ArticleMutation research2019
Frequent homozygous deletions of the CDKN2A locus in somatic cancer tissues.
Article in Mutation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Pitfalls in the evaluation of CDKN2A copy number status in meningioma.Journal of neuro-oncology · 2025Article
- Editorial: Methods in cancer genetics.Frontiers in oncology · 2023Article
- Fusion transcripts and their genomic breakpoints in polyadenylated and ribosomal RNA-minus RNA sequencing data.GigaScience · 2021Article
- Chromosomal translocations inactivating CDKN2A support a single path for malignant peripheral nerve sheath tumor initiation.Human genetics · 2021Article
- Clinical significance of CDKN2A homozygous deletion in combination with methylated MGMT status for IDH-wildtype glioblastoma.Cancer medicine · 2021Article
- Operationalization of Next-Generation Sequencing and Decision Support for Precision Oncology.JCO clinical cancer informatics · 2019Review
- Distribution of copy number variations and rearrangement endpoints in human cancers with a review of literature.Mutation researchReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Here we present and describe data on homozygous deletions (HD) of human CDKN2 A and neighboring regions on the p arm of Chromosome 9 from cancer genome sequences deposited on the online Catalogue of Somatic Mutations in Cancer (COSMIC) database. Although CDKN2 A HDs have been previously described in many cancers, this is a pan-cancer report of these aberrations with the aim to map the distribution of the breakpoints. We find that HDs of this locus have a median range of 1,255,650bps. When the deletion breakpoints were mapped on both the telomere and centromere proximal sides of CDKN2A, most of the telomere proximal breakpoints concentrate to a narrow region of the chromosome which includes the gene MTAP.. The centromere proximal breakpoints of the deletions are distributed over a wider chromosomal region. Furthermore, gene expression analysis shows that the deletions that include the CDKN2A region also include the MTAP region and this observation is tissue independent. We propose a model that may explain the origin of the telomere proximal CDKN2A breakpoints Finally, we find that HD distributions for at least three other loci, RB1, SMAD4 and PTEN are also not random.
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