CDKN2A/p16 in ependymomas

S. Bortolotto, L. Chiado-Piat, P. Cavalla, I. Bosone, A. Mauro, D. Schiffer

Research output: Contribution to journalArticle

Abstract

Sixteen cases of ependymoma were studied for CDKN2A/p16 inactivation by immunohistochemistry using a p16 monoclonal antibody, by homozygous deletion (HD) assay and 5′CpG promoter methylation assay (methylation-specific PCR). Three out of 16 cases were p16 immuno-negative: two corresponded to grade II ependymomas and one to grade III. The latter ependymoma, characterized by a high Ki-67/MIB-1 LI, was the only one of the whole series to show CDKN2A HD. No promoter methylation was found in the two immuno-negative cases without CDKN2A HD. Alternative mechanisms, such as point mutations or alterations in p16 post-translational regulation, may be responsible for p16 inactivation. Since in our series just one out of eight anaplastic cases showed negative immunostaining and CDKN2A HD, p16/CDKN2A inactivation may not play an important role in the malignant transformation of ependymomas. Amplification of CCND1 and CDK4, p27/Kip1 degradation and TP53 mutations were previously studied by other authors and were demonstrated not to correlate with anaplasia. Up to date, molecular genetic studies have not been useful in recognizing the anaplastic variant in ependymomas.

Original languageEnglish
Pages (from-to)9-13
Number of pages5
JournalJournal of Neuro-Oncology
Volume54
Issue number1
DOIs
Publication statusPublished - 2001

Fingerprint

Ependymoma
Methylation
Anaplasia
Point Mutation
Molecular Biology
Immunohistochemistry
Monoclonal Antibodies
Polymerase Chain Reaction
Mutation

Keywords

  • Cancer biology
  • CDKN2A/p16
  • Ependymomas

ASJC Scopus subject areas

  • Clinical Neurology
  • Cancer Research
  • Oncology
  • Neuroscience(all)

Cite this

Bortolotto, S., Chiado-Piat, L., Cavalla, P., Bosone, I., Mauro, A., & Schiffer, D. (2001). CDKN2A/p16 in ependymomas. Journal of Neuro-Oncology, 54(1), 9-13. https://doi.org/10.1023/A:1012537105775

CDKN2A/p16 in ependymomas. / Bortolotto, S.; Chiado-Piat, L.; Cavalla, P.; Bosone, I.; Mauro, A.; Schiffer, D.

In: Journal of Neuro-Oncology, Vol. 54, No. 1, 2001, p. 9-13.

Research output: Contribution to journalArticle

Bortolotto, S, Chiado-Piat, L, Cavalla, P, Bosone, I, Mauro, A & Schiffer, D 2001, 'CDKN2A/p16 in ependymomas', Journal of Neuro-Oncology, vol. 54, no. 1, pp. 9-13. https://doi.org/10.1023/A:1012537105775
Bortolotto S, Chiado-Piat L, Cavalla P, Bosone I, Mauro A, Schiffer D. CDKN2A/p16 in ependymomas. Journal of Neuro-Oncology. 2001;54(1):9-13. https://doi.org/10.1023/A:1012537105775
Bortolotto, S. ; Chiado-Piat, L. ; Cavalla, P. ; Bosone, I. ; Mauro, A. ; Schiffer, D. / CDKN2A/p16 in ependymomas. In: Journal of Neuro-Oncology. 2001 ; Vol. 54, No. 1. pp. 9-13.
@article{dfa278db82ca40f9874d6f4ea72dced2,
title = "CDKN2A/p16 in ependymomas",
abstract = "Sixteen cases of ependymoma were studied for CDKN2A/p16 inactivation by immunohistochemistry using a p16 monoclonal antibody, by homozygous deletion (HD) assay and 5′CpG promoter methylation assay (methylation-specific PCR). Three out of 16 cases were p16 immuno-negative: two corresponded to grade II ependymomas and one to grade III. The latter ependymoma, characterized by a high Ki-67/MIB-1 LI, was the only one of the whole series to show CDKN2A HD. No promoter methylation was found in the two immuno-negative cases without CDKN2A HD. Alternative mechanisms, such as point mutations or alterations in p16 post-translational regulation, may be responsible for p16 inactivation. Since in our series just one out of eight anaplastic cases showed negative immunostaining and CDKN2A HD, p16/CDKN2A inactivation may not play an important role in the malignant transformation of ependymomas. Amplification of CCND1 and CDK4, p27/Kip1 degradation and TP53 mutations were previously studied by other authors and were demonstrated not to correlate with anaplasia. Up to date, molecular genetic studies have not been useful in recognizing the anaplastic variant in ependymomas.",
keywords = "Cancer biology, CDKN2A/p16, Ependymomas",
author = "S. Bortolotto and L. Chiado-Piat and P. Cavalla and I. Bosone and A. Mauro and D. Schiffer",
year = "2001",
doi = "10.1023/A:1012537105775",
language = "English",
volume = "54",
pages = "9--13",
journal = "Journal of Neuro-Oncology",
issn = "0167-594X",
publisher = "Springer New York LLC",
number = "1",

