Evidence map›Paper›PMID 25703329›Full record

ReviewOncogene2015

Adaptive stress signaling in targeted cancer therapy resistance.

E Pazarentzos, T G Bivona

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Pleiotropic Effects of 3-International journal of molecular sciences · 2026
    Article
  12. Article
  13. Regulatory roles of MKP7/DUSP16 in cancer.Medical oncology (Northwood, London, England) · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The emergence of nanoporous materials in lung cancer therapy.Science and technology of advanced materials · 2022
    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

2 authors at 1 institution in 1 country.

E PazarentzosDivision of Hematology-Oncology, Department of Medicine, San Francisco, CA, USA.ORCID http://orcid.org/0000-0002-5453-1646
T G BivonaDivision of Hematology-Oncology, Department of Medicine, San Francisco, CA, USA.
University of California, San Francisco · US

Funding

Rational Combined Inhibition of NF-kB and EGFR to Optimize Lung Cancer TreatmentR01CA169338 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BIVONA, TREVER G · 2013 to 2023
$3.4M
Discovery of Rational Companion Therapeutic Targets to Optimize Cancer TreatmentDP2CA174497 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BIVONA, TREVER G · 2012 to 2012
$2.3M
Genetic Modifiers such as Fas Regulate Tumor-Cell Dependence on Mutant EGFRK08CA154787 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BIVONA, TREVER G · 2011 to 2014
$660k
Howard Hughes Medical InstituteNCI NIH HHS DP2 CA174497NCI NIH HHS K08 CA154787NCI NIH HHS R01 CA169338
6 · The paper itself

Abstract

The identification of specific genetic alterations that drive the initiation and progression of cancer and the development of targeted drugs that act against these driver alterations has revolutionized the treatment of many human cancers. Although substantial progress has been achieved with the use of such targeted cancer therapies, resistance remains a major challenge that limits the overall clinical impact. Hence, despite progress, new strategies are needed to enhance response and eliminate resistance to targeted cancer therapies in order to achieve durable or curative responses in patients. To date, efforts to characterize mechanisms of resistance have primarily focused on molecular events that mediate primary or secondary resistance in patients. Less is known about the initial molecular response and adaptation that may occur in tumor cells early upon exposure to a targeted agent. Although understudied, emerging evidence indicates that the early adaptive changes by which tumor cells respond to the stress of a targeted therapy may be crucial for tumo r cell survival during treatment and the development of resistance. Here we review recent data illuminating the molecular architecture underlying adaptive stress signaling in tumor cells. We highlight how leveraging this knowledge could catalyze novel strategies to minimize or eliminate targeted therapy resistance, thereby unleashing the full potential of targeted therapies to transform many cancers from lethal to chronic or curable conditions.

Indexed as

Adaptation, PhysiologicalSignal TransductionAnimalsCell SurvivalHumansNeoplasms

Identifiers

PMID25703329
PMCPMC4546915
OpenAlexW2098493786

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.