Evidence map›Paper›PMID 40064710›Full record

ReviewMedical oncology (Northwood, London, England)2025

Targeting EGFR and PI3K/mTOR pathways in glioblastoma: innovative therapeutic approaches.

Gursimran Singh, Rohit, Pankaj Kumar, Khadga Raj Aran

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
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  6. Review
  7. Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
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  14. PI3 K/AKT/mTOR pathway and its role in breast cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  15. Review
  16. Article
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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

4 authors.

Gursimran SinghDepartment of Pharmacy Practice, ISF College of Pharmacy (an Autonomous College), Moga, Punjab, 142001, India.
RohitResearch Scholar, I.K. Gujral Punjab Technical University, Kapurthala, Punjab, 144603, India.
Pankaj KumarDepartment of Pharmacology, Himachal Institute of Pharmaceutical Education and Research (HIPER), Tehsil-Nadaun, Hamirpur, Himachal Pradesh, 177033, India.
Khadga Raj AranNeuropharmacology Division, Department of Pharmacology, ISF College of Pharmacy (an Autonomous College), Moga, Punjab, 142001, India. bishalarann@gmail.com.ORCID http://orcid.org/0000-0002-2450-2975

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) stands as the most aggressive form of primary brain cancer in adults, characterized by its rapid growth, invasive nature, and a robust propensity to induce angiogenesis, forming new blood vessels to sustain its expansion. GBM arises from astrocytes, star-shaped glial cells, and despite significant progress in understanding its molecular mechanisms, its prognosis remains grim. It is frequently associated with mutations or overexpression of the epidermal growth factor receptor (EGFR), which initiates several downstream signaling pathways. Dysregulation of key signaling pathways, such as EGFR/PTEN/AKT/mTOR, drives tumorigenesis, promotes metastasis and leads to treatment resistance. The modest survival benefits of the conventional treatment of surgical resection followed by radiation and chemotherapy underscore the pressing need for innovative therapeutic approaches. In most the tumor, overexpression of EGFR is found associated with GBM and mutations in its several variants are important for promoting ongoing mitogenic signaling and tumor growth. This receptor inhibits apoptosis and promotes cell survival and proliferation by activating downstream PI3K/AKT/mTOR pathways. This route is typically blocked by PTEN, a crucial tumor suppressor, however, GBM frequently results in abnormalities in this protein. The aim of this review is to explore the molecular foundations of GBM, with a focus on the EGFR and PI3K/mTOR pathways and their impact on tumor behavior. Additionally, this review highlights EGFR and PI3K/AKT/mTOR inhibitors currently in clinical and preclinical trials, addressing treatment resistance, challenges, and future directions.

Indexed as

Antineoplastic AgentsBrain NeoplasmsErbB ReceptorsGlioblastomaPhosphoinositide-3 Kinase InhibitorsTOR Serine-Threonine KinasesAnimalsHumansMolecular Targeted TherapyPhosphatidylinositol 3-KinasesSignal TransductionAntineoplastic AgentsEGFR protein, humanErbB ReceptorsMTOR protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsTOR Serine-Threonine KinasesAngiogenesisEGRFGlioblastomaMTORPI3KPTEN

Identifiers

What Socratic 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 Socratic graph.