ArticleBrain pathology (Zurich, Switzerland)1998
Frequent inactivation of CDKN2A and rare mutation of TP53 in PCNSL.
Article in Brain pathology (Zurich, Switzerland), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 74 citations in OpenAlex.
- Trial
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- Liquid biopsy for improving diagnosis and monitoring of CNS lymphomas: A RANO review.Neuro-oncology · 2024Review
- The Molecular Landscape of Primary CNS Lymphomas (PCNSLs) in Children and Young Adults.Cancers · 2024Article
- Primary central nervous system lymphoma.Nature reviews. Disease primers · 2023Review
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- Rare cases of primary central nervous system anaplastic variant of diffuse large B-cell lymphoma.Diagnostic pathology · 2019Article
- Introduction of novel agents in the treatment of primary CNS lymphoma.Neuro-oncology · 2019Review
- TP53 hotspot mutations are predictive of survival in primary central nervous system lymphoma patients treated with combination chemotherapy.Acta neuropathologica communications · 2016Article
- Modern concepts in the biology, diagnosis, differential diagnosis and treatment of primary central nervous system lymphoma.Leukemia · 2011Review
- Differential micro-RNA expression in primary CNS and nodal diffuse large B-cell lymphomas.Neuro-oncology · 2011Article
- Significance of CDKN2A gene A148T variant in patients with bladder cancer.Central European journal of urology · 2011Article
- Array-based DNA methylation profiling of primary lymphomas of the central nervous system.BMC cancer · 2009Article
- Biology and treatment of primary central nervous system lymphoma.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
- Epigenetic inactivation of tumor suppressor genes in hematologic malignancies.International journal of hematology · 2004Review
- Characterization of gene expression profiles associated with glioma progression using oligonucleotide-based microarray analysis and real-time reverse transcription-polymerase chain reaction.The American journal of pathology · 2003Article
- Analysis of chromosomal copy number changes and oncoprotein expression in primary central nervous system lymphomas: frequent loss of chromosome arm 6q.Virchows Archiv : an international journal of pathology · 2003Article
- Homozygous deletion of INK4a/ARF genes and overexpression of bcl-2 in relation with poor prognosis in immunocompetent patients with primary central nervous system lymphoma of the diffuse large B-cell type.Journal of neuro-oncology · 2001Article
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Twenty primary central nervous system lymphomas (PCNSL) from immunocompetent patients (nineteen B-cell lymphomas and one T-cell lymphoma) were investigated for genetic alterations and/or expression of the genes BCL2, CCND1, CDK4, CDKN1A, CDKN2A, MDM2, MYC, RB1, REL, and TP53. The gene found to be altered most frequently was CDKN2A. Eight tumors (40%) showed homozygous and two tumors (10%) hemizygous CDKN2A deletions. Furthermore, methylation analysis of six PCNSL without homozygous CDKN2A loss revealed methylation of the CpG island within exon 1 of CDKN2A in three instances. Reverse transcription PCR analysis of CDKN2A mRNA expression was performed for 11 tumors and showed either no or weak signals. Similarly, immunocytochemistry for the CDKN2A gene product (p16) remained either completely negative or showed expression restricted to single tumor cells. None of the PCNSL showed amplification of CDK4. Similarly, investigation of CCND1 revealed no amplification, rearrangement or overexpression. The retinoblastoma protein was strongly expressed in all tumors. Only one PCNSL showed a mutation of the TP53 gene, i.e., a missense mutation at codon 248 (CGG to TGG:Arg to Trp). No evidence of BCL2 gene rearrangement was found in 11 tumors investigated. The bcl-2 protein, however, was strongly expressed in most tumors. None of the 20 PCNSL demonstrated gene amplification of MDM2, MYC or REL. In summary, inactivation of CDKN2A by either homozygous deletion or DNA methylation represents an important molecular mechanism in PCNSL. Mutation of the TP53 gene and alterations of the other genes investigated appear to be of minor significance in these tumors.
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