Evidence map›Paper›PMID 30192422›Full record

ArticleBrain pathology (Zurich, Switzerland)2019

Alternative lengthening of telomeres, ATRX loss and H3-K27M mutations in histologically defined pilocytic astrocytoma with anaplasia.

Fausto J Rodriguez, Jacqueline A Brosnan-Cashman, Sariah J Allen, M Adelita Vizcaino, Caterina Giannini, Sandra Camelo-Piragua, Milad Webb, Marcus Matsushita, Nitin Wadhwani, Abeer Tabbarah and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% of its field
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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Molecular Biomarker Testing for the Diagnosis of Diffuse Gliomas.Archives of pathology & laboratory medicine · 2022
    Guideline
  2. Article
  3. Article
  4. Adult spinal cord diffuse midline gliomas with piloid features have a better prognosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  5. Article
  6. Article
  7. Paediatric low-grade glioma: the role of classical pathology in integrated diagnostic practice.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Pediatric-Like Brain Tumors in Adults.Advances and technical standards in neurosurgery · 2024
    Review
  12. Review
  13. Article
  14. Review
  15. Article
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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

19 authors at 11 institutions in 3 countries.

Fausto J RodriguezDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Jacqueline A Brosnan-CashmanDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Sariah J AllenDepartment of Pathology, UMAE, Pediatric Hospital CMN SXXI IMSS, Mexico City, Mexico.
M Adelita VizcainoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Caterina GianniniDepartment of Pathology, Mayo Clinic College of Medicine, Rochester, MN.
Sandra Camelo-PiraguaDepartment of Pathology, University of Michigan, Ann Arbor, MI.
Milad WebbDepartment of Pathology, University of Michigan, Ann Arbor, MI.
Marcus MatsushitaDepartment of Pathology, Barretos Cancer Hospital, Barretos, Brasil.
Nitin WadhwaniDepartment of Pathology and Laboratory Medicine, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL.
Abeer TabbarahDepartment of Pathology, American University of Beirut, Lebanon.
Dima HamidehDepartment of Pediatric Oncology, American University of Beirut, Lebanon.
Liqun JiangDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Liam ChenDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Leonidas D ArvanitisDepartment of Pathology, Rush University Medical Center, Chicago, IL.
Hussein H AlnajarDepartment of Pathology, Rush University Medical Center, Chicago, IL.
John R BarberDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
Alicia Rodríguez-VelascoDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Brent OrrDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN.
Christopher M HeaphyDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Johns Hopkins University · USAmerican University of Beirut · LBRush University Medical Center · USUniversity of Michigan–Ann Arbor · USJohns Hopkins Medicine · USLurie Children's Hospital · USMayo Clinic · USMexican Social Security Institute · MXSidney Kimmel Cancer Center · USSidney Kimmel Comprehensive Cancer Center · USSt. Jude Children's Research Hospital · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
TRAINING IN AREAS FUNDAMENTAL TO CANCER RESEARCHT32CA009110 · NCI · JOHNS HOPKINS UNIVERSITY · PI MATUNIS, MICHAEL J., WEERARATNA, ASHANI T · 1985 to 2025
$13.1M
Foundation for the National Institutes of Health 2T32CA009110-39A1NCI NIH HHS P30 CA006973NCI NIH HHS T32 CA009110
6 · The paper itself

Abstract

Anaplasia may be identified in a subset of tumors with a presumed pilocytic astrocytoma (PA) component or piloid features, which may be associated with aggressive behavior, but the biologic basis of this change remains unclear. Fifty-seven resections from 36 patients (23 M, 13 F, mean age 32 years, range 3-75) were included. A clinical diagnosis of NF1 was present in 8 (22%). Alternative lengthening of telomeres (ALT) was assessed by telomere-specific FISH and/or CISH. A combination of immunohistochemistry, DNA sequencing and FISH were used to study BRAF, ATRX, CDKN2A/p16, mutant IDH1 p.R132H and H3-K27M proteins. ALT was present in 25 (69%) cases and ATRX loss in 20 (57%), mostly in the expected association of ALT+/ATRX- (20/24, 83%) or ALT-/ATRX+ (11/11, 100%). BRAF duplication was present in 8 (of 26) (31%). H3-K27M was present in 5 of 32 (16%) cases, all with concurrent ATRX loss and ALT. ALT was also present in 9 (of 11) cases in the benign PA precursor, 7 of which also had ATRX loss in both the precursor and the anaplastic tumor. In a single pediatric case, ALT and ATRX loss developed in the anaplastic component only, and in another adult case, ALT was present in the PA-A component only, but ATRX was not tested. Features associated with worse prognosis included subtotal resection, adult vs. pediatric, presence of a PA precursor preceding a diagnosis of anaplasia, necrosis, presence of ALT and ATRX expression loss. ALT and ATRX loss, as well as alterations involving the MAPK pathway, are frequent in PA with anaplasia at the time of development of anaplasia or in their precursors. Additionally, a small subset of PA with anaplasia have H3-K27M mutations. These findings further support the concept that PA with anaplasia is a neoplasm with heterogeneous genetic features and alterations typical of both PA and diffuse gliomas.

Indexed as

AdolescentAdultAgedAnaplasiaAstrocytomaBiomarkers, TumorBrainBrain NeoplasmsChildChild, PreschoolFemaleGliomaHistonesHumansImmunohistochemistryIn Situ Hybridization, FluorescenceATRX protein, humanBiomarkers, TumorHistonesNuclear ProteinsX-linked Nuclear Proteinalternative lengthening of telomeresATRXgliomaH3-K27Mpilocytic astrocytoma

Identifiers

PMID30192422
PMCPMC6314894
OpenAlexW2889619176

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.