Evidence map›Paper›PMID 26967052›Full record

ReviewOncotarget2016

PI3K/Akt/mTOR signaling pathway and targeted therapy for glioblastoma.

Xiaoman Li, Changjing Wu, Nianci Chen, Huadi Gu, Allen Yen, Liu Cao, Enhua Wang, Liang Wang

Abstract readReview
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 345 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
345citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

345 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Oncoimmunology · 2026
    Article
  4. Review
  5. Article
  6. The novel [RSC advances · 2026
    Article
  7. Review
  8. Article
  9. Rapamycin Targets Cancer Stem Cells to Decrease Cisplatin Resistance in a Head and Neck Cancer Mouse Xenograft Model.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026
    Article
  10. Mechanisms, Microenvironments, and Models: Understanding Therapeutic Resistance in Glioblastoma.International journal of radiation oncology, biology, physics · 2026
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Role of CRISPR and Its Therapeutic Applications in Glioblastoma.International journal of molecular sciences · 2026
    Review

285 more citing papers are in PubMed but not listed here.

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

8 authors.

Xiaoman LiKey Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
Changjing WuKey Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
Nianci ChenClass 9 of The 97th Clinical Medicine of Seven-Year Program, China Medical University, Shenyang, China.
Huadi GuDepartment of Pathology, The College of Basic Medical Sciences, China Medical University, Shenyang, China.
Allen YenSchool of Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
Liu CaoKey Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China.
Enhua WangDepartment of Pathology, The College of Basic Medical Sciences, China Medical University, Shenyang, China.
Liang WangDepartment of Pathology, The College of Basic Medical Sciences, China Medical University, Shenyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiform (GBM) is the most common malignant glioma of all the brain tumors and currently effective treatment options are still lacking. GBM is frequently accompanied with overexpression and/or mutation of epidermal growth factor receptor (EGFR), which subsequently leads to activation of many downstream signal pathways such as phosphatidylinositol 3-kinase (PI3K)/Akt/rapamycin-sensitive mTOR-complex (mTOR) pathway. Here we explored the reason why inhibition of the pathway may serve as a compelling therapeutic target for the disease, and provided an update data of EFGR and PI3K/Akt/mTOR inhibitors in clinical trials.

Indexed as

Molecular Targeted TherapyPhosphoinositide-3 Kinase InhibitorsAnimalsAntineoplastic AgentsBrain NeoplasmsErbB ReceptorsGlioblastomaHumansPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTreatment OutcomeAntineoplastic AgentsEGFR protein, humanErbB ReceptorsMTOR protein, humanPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesEGFRglioblastomaPI3K/Akt/mTOR pathwaytargeted therapy

Identifiers

PMID26967052
PMCPMC5078108

What OpenQuestion holds

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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.