Evidence map›Paper›PMID 39042515›Full record

ArticleJournal of neuropathology and experimental neurology2024

Comparing loss of p16 and MTAP expression in detecting CDKN2A homozygous deletion in pleomorphic xanthoastrocytoma.

M Adelita Vizcaino, Caterina Giannini, Rachael A Vaubel, Aivi T Nguyen, Jorge A Trejo-Lopez, Aditya Raghunathan, Sarah M Jenkins, Robert B Jenkins, Cinthya J Zepeda Mendoza

Abstract readComparative Study
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Association of CDKN2A/B and MTAP deletions in adult-type diffuse gliomas.Journal of neuropathology and experimental neurology · 2026
    Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

M Adelita VizcainoDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.ORCID 0000-0003-4636-8743
Caterina GianniniDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.
Rachael A VaubelDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.
Aivi T NguyenDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.
Jorge A Trejo-LopezDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.
Aditya RaghunathanDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.
Sarah M JenkinsDepartment of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, United States.
Robert B JenkinsDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.
Cinthya J Zepeda MendozaDepartment of Laboratory of Medicine and Pathology, Mayo Clinic, Rochester, MN, United States.

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Lila J. Rutten · 1985 to 2026
$151.3M
Mayo Clinic Department of Laboratory Medicine and Pathology 23-03Mayo Clinic Department of Laboratory Medicine and Pathology AP No. 23-03Mayo Clinic institutional 07-3653Mayo Clinic institutional funding IRB No. 07-3653NCI NIH HHS P30 CA015083
6 · The paper itself

Abstract

Pleomorphic xanthoastrocytomas (PXAs) harbor CDKN2A homozygous deletion in >90% of cases, resulting in loss of p16 expression by immunohistochemistry. Considering the proximity of MTAP to CDKN2A and their frequent concurrent deletions, loss of MTAP expression may be a surrogate for CDKN2A homozygous deletion. We evaluated p16 and MTAP expression in 38 patient PXAs (CNS WHO grade 2: n = 23, 60.5%; grade 3: n = 15, 39.5%) with available chromosomal microarray data to determine whether MTAP can be utilized independently or in combination with p16 to predict CDKN2A status. CDKN2A, CDKN2B, and MTAP homozygous deletion were present in 37 (97.4%), 36 (94.7%), and 25 (65.8%) cases, respectively. Expression of p16 was lost in 35 (92.1%) cases, equivocal in one (2.6%), and failed in 2 (5.3%), while MTAP expression was lost in 27 (71.1%) cases, retained in 10 (26.3%), and equivocal in one (2.6%). This yielded a sensitivity of 94.6% for p16 and 73.0% for MTAP in detecting CDKN2A homozygous deletion through immunohistochemistry. MTAP expression was lost in the 2 cases with failed p16 staining (combined sensitivity of 100%). Our findings demonstrate that combined p16 and MTAP immunostains correctly detect CDKN2A homozygous deletion in PXA, while MTAP expression alone shows reduced sensitivity.

Indexed as

AstrocytomaBrain NeoplasmsCyclin-Dependent Kinase Inhibitor p16AdolescentAdultAgedChildFemaleGene DeletionHomozygoteHumansMaleMiddle AgedPurine-Nucleoside PhosphorylaseYoung Adult5'-methylthioadenosine phosphorylaseCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Purine-Nucleoside PhosphorylaseCDKN2A homozygous deletionchromosomal copy number variationImmunohistochemistryMTAPp16pleomorphic xanthoastrocytoma

Identifiers

PMID39042515
PMCPMC11576554

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.