Evidence map›Paper›PMID 27450453›Full record

ArticleCancer research2016

JNK Pathway Activation Modulates Acquired Resistance to EGFR/HER2-Targeted Therapies.

Simin Manole, Edward J Richards, Aaron S Meyer

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. JNK Pathway in CNS Pathologies.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. Cancer biotherapy & radiopharmaceuticals · 2019
    Article
  17. Article
  18. A biomaterial screening approach reveals microenvironmental mechanisms of drug resistance.Integrative biology : quantitative biosciences from nano to macro · 2017
    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

3 authors at 2 institutions in 1 country.

Simin ManoleKoch Institute for Integrative Cancer Research at MIT, Cambridge, Massachusetts.
Edward J RichardsKoch Institute for Integrative Cancer Research at MIT, Cambridge, Massachusetts.
Aaron S MeyerKoch Institute for Integrative Cancer Research at MIT, Cambridge, Massachusetts a@ameyer.me.
Koch Institute for Integrative Cancer Research At MITAllen Institute · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Jacqueline A. Lees · 1985 to 2026
$93.9M
Adapter-Layer RTK Signaling: Basic Understanding & Targeted DrugResistanceDP5OD019815 · OD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MEYER, AARON SAMUEL · 2014 to 2018
$2.0M
NCI NIH HHS P30 CA014051NIH HHS DP5 OD019815
6 · The paper itself

Abstract

Resistance limits the effectiveness of receptor tyrosine kinase (RTK)-targeted therapies. Combination therapies targeting resistance mechanisms can considerably improve response, but will require an improved understanding of when particular combinations will be effective. One common form of resistance is bypass signaling, wherein RTKs not targeted by an inhibitor can direct reactivation of pathways essential for survival. Although this mechanism of resistance is well appreciated, it is unclear which downstream signaling events are responsible. Here, we apply a combined experimental- and statistical modeling-based approach to identify a set of pathway reactivation essential for RTK-mediated bypass resistance. Differences in the downstream pathway activation provided by particular RTKs lead to qualitative differences in the capacity of each receptor to drive therapeutic resistance. We identify and validate that the JNK pathway is activated during and strongly modulates bypass resistance. These results identify effective therapeutic combinations that block bypass-mediated resistance and provide a basic understanding of this network-level change in kinase dependence that will inform the design of prognostic assays for identifying effective therapeutic combinations in individual patients. Cancer Res; 76(18); 5219-28. ©2016 AACR.

Indexed as

Cell Line, TumorComputer SimulationDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesErbB ReceptorsErlotinib HydrochlorideHumansLapatinibLeast-Squares AnalysisLinear ModelsMAP Kinase Signaling SystemQuinazolinesEGFR protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesErbB ReceptorsErlotinib HydrochlorideLapatinibQuinazolines

Identifiers

PMID27450453
PMCPMC5026573
OpenAlexW2489870930

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.