Evidence map›Paper›PMID 23542173›Full record

ReviewOncogene2014

Signaling cross-talk in the resistance to HER family receptor targeted therapy.

H Yamaguchi, S-S Chang, J L Hsu, M-C Hung

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 114 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Wnt Signaling in the Breast: From Development to Disease.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Review
  16. 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
  17. Article
  18. Article
  19. Article
  20. Article

18 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

4 authors at 2 institutions in 1 country.

H YamaguchiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
S-S Chang1] Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] Graduate School of Biomedical Sciences, The University of Texas, Health Science Center at Houston, Houston, TX, USA.
J L Hsu1] Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University, Taichung, Taiwan [3] Department of Biotechnology, Asia University, Taichung, Taiwan.
M-C Hung1] Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA [2] Graduate School of Biomedical Sciences, The University of Texas, Health Science Center at Houston, Houston, TX, USA [3] Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University, Taichung, Taiwan [4] Department of Biotechnology, Asia University, Taichung, Taiwan.
The University of Texas MD Anderson Cancer Center · USThe University of Texas Health Science Center at Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tumor Progression of Nuclear EGFR in Breast CancerR01CA109311 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUNG, MIEN-CHIE · 2004 to 2014
$3.0M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA109311
6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) and human EGFR 2 (HER2) have an important role in the initiation and progression of various types of cancer. Inhibitors targeting these receptor tyrosine kinases are some of the most successful targeted anticancer drugs widely used for cancer treatment; however, cancer cells have mechanisms of intrinsic and acquired drug resistance that pose as major obstacles in drug efficacy. Extensive studies from both clinical and laboratory research have identified several molecular mechanisms underlying resistance. Among them is the role of signaling cross-talk between the EGFR/HER2 and other signaling pathways. In this review, we focus particularly on this signaling cross-talk at the receptor, mediator and effector levels, and further discuss alternative approaches to overcome resistance. In addition to well-recognized signaling cross-talk involved in the resistance, we also introduce the cross-talk between EGFR/HER2-mediated pathways and pathways triggered by other types of receptors, including those of the Notch, Wnt and TNFR/IKK/NF-κB pathways, and discuss the potential role of targeting this cross-talk to sensitize cells to EGFR/HER2 inhibitors.

Indexed as

AnimalsAntineoplastic AgentsErb-b2 Receptor Tyrosine KinasesErbB ReceptorsHumansMolecular Targeted TherapyNeoplasmsReceptor Cross-TalkSignal TransductionAntineoplastic AgentsErb-b2 Receptor Tyrosine KinasesErbB Receptors

Identifiers

PMID23542173
PMCPMC3874419
OpenAlexW2098983774

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.