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Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity.

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Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity. / Holtkamp, Nikola; Okuducu, Ali Fuat; Mucha, Jana; Afanasieva, Anastasia; Hartmann, Christian; Atallah, Isis; Estevez-Schwarz, Lope; Mawrin, Christian; Friedrich, Reinhard; Mautner, Viktor Felix; von Deimling, Andreas.

In: CARCINOGENESIS, Vol. 27, No. 3, 3, 2006, p. 664-671.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Holtkamp, N, Okuducu, AF, Mucha, J, Afanasieva, A, Hartmann, C, Atallah, I, Estevez-Schwarz, L, Mawrin, C, Friedrich, R, Mautner, VF & von Deimling, A 2006, 'Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity.', CARCINOGENESIS, vol. 27, no. 3, 3, pp. 664-671. <http://www.ncbi.nlm.nih.gov/pubmed/16357008?dopt=Citation>

APA

Holtkamp, N., Okuducu, A. F., Mucha, J., Afanasieva, A., Hartmann, C., Atallah, I., Estevez-Schwarz, L., Mawrin, C., Friedrich, R., Mautner, V. F., & von Deimling, A. (2006). Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity. CARCINOGENESIS, 27(3), 664-671. [3]. http://www.ncbi.nlm.nih.gov/pubmed/16357008?dopt=Citation

Vancouver

Holtkamp N, Okuducu AF, Mucha J, Afanasieva A, Hartmann C, Atallah I et al. Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity. CARCINOGENESIS. 2006;27(3):664-671. 3.

Bibtex

@article{7bdbd8b8a3904928b9b300e4cd6c9f16,
title = "Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity.",
abstract = "Platelet-derived growth factor receptor alpha (PDGFRalpha) and c-Kit are receptor tyrosine kinases. Both are targets of the tyrosine kinase inhibitor imatinib mesylate which is approved for treatment of some cancers. In order to assess the role of PDGFRalpha and c-Kit in malignant peripheral nerve sheath tumours (MPNST) we examined human tumours for structural alterations, protein and ligand expression. We investigated 34 MPNST, 6 corresponding plexiform neurofibromas (pNF) and 1 MPNST cell culture from 31 patients for mutations and polymorphisms in PDGFRA (exon 2-21) and KIT (exon 9, 11, 13, 17). PDGFRA was amplified in seven tumours from six patients and MPNST cell culture S462. KIT was amplified in five tumours from four patients and in the cell culture. Two MPNST carried somatic PDGFRA mutations in exons coding for the extracellular domain. In addition we detected several polymorphisms in PDGFRA. No point mutations or polymorphisms were detected in the four KIT exons analysed. PDGFRalpha expression was present in 21 of 28 MPNST patients (75%) and the MPNST cell culture. Expression analysis of PDGFRalpha ligands in MPNST and neurofibromas revealed that PDGF-A was more widely expressed than PDGF-B. Focal c-Kit expression was detected in 2 of 29 (7%) MPNST patients. Imatinib treatment of MPNST cell culture S462 exerted a growth inhibitory effect and prevented PDGF-AA induced PDGFRalpha phosphorylation. In summary, PDGFRA, PDGF and KIT dysregulation as well as growth inhibition of cell culture S462 by imatinib may suggest that MPNST patients benefit from treatment with imatinib.",
author = "Nikola Holtkamp and Okuducu, {Ali Fuat} and Jana Mucha and Anastasia Afanasieva and Christian Hartmann and Isis Atallah and Lope Estevez-Schwarz and Christian Mawrin and Reinhard Friedrich and Mautner, {Viktor Felix} and {von Deimling}, Andreas",
year = "2006",
language = "Deutsch",
volume = "27",
pages = "664--671",
journal = "CARCINOGENESIS",
issn = "0143-3334",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Mutation and expression of PDGFRA and KIT in malignant peripheral nerve sheath tumors, and its implications for imatinib sensitivity.

