Evidence map›Paper›PMID 24349829›Full record

ReviewCancer biology & medicine2013

Therapeutic resistance in cancer: microRNA regulation of EGFR signaling networks.

German G Gomez, Jill Wykosky, Ciro Zanca, Frank B Furnari, Webster K Cavenee

Open access · greenAbstract readReview
In one paragraph

Review in Cancer biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.6field-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.

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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Histological examination of the effects of epidermal growth factor on regeneration of acute peripheral nerve injuries on rabbit model.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2022
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Regulatory mechanisms of EGFR signalling during Drosophila eye development.Cellular and molecular life sciences : CMLS · 2016
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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.

German G GomezLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA.
Jill WykoskyLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA.
Ciro ZancaLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA.
Frank B FurnariLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA.
Webster K CaveneeLudwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA.
University of California, San Diego · USLudwig Cancer Research · US

Funding

Transgenic Mouse and Biobank CoreP01CA095616 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DEPINHO, RONALD ANTHONY · 2003 to 2012
$20.3M
Genotypic Interactions in Brain Cancer HeterogeneityR01NS080939 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FURNARI, FRANK · 2012 to 2022
$3.5M
NCI NIH HHS P01 CA095616NINDS NIH HHS R01 NS080939
6 · The paper itself

Abstract

Receptor tyrosine kinases (RTKs) such as the epidermal growth factor receptor (EGFR) regulate cellular homeostatic processes. EGFR activates downstream signaling cascades that promote tumor cell survival, proliferation and migration. Dysregulation of EGFR signaling as a consequence of overexpression, amplification and mutation of the EGFR gene occurs frequently in several types of cancers and many become dependent on EGFR signaling to maintain their malignant phenotypes. Consequently, concerted efforts have been mounted to develop therapeutic agents and strategies to effectively inhibit EGFR. However, limited therapeutic benefits to cancer patients have been derived from EGFR-targeted therapies. A well-documented obstacle to improved patient survival is the presence of EGFR-inhibitor resistant tumor cell variants within heterogeneous tumor cell masses. Here, we summarize the mechanisms by which tumors resist EGFR-targeted therapies and highlight the emerging role of microRNAs (miRs) as downstream effector molecules utilized by EGFR to promote tumor initiation, progression and that play a role in resistance to EGFR inhibitors. We also examine evidence supporting the utility of miRs as predictors of response to targeted therapies and novel therapeutic agents to circumvent EGFR-inhibitor resistance mechanisms.

Indexed as

Epidermal growth factor receptormicroRNAtherapeutic resistancetyrosine kinase inhibitors

Identifiers

PMID24349829
PMCPMC3860350
OpenAlexW1507295026

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.