.uk organization: Northern Institute for Cancer Research, University of Newcastle, The Medical School, Framlington Place, Newcastle-upon-Tyne, NE2 4HH, UK |
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Keywords | PDGFR BRAF RAS Medulloblastoma Human Platelet derived growth factor receptor Enzyme Mitogen-activated protein kinase Pharmacology BRAF Gene Cancerology C-Onc gene Genetics Medulloblastoma PDGFR BRAF RAS Mutation Child Protooncogene |
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SubjectTerms | Adolescent Adult Biological and medical sciences BRAF Cerebellar Neoplasms - genetics Child Child, Preschool Exons Female Genes, ras - genetics Humans Infant Male MAP Kinase Signaling System Medical sciences Medulloblastoma Medulloblastoma - genetics Mitogen-Activated Protein Kinases - genetics Mutation - genetics PDGFR Pharmacology. Drug treatments Polymorphism, Restriction Fragment Length RAS Receptor, Platelet-Derived Growth Factor alpha - genetics Receptor, Platelet-Derived Growth Factor alpha - metabolism Receptors, Platelet-Derived Growth Factor - genetics Tumors |
Title | Mutational analysis of PDGFR–RAS/MAPK pathway activation in childhood medulloblastoma |
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