Evidence map›Paper›PMID 29866745›Full record

ArticleMolecular cancer therapeutics2018

The XPO1 Inhibitor Selinexor Inhibits Translation and Enhances the Radiosensitivity of Glioblastoma Cells Grown

Amy Wahba, Barbara H Rath, John W O'Neill, Kevin Camphausen, Philip J Tofilon

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

35 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Small-Molecule Drugs in Pediatric Neuro-Oncology.Current oncology (Toronto, Ont.) · 2025
    Review
  6. Article
  7. Review
  8. The translatome of glioblastoma.Molecular oncology · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Pediatric Diffuse Midline Gliomas: An Unfinished Puzzle.Diagnostics (Basel, Switzerland) · 2022
    Review
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Amy WahbaRadiation Oncology Branch, National Cancer Institute, Bethesda, Maryland.
Barbara H RathRadiation Oncology Branch, National Cancer Institute, Bethesda, Maryland.
John W O'NeillRadiation Oncology Branch, National Cancer Institute, Bethesda, Maryland.
Kevin CamphausenRadiation Oncology Branch, National Cancer Institute, Bethesda, Maryland.
Philip J TofilonRadiation Oncology Branch, National Cancer Institute, Bethesda, Maryland. tofilonp@mail.nih.gov.
National Cancer Institute · US

Funding

The Synergy Between Radiotherapy and Molecularly Targeted AgentsZIASC010373 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI CAMPHAUSEN, KEVIN · 2009 to 2025
$22.2M
Microenvironmental regulation of glioblastoma radiosensitivityZIABC011372 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TOFILON, PHILIP · 2011 to 2025
$11.7M
Radiation-induced translational control of gene expressionZIABC011373 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TOFILON, PHILIP · 2011 to 2025
$11.7M
Intramural NIH HHS ZIA BC011372Intramural NIH HHS ZIA BC011373
6 · The paper itself

Abstract

Analysis of the radiation-induced translatome of glioblastoma stem-like cells (GSC) identified an interacting network in which XPO1 serves as a major hub protein. To determine whether this nuclear export protein provides a target for radiosensitization, we defined the effects of clinically relevant XPO1 inhibitor selinexor on the radiosensitivity of glioblastoma cells. As determined by clonogenic survival analysis, selinexor enhanced the radiosensitivity of GSCs but not normal fibroblast cell lines. On the basis of γH2AX foci and neutral comet analyses, selinexor inhibited the repair of radiation-induced DNA double-strand breaks in GSCs, suggesting that the selinexor-induced radiosensitization is mediated by an inhibition of DNA repair. Consistent with a role for XPO1 in the nuclear to cytoplasm export of rRNA, selinexor reduced 5S and 18S rRNA nuclear export in GSCs, which was accompanied by a decrease in gene translation efficiency, as determined from polysome profiles, as well as in protein synthesis. In contrast, rRNA nuclear export and protein synthesis were not reduced in normal cells treated with selinexor. Orthotopic xenografts initiated from a GSC line were then used to define the

Indexed as

AnimalsBrain NeoplasmsFemaleGlioblastomaHumansHydrazinesMiceMice, NudeRadiation ToleranceTriazolesHydrazinesselinexorTriazoles

Identifiers

PMID29866745
PMCPMC6072610
OpenAlexW2807564425

What OpenQuestion holds

Textmetadata
LicenceTDM
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.