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Long-term survival in primary glioblastoma with versus without isocitrate dehydrogenase mutations

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Long-term survival in primary glioblastoma with versus without isocitrate dehydrogenase mutations. / Hartmann, Christian; Hentschel, Bettina; Simon, Matthias; Westphal, Manfred; Schackert, Gabriele; Tonn, Jörg C; Loeffler, Markus; Reifenberger, Guido; Pietsch, Torsten; von Deimling, Andreas; Weller, Michael; German Glioma Network.

in: CLIN CANCER RES, Jahrgang 19, Nr. 18, 15.09.2013, S. 5146-57.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Hartmann, C, Hentschel, B, Simon, M, Westphal, M, Schackert, G, Tonn, JC, Loeffler, M, Reifenberger, G, Pietsch, T, von Deimling, A, Weller, M & German Glioma Network 2013, 'Long-term survival in primary glioblastoma with versus without isocitrate dehydrogenase mutations', CLIN CANCER RES, Jg. 19, Nr. 18, S. 5146-57. https://doi.org/10.1158/1078-0432.CCR-13-0017

APA

Hartmann, C., Hentschel, B., Simon, M., Westphal, M., Schackert, G., Tonn, J. C., Loeffler, M., Reifenberger, G., Pietsch, T., von Deimling, A., Weller, M., & German Glioma Network (2013). Long-term survival in primary glioblastoma with versus without isocitrate dehydrogenase mutations. CLIN CANCER RES, 19(18), 5146-57. https://doi.org/10.1158/1078-0432.CCR-13-0017

Vancouver

Hartmann C, Hentschel B, Simon M, Westphal M, Schackert G, Tonn JC et al. Long-term survival in primary glioblastoma with versus without isocitrate dehydrogenase mutations. CLIN CANCER RES. 2013 Sep 15;19(18):5146-57. https://doi.org/10.1158/1078-0432.CCR-13-0017

Bibtex

@article{d6ec4c751f6b469d840687dd9a2db9c9,
title = "Long-term survival in primary glioblastoma with versus without isocitrate dehydrogenase mutations",
abstract = "PURPOSE: The determinants of long-term survival in glioblastoma have remained largely obscure. Isocitrate dehydrogenase (IDH) 1 or 2 mutations are common in World Health Organization (WHO) grades II and III gliomas, but rare in primary glioblastomas, and associated with longer survival.EXPERIMENTAL DESIGN: We compared clinical and molecular characteristics of 69 patients with centrally confirmed glioblastoma and survival >36 months (LTS-36), including 33 patients surviving >60 months (LTS-60), with 257 patients surviving <36 months. MGMT promoter methylation, 1p/19q codeletions, EGFR amplification, TP53 mutations, and IDH1/2 mutations were determined by standard techniques.RESULTS: The rate of IDH1/2 mutations in LTS-36 patients was 34% (23 of 67 patients) as opposed to 4.3% in controls (11 of 257 patients). Long-term survivors with IDH1/2-mutant glioblastomas were younger, had almost no EGFR amplifications, but exhibited more often 1p/19q codeletions and TP53 mutations than LTS patients with IDH1/2 wild-type glioblastomas. Long-term survivors with IDH1/2 wild-type showed no distinguishing features from other patients with IDH1/2 wild-type glioblastomas except for a higher rate of MGMT promoter methylation. Similarly, among 11 patients with IDH1/2-mutant glioblastomas without long-term survival, the only difference to IDH1/2-mutant long-term survivors was less-frequent MGMT promoter methylation. Compared with LTS-36 patients, LTS-60 patients had less frequently TP53 mutations and radiotherapy alone as initial treatment.CONCLUSIONS: IDH1/2 mutations define a subgroup of tumors of LTS patients that exhibit molecular characteristics of WHO grade II/III gliomas and secondary glioblastomas. Determinants of LTS with IDH1/2 wild-type glioblastomas, which exhibit typical molecular features of primary glioblastomas, beyond MGMT promoter methylation, remain to be identified.",
keywords = "Adult, Aged, Aged, 80 and over, Brain Neoplasms, Cohort Studies, Combined Modality Therapy, DNA Methylation, DNA Modification Methylases, DNA Repair Enzymes, DNA, Neoplasm, Female, Follow-Up Studies, Gene Amplification, Glioblastoma, Humans, Isocitrate Dehydrogenase, Male, Middle Aged, Mutation, Neoplasm Staging, Polymerase Chain Reaction, Prognosis, Promoter Regions, Genetic, Receptor, Epidermal Growth Factor, Survival Rate, Survivors, Tumor Suppressor Protein p53, Tumor Suppressor Proteins, Young Adult",
author = "Christian Hartmann and Bettina Hentschel and Matthias Simon and Manfred Westphal and Gabriele Schackert and Tonn, {J{\"o}rg C} and Markus Loeffler and Guido Reifenberger and Torsten Pietsch and {von Deimling}, Andreas and Michael Weller and {German Glioma Network}",
note = "{\textcopyright}2013 AACR.",
year = "2013",
month = sep,
day = "15",
doi = "10.1158/1078-0432.CCR-13-0017",
language = "English",
volume = "19",
pages = "5146--57",
journal = "CLIN CANCER RES",
issn = "1078-0432",
publisher = "American Association for Cancer Research Inc.",
number = "18",

}

RIS

TY - JOUR

T1 - Long-term survival in primary glioblastoma with versus without isocitrate dehydrogenase mutations

AU - Hartmann, Christian

AU - Hentschel, Bettina

AU - Simon, Matthias

AU - Westphal, Manfred

AU - Schackert, Gabriele

AU - Tonn, Jörg C

AU - Loeffler, Markus

AU - Reifenberger, Guido

AU - Pietsch, Torsten

AU - von Deimling, Andreas

AU - Weller, Michael

AU - German Glioma Network

N1 - ©2013 AACR.

