Evidence map›Paper›PMID 22229414›Full record

ReviewCurrent medicinal chemistry2012

Pharmacological strategies to overcome HER2 cross-talk and Trastuzumab resistance.

R Nahta

Open access · greenAbstract readReview
In one paragraph

Review in Current medicinal chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. JCO precision oncology · 2025
    Article
  4. Evidence for cytoprotective autophagy in response to HER2-targeted monoclonal antibodies.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  5. Article
  6. Review
  7. Combining Neratinib with CDK4/6, mTOR, and MEK Inhibitors in Models of HER2-positive Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  8. Article
  9. Article
  10. International journal of molecular sciences · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

1 author at 1 institution in 1 country.

R NahtaDepartments of Pharmacology, Emory University School of Medicine, USA. rnahta@emory.edu
Emory University · US

Funding

HER-2/IGF-IR cross-talk and Herceptin resistanceK01CA118174 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI NAHTA, RITA · 2006 to 2010
$807k
NCI NIH HHS 3K01CA118174-5S1NCI NIH HHS K01 CA118174NCI NIH HHS K01CA118174
6 · The paper itself

Abstract

Approximately 20-30% of breast cancers show increased expression of the HER2 receptor tyrosine kinase. Trastuzumab (Herceptin) is a clinically approved anti-HER2 monoclonal antibody. Many patients with HER2-overexpressing metastatic breast cancer respond to trastuzumab; however, a subset display primary drug resistance. In addition, many patients who initially respond to trastuzumab ultimately develop disease progression. Multiple molecular mechanisms contributing to trastuzumab resistance have been proposed in the literature. These mechanisms include cross-signaling from related HER/erbB receptors and compensatory signaling from receptors outside of the HER/erbB family, including receptors for insulin-like growth factor-I, vascular endothelial growth factor, and transforming growth factor beta. The major downstream signaling pathway activated by HER2 cross-talk is PI3K/mTOR, and a potential integrator of receptor cross-talk is Src-focal adhesion kinase (FAK) signaling. PI3K, Src, and FAK have independently been implicated in trastuzumab resistance. In this review, we will discuss pharmacological inhibition of HER2 cross-talk as a strategy to treat trastuzumab-refractory HER2-overexpresssing breast cancer.

Indexed as

Drug DesignAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBreast NeoplasmsChemistry, PharmaceuticalDimerizationDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesFemaleHumansReceptor Cross-TalkReceptor, ErbB-3TrastuzumabAntibodies, Monoclonal, HumanizedAntineoplastic AgentsErb-b2 Receptor Tyrosine KinasesReceptor, ErbB-3Trastuzumab

Identifiers

PMID22229414
PMCPMC3294049
OpenAlexW2055831769

What OpenQuestion holds

Textmetadata
LicenceTDM
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.