AU - Holtkamp, Nikola

AU - Okuducu, Ali Fuat

AU - Mucha, Jana

AU - Afanasieva, Anastasia

AU - Hartmann, Christian

AU - Atallah, Isis

AU - Estevez-Schwarz, Lope

AU - Mawrin, Christian

AU - Friedrich, Reinhard

AU - Mautner, Viktor Felix

AU - von Deimling, Andreas

PY - 2006

Y1 - 2006

N2 - Platelet-derived growth factor receptor alpha (PDGFRalpha) and c-Kit are receptor tyrosine kinases. Both are targets of the tyrosine kinase inhibitor imatinib mesylate which is approved for treatment of some cancers. In order to assess the role of PDGFRalpha and c-Kit in malignant peripheral nerve sheath tumours (MPNST) we examined human tumours for structural alterations, protein and ligand expression. We investigated 34 MPNST, 6 corresponding plexiform neurofibromas (pNF) and 1 MPNST cell culture from 31 patients for mutations and polymorphisms in PDGFRA (exon 2-21) and KIT (exon 9, 11, 13, 17). PDGFRA was amplified in seven tumours from six patients and MPNST cell culture S462. KIT was amplified in five tumours from four patients and in the cell culture. Two MPNST carried somatic PDGFRA mutations in exons coding for the extracellular domain. In addition we detected several polymorphisms in PDGFRA. No point mutations or polymorphisms were detected in the four KIT exons analysed. PDGFRalpha expression was present in 21 of 28 MPNST patients (75%) and the MPNST cell culture. Expression analysis of PDGFRalpha ligands in MPNST and neurofibromas revealed that PDGF-A was more widely expressed than PDGF-B. Focal c-Kit expression was detected in 2 of 29 (7%) MPNST patients. Imatinib treatment of MPNST cell culture S462 exerted a growth inhibitory effect and prevented PDGF-AA induced PDGFRalpha phosphorylation. In summary, PDGFRA, PDGF and KIT dysregulation as well as growth inhibition of cell culture S462 by imatinib may suggest that MPNST patients benefit from treatment with imatinib.

AB - Platelet-derived growth factor receptor alpha (PDGFRalpha) and c-Kit are receptor tyrosine kinases. Both are targets of the tyrosine kinase inhibitor imatinib mesylate which is approved for treatment of some cancers. In order to assess the role of PDGFRalpha and c-Kit in malignant peripheral nerve sheath tumours (MPNST) we examined human tumours for structural alterations, protein and ligand expression. We investigated 34 MPNST, 6 corresponding plexiform neurofibromas (pNF) and 1 MPNST cell culture from 31 patients for mutations and polymorphisms in PDGFRA (exon 2-21) and KIT (exon 9, 11, 13, 17). PDGFRA was amplified in seven tumours from six patients and MPNST cell culture S462. KIT was amplified in five tumours from four patients and in the cell culture. Two MPNST carried somatic PDGFRA mutations in exons coding for the extracellular domain. In addition we detected several polymorphisms in PDGFRA. No point mutations or polymorphisms were detected in the four KIT exons analysed. PDGFRalpha expression was present in 21 of 28 MPNST patients (75%) and the MPNST cell culture. Expression analysis of PDGFRalpha ligands in MPNST and neurofibromas revealed that PDGF-A was more widely expressed than PDGF-B. Focal c-Kit expression was detected in 2 of 29 (7%) MPNST patients. Imatinib treatment of MPNST cell culture S462 exerted a growth inhibitory effect and prevented PDGF-AA induced PDGFRalpha phosphorylation. In summary, PDGFRA, PDGF and KIT dysregulation as well as growth inhibition of cell culture S462 by imatinib may suggest that MPNST patients benefit from treatment with imatinib.

M3 - SCORING: Zeitschriftenaufsatz

VL - 27

SP - 664

EP - 671

JO - CARCINOGENESIS

JF - CARCINOGENESIS

SN - 0143-3334

IS - 3

M1 - 3

ER -