Research ExplorerPublicationsDemonstration of p53 protein and TP53 gene mutations in olig...

Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas

Standard

Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas. / Hagel, C; Laking, G; Laas, R; Scheil, S; Jung, R; Milde-Langosch, K; Stavrou, D K.

In: EUR J CANCER, Vol. 32A, No. 13, 13, 12.1996, p. 2242-2248.

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

Harvard

Hagel, C, Laking, G, Laas, R, Scheil, S, Jung, R, Milde-Langosch, K & Stavrou, DK 1996, 'Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas', EUR J CANCER, vol. 32A, no. 13, 13, pp. 2242-2248. https://doi.org/10.1016/s0959-8049(96)00259-6

APA

Hagel, C., Laking, G., Laas, R., Scheil, S., Jung, R., Milde-Langosch, K., & Stavrou, D. K. (1996). Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas. EUR J CANCER, 32A(13), 2242-2248. [13]. https://doi.org/10.1016/s0959-8049(96)00259-6

Vancouver

Hagel C, Laking G, Laas R, Scheil S, Jung R, Milde-Langosch K et al. Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas. EUR J CANCER. 1996 Dec;32A(13):2242-2248. 13. https://doi.org/10.1016/s0959-8049(96)00259-6

Bibtex

@article{c056c80847194ae997c685960c1053c3,
title = "Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas",
abstract = "Paraffin embedded tissue of 84 oligodendrogliomas (63 primary tumours, 21 recurrences), 21 glioblastomas with oligodendroglial growth pattern (15 primaries, 6 recurrences) and 17 mixed gliomas was investigated for the presence of mutations in exons 5-9 by means of single stranded conformation polymorphism (SCCP), temperature gradient gel electrophoresis (TGGE) and direct DNA sequencing. In parallel, p53 protein accumulation was determined by means of immunohistochemistry. The percentage of mutations was found to be higher than previously reported (6 of 44 grade II oligodendrogliomas, 4 of 19 grade III oligodendrogliomas, 4 of 15 glioblastomas). In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine-->tyrosine, proline-->leucine) and were associated with marked accumulation of p53 protein. A significant correlation between p53 protein accumulation and TP53 gene aberrations was found (P < 0.001), although p53 protein accumulation was detected more often than TP53 gene anomalies, indicating that factors other than TP53 gene mutation may also lead to a p53 protein accumulation in the tumour cells. A significant correlation was found for p53 protein accumulation and tumour grade but not TP53 gene mutations. In conclusion, evaluation of p53 protein accumulation reflected the clinical course of oligodendrogliomas better than the mere presence of TP53 gene mutations.",
keywords = "Adult, Brain Neoplasms/genetics, Female, Genes, p53, Humans, Immunoenzyme Techniques, Male, Middle Aged, Mutation, Neoplasm Proteins/metabolism, Oligodendroglioma/genetics, Polymerase Chain Reaction, Polymorphism, Single-Stranded Conformational, Tumor Suppressor Protein p53/metabolism",
author = "C Hagel and G Laking and R Laas and S Scheil and R Jung and K Milde-Langosch and Stavrou, {D K}",
year = "1996",
month = dec,
doi = "10.1016/s0959-8049(96)00259-6",
language = "English",
volume = "32A",
pages = "2242--2248",
journal = "EUR J CANCER",
issn = "0959-8049",
publisher = "Elsevier Limited",
number = "13",

}

RIS

TY - JOUR

T1 - Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas

AU - Hagel, C

AU - Laking, G

AU - Laas, R

AU - Scheil, S

AU - Jung, R

AU - Milde-Langosch, K

AU - Stavrou, D K

PY - 1996/12

Y1 - 1996/12

N2 - Paraffin embedded tissue of 84 oligodendrogliomas (63 primary tumours, 21 recurrences), 21 glioblastomas with oligodendroglial growth pattern (15 primaries, 6 recurrences) and 17 mixed gliomas was investigated for the presence of mutations in exons 5-9 by means of single stranded conformation polymorphism (SCCP), temperature gradient gel electrophoresis (TGGE) and direct DNA sequencing. In parallel, p53 protein accumulation was determined by means of immunohistochemistry. The percentage of mutations was found to be higher than previously reported (6 of 44 grade II oligodendrogliomas, 4 of 19 grade III oligodendrogliomas, 4 of 15 glioblastomas). In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine-->tyrosine, proline-->leucine) and were associated with marked accumulation of p53 protein. A significant correlation between p53 protein accumulation and TP53 gene aberrations was found (P < 0.001), although p53 protein accumulation was detected more often than TP53 gene anomalies, indicating that factors other than TP53 gene mutation may also lead to a p53 protein accumulation in the tumour cells. A significant correlation was found for p53 protein accumulation and tumour grade but not TP53 gene mutations. In conclusion, evaluation of p53 protein accumulation reflected the clinical course of oligodendrogliomas better than the mere presence of TP53 gene mutations.

AB - Paraffin embedded tissue of 84 oligodendrogliomas (63 primary tumours, 21 recurrences), 21 glioblastomas with oligodendroglial growth pattern (15 primaries, 6 recurrences) and 17 mixed gliomas was investigated for the presence of mutations in exons 5-9 by means of single stranded conformation polymorphism (SCCP), temperature gradient gel electrophoresis (TGGE) and direct DNA sequencing. In parallel, p53 protein accumulation was determined by means of immunohistochemistry. The percentage of mutations was found to be higher than previously reported (6 of 44 grade II oligodendrogliomas, 4 of 19 grade III oligodendrogliomas, 4 of 15 glioblastomas). In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine-->tyrosine, proline-->leucine) and were associated with marked accumulation of p53 protein. A significant correlation between p53 protein accumulation and TP53 gene aberrations was found (P < 0.001), although p53 protein accumulation was detected more often than TP53 gene anomalies, indicating that factors other than TP53 gene mutation may also lead to a p53 protein accumulation in the tumour cells. A significant correlation was found for p53 protein accumulation and tumour grade but not TP53 gene mutations. In conclusion, evaluation of p53 protein accumulation reflected the clinical course of oligodendrogliomas better than the mere presence of TP53 gene mutations.

KW - Adult

KW - Brain Neoplasms/genetics

KW - Female

KW - Genes, p53

KW - Humans

KW - Immunoenzyme Techniques

KW - Male

KW - Middle Aged

KW - Mutation

KW - Neoplasm Proteins/metabolism

KW - Oligodendroglioma/genetics

KW - Polymerase Chain Reaction

KW - Polymorphism, Single-Stranded Conformational

KW - Tumor Suppressor Protein p53/metabolism

U2 - 10.1016/s0959-8049(96)00259-6

DO - 10.1016/s0959-8049(96)00259-6

M3 - SCORING: Journal article

C2 - 9038605

VL - 32A

SP - 2242

EP - 2248

JO - EUR J CANCER

JF - EUR J CANCER

SN - 0959-8049

IS - 13

M1 - 13

ER -