Evidence map›Paper›PMID 24335351›Full record

ReviewCell cycle (Georgetown, Tex.)2014

EGFR signaling and autophagy dependence for growth, survival, and therapy resistance.

Barry Jutten, Kasper M A Rouschop

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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.

NCT02378532 phase1completednot on this mapstarted 2016, after this paper: background citation

A Phase I Trial for the Addition of Chloroquine, an Autophagy Inhibitor, to Concurrent Chemoradiation for Newly Diagnosed Glioblastoma

TypeinterventionalSponsorMaastricht Radiation OncologyRan2016 to 2019Enrolled13ConditionsGlioblastoma MultiformeArmsChloroquine, Radiotherapy, Temozolomide
NCT02432417 phase2withdrawnnot on this mapstarted 2023, after this paper: background citation

A Phase II Randomized Controlled Trial for the Addition of Chloroquine, an Autophagy Inhibitor, to Concurrent Chemoradiation for Newly Diagnosed Glioblastoma

TypeinterventionalSponsorMaastricht Radiation OncologyRan2023 to 2023Enrolled0ConditionsGlioblastoma, Astrocytoma, Grade IVArmsChloroquine
3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
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  10. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
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17 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

2 authors at 2 institutions in 2 countries.

Barry JuttenMaastricht Radiation Oncology (MaastRO) Lab; GROW - School for Oncology and Developmental Biology; Maastricht University; Maastricht, the Netherlands.
Kasper M A RouschopMaastricht Radiation Oncology (MaastRO) Lab; GROW - School for Oncology and Developmental Biology; Maastricht University; Maastricht, the Netherlands.
Children's Oncology Group · CHMaastro Clinic · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) is amplified or mutated in various human epithelial tumors. Its expression and activation leads to cell proliferation, differentiation, and survival. Consistently, EGFR amplification or expression of EGFR variant 3 (EGFRvIII) is associated with resistance to conventional cancer therapy through activation of pro-survival signaling and DNA-repair mechanisms. EGFR targeting has successfully been exploited as strategy to increase treatment efficacy. Nevertheless, these targeting strategies have only been proven effective in a limited percentage of human tumors. Recent knowledge indicates that EGFR deregulated tumors display differences in autophagy and dependence on autophagy for growth and survival and the use of autophagy to increase resistance to EGFR-targeting drugs. In this review the dependency on autophagy and its role in mediating resistance to EGFR-targeting agents will be discussed. Considering the current knowledge, autophagy inhibition could provide a novel strategy to enhance therapy efficacy in treatment of EGFR deregulated tumors.

Indexed as

Signal TransductionAntineoplastic AgentsAutophagyCell DifferentiationCell ProliferationCell SurvivalDrug Resistance, NeoplasmErbB ReceptorsHumansNeoplasmsAntineoplastic AgentsEGFR protein, humanErbB Receptorsautophagycancer treatmentEGFREGFRvIIIhypoxiametabolic stressmutationsstarvationtreatment resistance

Identifiers

PMID24335351
PMCPMC3925733
OpenAlexW2106426363

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.