Evidence map›Paper›PMID 34206026›Full record

ReviewCancers2021

EGFR in Cancer: Signaling Mechanisms, Drugs, and Acquired Resistance.

Mary Luz Uribe, Ilaria Marrocco, Yosef Yarden

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 337 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
337citing papers in PubMed, 2 pooled it
45.4field-weighted citation impact, top 1% 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

337 citing papers in PubMed, 2 syntheses or guidelines pooled it, 528 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Observational
  18. Review
  19. Ligand regulation and function of preformed EGFR dimers.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  20. Article

277 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

3 authors at 1 institution in 1 country.

Mary Luz UribeDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.ORCID 0000-0002-6567-2436
Ilaria MarroccoDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.
Yosef YardenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.
Weizmann Institute of Science · IL

Funding

Dr. Miriam and Sheldon G. Adelson Medical Research Foundation 15FP7 Ideas: European Research Council 740469Israel Cancer Research Fund 18-304-MIIsrael Science Foundation 1931/20Samuel Waxman Cancer Research Foundation 432/2020
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) has served as the founding member of the large family of growth factor receptors harboring intrinsic tyrosine kinase function. High abundance of EGFR and large internal deletions are frequently observed in brain tumors, whereas point mutations and small insertions within the kinase domain are common in lung cancer. For these reasons EGFR and its preferred heterodimer partner, HER2/ERBB2, became popular targets of anti-cancer therapies. Nevertheless, EGFR research keeps revealing unexpected observations, which are reviewed herein. Once activated by a ligand, EGFR initiates a time-dependent series of molecular switches comprising downregulation of a large cohort of microRNAs, up-regulation of newly synthesized mRNAs, and covalent protein modifications, collectively controlling phenotype-determining genes. In addition to microRNAs, long non-coding RNAs and circular RNAs play critical roles in EGFR signaling. Along with driver mutations, EGFR drives metastasis in many ways. Paracrine loops comprising tumor and stromal cells enable EGFR to fuel invasion across tissue barriers, survival of clusters of circulating tumor cells, as well as colonization of distant organs. We conclude by listing all clinically approved anti-cancer drugs targeting either EGFR or HER2. Because emergence of drug resistance is nearly inevitable, we discuss the major evasion mechanisms.

Indexed as

anti-cancer drugdrug resistancegrowth factorsignaling pathwaysignal transductiontranscription networktyrosine kinase

Identifiers

PMID34206026
PMCPMC8197917
OpenAlexW3169321271

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.