PY - 2013/9/15

Y1 - 2013/9/15

N2 - PURPOSE: The determinants of long-term survival in glioblastoma have remained largely obscure. Isocitrate dehydrogenase (IDH) 1 or 2 mutations are common in World Health Organization (WHO) grades II and III gliomas, but rare in primary glioblastomas, and associated with longer survival.EXPERIMENTAL DESIGN: We compared clinical and molecular characteristics of 69 patients with centrally confirmed glioblastoma and survival >36 months (LTS-36), including 33 patients surviving >60 months (LTS-60), with 257 patients surviving <36 months. MGMT promoter methylation, 1p/19q codeletions, EGFR amplification, TP53 mutations, and IDH1/2 mutations were determined by standard techniques.RESULTS: The rate of IDH1/2 mutations in LTS-36 patients was 34% (23 of 67 patients) as opposed to 4.3% in controls (11 of 257 patients). Long-term survivors with IDH1/2-mutant glioblastomas were younger, had almost no EGFR amplifications, but exhibited more often 1p/19q codeletions and TP53 mutations than LTS patients with IDH1/2 wild-type glioblastomas. Long-term survivors with IDH1/2 wild-type showed no distinguishing features from other patients with IDH1/2 wild-type glioblastomas except for a higher rate of MGMT promoter methylation. Similarly, among 11 patients with IDH1/2-mutant glioblastomas without long-term survival, the only difference to IDH1/2-mutant long-term survivors was less-frequent MGMT promoter methylation. Compared with LTS-36 patients, LTS-60 patients had less frequently TP53 mutations and radiotherapy alone as initial treatment.CONCLUSIONS: IDH1/2 mutations define a subgroup of tumors of LTS patients that exhibit molecular characteristics of WHO grade II/III gliomas and secondary glioblastomas. Determinants of LTS with IDH1/2 wild-type glioblastomas, which exhibit typical molecular features of primary glioblastomas, beyond MGMT promoter methylation, remain to be identified.

AB - PURPOSE: The determinants of long-term survival in glioblastoma have remained largely obscure. Isocitrate dehydrogenase (IDH) 1 or 2 mutations are common in World Health Organization (WHO) grades II and III gliomas, but rare in primary glioblastomas, and associated with longer survival.EXPERIMENTAL DESIGN: We compared clinical and molecular characteristics of 69 patients with centrally confirmed glioblastoma and survival >36 months (LTS-36), including 33 patients surviving >60 months (LTS-60), with 257 patients surviving <36 months. MGMT promoter methylation, 1p/19q codeletions, EGFR amplification, TP53 mutations, and IDH1/2 mutations were determined by standard techniques.RESULTS: The rate of IDH1/2 mutations in LTS-36 patients was 34% (23 of 67 patients) as opposed to 4.3% in controls (11 of 257 patients). Long-term survivors with IDH1/2-mutant glioblastomas were younger, had almost no EGFR amplifications, but exhibited more often 1p/19q codeletions and TP53 mutations than LTS patients with IDH1/2 wild-type glioblastomas. Long-term survivors with IDH1/2 wild-type showed no distinguishing features from other patients with IDH1/2 wild-type glioblastomas except for a higher rate of MGMT promoter methylation. Similarly, among 11 patients with IDH1/2-mutant glioblastomas without long-term survival, the only difference to IDH1/2-mutant long-term survivors was less-frequent MGMT promoter methylation. Compared with LTS-36 patients, LTS-60 patients had less frequently TP53 mutations and radiotherapy alone as initial treatment.CONCLUSIONS: IDH1/2 mutations define a subgroup of tumors of LTS patients that exhibit molecular characteristics of WHO grade II/III gliomas and secondary glioblastomas. Determinants of LTS with IDH1/2 wild-type glioblastomas, which exhibit typical molecular features of primary glioblastomas, beyond MGMT promoter methylation, remain to be identified.

KW - Adult

KW - Aged

KW - Aged, 80 and over

KW - Brain Neoplasms

KW - Cohort Studies

KW - Combined Modality Therapy

KW - DNA Methylation

KW - DNA Modification Methylases

KW - DNA Repair Enzymes

KW - DNA, Neoplasm

KW - Female

KW - Follow-Up Studies

KW - Gene Amplification

KW - Glioblastoma

KW - Humans

KW - Isocitrate Dehydrogenase

KW - Male

KW - Middle Aged

KW - Mutation

KW - Neoplasm Staging

KW - Polymerase Chain Reaction

KW - Prognosis

KW - Promoter Regions, Genetic

KW - Receptor, Epidermal Growth Factor

KW - Survival Rate

KW - Survivors

KW - Tumor Suppressor Protein p53

KW - Tumor Suppressor Proteins

KW - Young Adult

U2 - 10.1158/1078-0432.CCR-13-0017

DO - 10.1158/1078-0432.CCR-13-0017

M3 - SCORING: Journal article

C2 - 23918605

VL - 19

SP - 5146

EP - 5157

JO - CLIN CANCER RES

JF - CLIN CANCER RES

SN - 1078-0432

IS - 18

ER -