Evidence map›Paper›PMID 25680965›Full record

ReviewEMBO reports2015

Oncogene addiction: pathways of therapeutic response, resistance, and road maps toward a cure.

Raymond Pagliarini, Wenlin Shao, William R Sellers

Abstract readReview
In one paragraph

Review in EMBO reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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

135 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
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  17. Oncogenic gene fusions in cancer: from biology to therapy.Signal transduction and targeted therapy · 2025
    Review
  18. Article
  19. Article
  20. Article

75 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

3 authors.

Raymond PagliariniDepartment of Oncology, Novartis Institutes for BioMedical Research, Cambridge, MA, USA.
Wenlin ShaoDepartment of Oncology, Novartis Institutes for BioMedical Research, Cambridge, MA, USA.
William R SellersDepartment of Oncology, Novartis Institutes for BioMedical Research, Cambridge, MA, USA william.sellers@novartis.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A key goal of cancer therapeutics is to selectively target the genetic lesions that initiate and maintain cancer cell proliferation and survival. While most cancers harbor multiple oncogenic mutations, a wealth of preclinical and clinical data supports that many cancers are sensitive to inhibition of single oncogenes, a concept referred to as 'oncogene addiction'. Herein, we describe the clinical evidence supporting oncogene addiction and discuss common mechanistic themes emerging from the response and acquired resistance to oncogene-targeted therapies. Finally, we suggest several opportunities toward exploiting oncogene addiction to achieve curative cancer therapies.

Indexed as

Antineoplastic AgentsCell ProliferationCell SurvivalDrug Delivery SystemsDrug Resistance, NeoplasmGenes, EssentialHumansModels, BiologicalNeoplasmsOncogenesAntineoplastic Agentsfeedbackoncogene addictiononcogenic shocktargeted therapy

Identifiers

PMID25680965
PMCPMC4364868

What OpenQuestion holds

Textmetadata
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.