Evidence map›Paper›PMID 27149220›Full record

ArticleNature medicine2016

A framework for understanding and targeting residual disease in oncogene-driven solid cancers.

Trever G Bivona, Robert C Doebele

Open access · greenAbstract read
In one paragraph

Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
8.6field-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

114 citing papers in PubMed, 186 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Radioresistance Mechanisms in Head and Neck Cancer.Clinical and experimental otorhinolaryngology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Pooled Nanoparticle Screening Using a Chemical Barcoding Approach.Angewandte Chemie (International ed. in English) · 2025
    Article
  12. Regulation of mFunctional & integrative genomics · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

54 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

2 authors at 2 institutions in 1 country.

Trever G BivonaDepartment of Medicine, University of California, San Francisco, San Francisco, California, USA.
Robert C DoebeleDepartment of Medicine and Medical Oncology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
University of California, San Francisco · USUniversity of Colorado Anschutz Medical Campus · US

Funding

Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
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
The role of EGFR as a mechanism of therapeutic resistance in gene fusion positive lung cancer.R01CA193935 · NCI · UNIVERSITY OF COLORADO DENVER · PI DOEBELE, ROBERT C · 2016 to 2020
$2.0M
Howard Hughes Medical InstituteNCI NIH HHS DP2 CA174497NCI NIH HHS P50 CA058187NCI NIH HHS R01 CA169338NCI NIH HHS R01 CA193935
6 · The paper itself

Abstract

Molecular targeted therapy has the potential to dramatically improve survival in patients with cancer. However, complete and durable responses to targeted therapy are rare in individuals with advanced-stage solid cancers. Even the most effective targeted therapies generally do not induce a complete tumor response, resulting in residual disease and tumor progression that limits patient survival. We discuss the emerging need to more fully understand the molecular basis of residual disease as a prelude to designing therapeutic strategies to minimize or eliminate residual disease so that we can move from temporary to chronic control of disease, or a cure, for patients with advanced-stage solid cancers. Ultimately, we propose a shift from the current reactive paradigm of analyzing and treating acquired drug resistance to a pre-emptive paradigm of defining the mechanisms that result in residual disease, to target and limit this disease reservoir.

Indexed as

Drug Resistance, NeoplasmAntineoplastic Combined Chemotherapy ProtocolsHumansImmunotherapyMolecular Targeted TherapyNeoplasm, ResidualNeoplasmsOncogenes

Identifiers

PMID27149220
PMCPMC5384713
OpenAlexW2346133077

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.