}

TY - JOUR

T1 - CDKN2A/p16 in ependymomas

AU - Bortolotto, S.

AU - Chiado-Piat, L.

AU - Cavalla, P.

AU - Bosone, I.

AU - Mauro, A.

AU - Schiffer, D.

PY - 2001

Y1 - 2001

N2 - Sixteen cases of ependymoma were studied for CDKN2A/p16 inactivation by immunohistochemistry using a p16 monoclonal antibody, by homozygous deletion (HD) assay and 5′CpG promoter methylation assay (methylation-specific PCR). Three out of 16 cases were p16 immuno-negative: two corresponded to grade II ependymomas and one to grade III. The latter ependymoma, characterized by a high Ki-67/MIB-1 LI, was the only one of the whole series to show CDKN2A HD. No promoter methylation was found in the two immuno-negative cases without CDKN2A HD. Alternative mechanisms, such as point mutations or alterations in p16 post-translational regulation, may be responsible for p16 inactivation. Since in our series just one out of eight anaplastic cases showed negative immunostaining and CDKN2A HD, p16/CDKN2A inactivation may not play an important role in the malignant transformation of ependymomas. Amplification of CCND1 and CDK4, p27/Kip1 degradation and TP53 mutations were previously studied by other authors and were demonstrated not to correlate with anaplasia. Up to date, molecular genetic studies have not been useful in recognizing the anaplastic variant in ependymomas.

AB - Sixteen cases of ependymoma were studied for CDKN2A/p16 inactivation by immunohistochemistry using a p16 monoclonal antibody, by homozygous deletion (HD) assay and 5′CpG promoter methylation assay (methylation-specific PCR). Three out of 16 cases were p16 immuno-negative: two corresponded to grade II ependymomas and one to grade III. The latter ependymoma, characterized by a high Ki-67/MIB-1 LI, was the only one of the whole series to show CDKN2A HD. No promoter methylation was found in the two immuno-negative cases without CDKN2A HD. Alternative mechanisms, such as point mutations or alterations in p16 post-translational regulation, may be responsible for p16 inactivation. Since in our series just one out of eight anaplastic cases showed negative immunostaining and CDKN2A HD, p16/CDKN2A inactivation may not play an important role in the malignant transformation of ependymomas. Amplification of CCND1 and CDK4, p27/Kip1 degradation and TP53 mutations were previously studied by other authors and were demonstrated not to correlate with anaplasia. Up to date, molecular genetic studies have not been useful in recognizing the anaplastic variant in ependymomas.

KW - Cancer biology

KW - CDKN2A/p16

KW - Ependymomas

UR - http://www.scopus.com/inward/record.url?scp=0035183193&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035183193&partnerID=8YFLogxK

U2 - 10.1023/A:1012537105775

DO - 10.1023/A:1012537105775

M3 - Article

C2 - 11763427

AN - SCOPUS:0035183193

VL - 54

SP - 9

EP - 13

JO - Journal of Neuro-Oncology

JF - Journal of Neuro-Oncology

SN - 0167-594X

IS - 1

ER -