Evidence map›Paper›PMID 31527477›Full record

ReviewCancers2019

Targeting Autophagy for Overcoming Resistance to Anti-EGFR Treatments.

Yoojung Kwon, Misun Kim, Hyun Suk Jung, Youngmi Kim, Dooil Jeoung

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.6field-weighted citation impact, top 2% 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, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Acquired multipleOncology letters · 2025
    Article
  4. Article
  5. Article
  6. Case report:Frontiers in oncology · 2024
    Article
  7. Article
  8. Modulating Glycolysis to Improve Cancer Therapy.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Essential role for STAT3/FOXM1/ATG7 signaling-dependent autophagy in resistance to Icotinib.Journal of experimental & clinical cancer research : CR · 2022
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

5 authors at 2 institutions in 1 country.

Yoojung KwonDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 24341, Korea. kkwon89@kangwon.ac.kr.
Misun KimDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 24341, Korea. misunjtl@naver.com.
Hyun Suk JungDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 24341, Korea. hsjung@kangwon.ac.kr.
Youngmi KimInstitute of New Frontier Research, College of Medicine, Hallym University, Chunchon 24251, Korea. kym8389@hanmail.net.
Dooil JeoungDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 24341, Korea. jeoungd@kangwon.ac.kr.
Kangwon National University · KRHallym University · KR

Funding

National Research Foundation Grants 2017M3A9G7072417National Research Foundation Grants 2017R1A2A2A05001029National Research Foundation Grants 2018R1D1A1B07043498
6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) plays critical roles in cell proliferation, tumorigenesis, and anti-cancer drug resistance. Overexpression and somatic mutations of EGFR result in enhanced cancer cell survival. Therefore, EGFR can be a target for the development of anti-cancer therapy. Patients with cancers, including non-small cell lung cancers (NSCLC), have been shown to response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) and anti-EGFR antibodies. However, resistance to these anti-EGFR treatments has developed. Autophagy has emerged as a potential mechanism involved in the acquired resistance to anti-EGFR treatments. Anti-EGFR treatments can induce autophagy and result in resistance to anti-EGFR treatments. Autophagy is a programmed catabolic process stimulated by various stimuli. It promotes cellular survival under these stress conditions. Under normal conditions, EGFR-activated phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase (AKT)/mammalian target of rapamycin (mTOR) signaling inhibits autophagy while EGFR/rat sarcoma viral oncogene homolog (RAS)/mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) signaling promotes autophagy. Thus, targeting autophagy may overcome resistance to anti-EGFR treatments. Inhibitors targeting autophagy and EGFR signaling have been under development. In this review, we discuss crosstalk between EGFR signaling and autophagy. We also assess whether autophagy inhibition, along with anti-EGFR treatments, might represent a promising approach to overcome resistance to anti-EGFR treatments in various cancers. In addition, we discuss new developments concerning anti-autophagy therapeutics for overcoming resistance to anti-EGFR treatments in various cancers.

Indexed as

anti-EGFR treatmentsautophagyco-targetingEGFR signaling

Identifiers

PMID31527477
PMCPMC6769649
OpenAlexW2974416662

What Socratic 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 Socratic graph.