Evidence map›Paper›PMID 22227013›Full record

ReviewBiochemical pharmacology2012

Acquired resistance to drugs targeting receptor tyrosine kinases.

Steven A Rosenzweig

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
8.5field-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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Identification of novel therapeutic target genes in acquired lapatinib-resistant breast cancer by integrative meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Receptor Tyrosine Kinase Signaling InvolvesTropical medicine and infectious disease · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  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

1 author at 1 institution in 1 country.

Steven A RosenzweigDepartment of Cell and Molecular Pharmacology & Experimental Therapeutics, Medical University of South Carolina, Charleston, 29425-5050, United States. rosenzsa@musc.edu
Medical University of South Carolina · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Jian Ouyang · 2009 to 2026
$42.7M
Receptor Crosstalk in HNSCC Metastatic ProgressionR01CA134845 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ROSENZWEIG, STEVEN ALAN · 2009 to 2016
$1.6M
NCI NIH HHS CA134845NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA134845
6 · The paper itself

Abstract

Development of resistance to chemotherapeutic drugs represents a significant hindrance to the effective treatment of cancer patients. The molecular mechanisms responsible have been investigated for over half a century and have revealed the lack of a single cause. Rather, a multitude of mechanisms have been delineated ranging from induction and expression of membrane transporters that pump drugs out of cells (multidrug resistance (MDR) phenotype), changes in the glutathione system and altered metabolism to name a few. Treatment of cancer patients/cancer cells with chemotherapeutic agents and/or molecularly targeted drugs is accompanied by acquisition of resistance to the treatment administered. Chemotherapeutic agent resistance was initially assumed to be due to induction of mutations leading to a resistant phenotype. This has also been true for molecularly targeted drugs. Considerable experience has been gained from the study of agents targeting the Bcr-Abl tyrosine kinase including imatinib, dasatinib and sunitinib. It is clear that mutations alone are not responsible for the many resistance mechanisms in play. Rather, additional mechanisms are involved, ranging from epigenetic changes, alternative splicing and the induction of alternative/compensatory signaling pathways. In this review, resistance to receptor tyrosine kinase inhibitors (RTKIs), RTK-directed antibodies and antibodies that inactivate ligands for RTKs are discussed. New approaches and concepts aimed at avoiding the generation of drug resistance will be examined. The recent observation that many RTKs, including the IGF-1R, are dependence receptors that induce apoptosis in a ligand-independent manner will be discussed and the implications this signaling paradigm has on therapeutic strategies will be considered.

Indexed as

Drug Resistance, NeoplasmAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsDrug Resistance, MultipleEpigenesis, GeneticErbB ReceptorsFusion Proteins, bcr-ablHumansNeoplasmsProtein Kinase InhibitorsProtein-Tyrosine KinasesReceptor, IGF Type 1Receptor Protein-Tyrosine KinasesSignal TransductionTrastuzumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsEGFR protein, humanErbB ReceptorsFusion Proteins, bcr-ablProtein Kinase InhibitorsProtein-Tyrosine KinasesReceptor, IGF Type 1Receptor Protein-Tyrosine KinasesTrastuzumab

Identifiers

PMID22227013
PMCPMC3299940
OpenAlexW2074136156

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.