Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas
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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, Jahrgang 32A, Nr. 13, 13, 12.1996, S. 2242-2248.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -