Evidence map›Paper›PMID 31280432›Full record

ArticleJournal of neuro-oncology2019

Absent in melanoma 2 regulates tumor cell proliferation in glioblastoma multiforme.

P A Chen, G Shrivastava, E F Balcom, B A McKenzie, J Fernandes, W G Branton, B M Wheatley, K Petruk, F K H van Landeghem, Christopher Power

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023
    Review
  8. Review
  9. Article
  10. Review
  11. Pattern recognition receptors in health and diseases.Signal transduction and targeted therapy · 2021
    Review
  12. Article
  13. Review
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

10 authors at 1 institution in 1 country.

P A ChenDepartment of Medicine (Neurology), HMRC 6-11, University of Alberta, Edmonton, AB, Canada.
G ShrivastavaDepartment of Medicine (Neurology), HMRC 6-11, University of Alberta, Edmonton, AB, Canada.
E F BalcomDepartment of Medicine (Neurology), HMRC 6-11, University of Alberta, Edmonton, AB, Canada.
B A McKenzieDepartment of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB, Canada.
J FernandesDepartment of Medicine (Neurology), HMRC 6-11, University of Alberta, Edmonton, AB, Canada.
W G BrantonDepartment of Medicine (Neurology), HMRC 6-11, University of Alberta, Edmonton, AB, Canada.
B M WheatleyDepartment of Surgery, University of Alberta, Edmonton, AB, Canada.
K PetrukDepartment of Surgery, University of Alberta, Edmonton, AB, Canada.
F K H van LandeghemLaboratory Medicine & Pathology, University of Alberta, Edmonton, AB, Canada.
Christopher PowerDepartment of Medicine (Neurology), HMRC 6-11, University of Alberta, Edmonton, AB, Canada. chris.power@ualberta.ca.ORCID http://orcid.org/0000-0002-5131-9711
University of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionInflammation is a key aspect of glioblastoma multiforme (GBM) although it remains unclear how it contributes to GBM pathogenesis. Inflammasomes are intracellular multi-protein complexes that are involved in innate immunity and are activated by cellular stress, principally in macrophages. This study examined the expression of inflammasome-associated genes in GBM, particularly absent in melanoma 2 (AIM2).

methodsTissue samples from surgically-resected GBM tumors (n = 10) were compared to resected brain specimens from patients with epilepsy (age- and sex-matched Other Disease Controls (ODC, n=5)) by qRT-PCR, western blotting and immunofluorescence. Gene expression studies in human astrocytoma U251 cells were performed and the effects of deleting the absent in melanoma 2 (AIM2) gene using the CRISPR-Cas9 system were analyzed.

resultsGBM tissues showed significantly elevated expression of multiple immune (CD3E, CD163, CD68, MX1, ARG1) and inflammasome (AIM2, NLRP1, IL18, CASP1, and IL-33) genes compared to ODC tissues, without induction of IL1B, IFNG or TNFA. An insert-containing AIM2 variant transcript was highly expressed in GBM tissues and in U251 cells. AIM2 immunoreactivity was concentrated in the tumor core in the absence of PCNA immunodetection and showed a predominant 52 kDa immunoreactive band on western blot. Deletion of AIM2 resulted in significantly enhanced proliferation of U251 cells, which also displayed increased resistance to temozolomide treatment.

conclusionsGBM tumors express a distinct profile of inflammasome-associated genes in a tumor-specific manner. AIM2 expression in tumor cells suppressed cell proliferation while also conferring increased susceptibility to contemporary GBM therapy.

Indexed as

Cell ProliferationBiomarkers, TumorCase-Control StudiesDNA-Binding ProteinsGlioblastomaHumansInflammasomesInflammationRNA, Small InterferingTumor Cells, CulturedAIM2 protein, humanBiomarkers, TumorDNA-Binding ProteinsInflammasomesRNA, Small InterferingAIM2GlioblastomaInflammasomeTemozolomideTranscript insertion

Identifiers

PMID31280432
OpenAlexW2955558978

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.