Evidence map›Paper›PMID 27588472›Full record

ArticleOncotarget2016

Targeting hexokinase 2 enhances response to radio-chemotherapy in glioblastoma.

Alenoush Vartanian, Sameer Agnihotri, Mark R Wilson, Kelly E Burrell, Peter D Tonge, Amir Alamsahebpour, Shahrzad Jalali, Michael S Taccone, Sheila Mansouri, Brian Golbourn and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 7% 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, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Frontiers in immunology · 2026
    Article
  6. Review
  7. Review
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  13. Interplay between altered metabolism and DNA damage and repair in ovarian cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  14. Article
  15. The PI3K/Akt Pathway and Glucose Metabolism: A Dangerous Liaison in Cancer.International journal of biological sciences · 2024
    Review
  16. Glioblastoma Metabolism: Insights and Therapeutic Strategies.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Review
  19. Article
  20. 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

12 authors at 1 institution in 1 country.

Alenoush VartanianMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Sameer AgnihotriMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Mark R WilsonMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Kelly E BurrellMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Peter D TongeMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Amir AlamsahebpourMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Shahrzad JalaliMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Michael S TacconeMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Sheila MansouriMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Brian GolbournArthur and Sonia Labatt Brain Tumour Research Centre, SickKids Hospital, Toronto, Canada.
Kenneth D AldapeMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
Gelareh ZadehMacFeeters Hamilton Center for Neuro-Oncology, Toronto, Canada.
SickKids Foundation · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

First-line cancer therapies such as alkylating agents and radiation have limited survival benefits for Glioblastoma (GBM) patients. Current research strongly supports the notion that inhibition of aberrant tumor metabolism holds promise as a therapeutic strategy when used in combination with radiation and chemotherapy. Hexokinase 2 (HK2) has been shown to be a key driver of altered metabolism in GBM, and presents an attractive therapeutic target. To date, no study has fully assessed the therapeutic value of targeting HK2 as a mechanism to sensitize cells to standard therapy, namely in the form of radiation and temozolomide (TMZ). Using cell lines and primary cultures of GBM, we showed that inducible knockdown of HK2 altered tumor metabolism, which could not be recapitulated by HK1 or HK3 loss. HK2 loss diminished both in vivo tumor vasculature as well as growth within orthotopic intracranial xenograft models of GBMs, and the survival benefit was additive with radiation and TMZ. Radio-sensitization following inhibition of HK2 was mediated by increased DNA damage, and could be rescued through constitutive activation of ERK signaling. This study supports HK2 as a potentially effective therapeutic target in GBM.

Indexed as

RNA InterferenceXenograft Model Antitumor AssaysAnimalsAntineoplastic Agents, AlkylatingBrain NeoplasmsCell Line, TumorCell ProliferationChemoradiotherapyDacarbazineDNA DamageGlioblastomaHEK293 CellsHexokinaseHumansMaleMAP Kinase Signaling SystemAntineoplastic Agents, AlkylatingDacarbazineHexokinaseHK2 protein, humanTemozolomidecell signalingglioblastomametabolismnovel treatments

Identifiers

PMID27588472
PMCPMC5342495
OpenAlexW2509057822

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.