Evidence map›Paper›PMID 32443649›Full record

ReviewCancers2020

Radiosensitising Cancer Using Phosphatidylinositol-3-Kinase (PI3K), Protein Kinase B (AKT) or Mammalian Target of Rapamycin (mTOR) Inhibitors.

Kasun Wanigasooriya, Robert Tyler, Joao D Barros-Silva, Yashashwi Sinha, Tariq Ismail, Andrew D Beggs

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025
    Review
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  7. Article
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  9. Article
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  12. Review
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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

6 authors at 2 institutions in 1 country.

Kasun WanigasooriyaCollege of Medical and Dental Sciences, Institute of Cancer and Genomic Science, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Robert TylerThe New Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Edgbaston, Birmingham B15 2TH, UK.
Joao D Barros-SilvaCollege of Medical and Dental Sciences, Institute of Cancer and Genomic Science, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Yashashwi SinhaCollege of Medical and Dental Sciences, Institute of Cancer and Genomic Science, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Tariq IsmailThe New Queen Elizabeth Hospital, University Hospitals Birmingham NHS Foundation Trust, Edgbaston, Birmingham B15 2TH, UK.
Andrew D BeggsCollege of Medical and Dental Sciences, Institute of Cancer and Genomic Science, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
University Hospitals Birmingham NHS Foundation Trust · GBUniversity of Birmingham · GB

Funding

Cancer Research UK 24430Medical Research Council MR/M009157/1
6 · The paper itself

Abstract

Radiotherapy is routinely used as a neoadjuvant, adjuvant or palliative treatment in various cancers. There is significant variation in clinical response to radiotherapy with or without traditional chemotherapy. Patients with a good response to radiotherapy demonstrate better clinical outcomes universally across different cancers. The PI3K/AKT/mTOR pathway upregulation has been linked to radiotherapy resistance. We reviewed the current literature exploring the role of inhibiting targets along this pathway, in enhancing radiotherapy response. We identified several studies using in vitro cancer cell lines, in vivo tumour xenografts and a few Phase I/II clinical trials. Most of the current evidence in this area comes from glioblastoma multiforme, non-small cell lung cancer, head and neck cancer, colorectal cancer, and prostate cancer. The biological basis for radiosensitivity following pathway inhibition was through inhibited DNA double strand break repair, inhibited cell proliferation, enhanced apoptosis and autophagy as well as tumour microenvironment changes. Dual PI3K/mTOR inhibition consistently demonstrated radiosensitisation of all types of cancer cells. Single pathway component inhibitors and other inhibitor combinations yielded variable outcomes especially within early clinical trials. There is ample evidence from preclinical studies to suggest that direct pharmacological inhibition of the PI3K/AKT/mTOR pathway components can radiosensitise different types of cancer cells. We recommend that future in vitro and in vivo research in this field should focus on dual PI3K/mTOR inhibitors. Early clinical trials are needed to assess the feasibility and efficacy of these dual inhibitors in combination with radiotherapy in brain, lung, head and neck, breast, prostate and rectal cancer patients.

Indexed as

AKTchemoradiotherapyglioblastoma multiformehead and neck cancermTOR inhibitorsnon-small cell lung cancerPI3Kprostate cancerradiosensitiserrectal cancer

Identifiers

PMID32443649
PMCPMC7281073
OpenAlexW3025069247

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.