Evidence map›Paper›PMID 30740553›Full record

ArticleCurrent opinion in systems biology2018

Drug persistence - from antibiotics to cancer therapies.

Karl Kochanowski, Leanna Morinishi, Steven Altschuler, Lani Wu

Abstract read
In one paragraph

Article in Current opinion in systems biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–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

23 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Glycerol-Driven Energy and Proteostasis Underpin Antibiotic Tolerance inbioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

4 authors.

Karl KochanowskiDepartment of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, California, USA.
Leanna MorinishiDepartment of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, California, USA.
Steven AltschulerDepartment of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, California, USA.
Lani WuDepartment of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, California, USA.

Funding

Maximizing the predictive power of high-throughput, microscopy-based phenotypic screensR01CA184984 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WU, LANI F · 2014 to 2025
$4.7M
Integrative Program in Complex Biological System (ipCBS)T32EB009383 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MARSHALL, WALLACE, WEINER, ORION D · 2009 to 2022
$3.2M
(PQD1) An Iterative Approach for Overcoming Evolving Targeted Therapy ResistanceR01CA185404 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WU, LANI F · 2014 to 2017
$1.3M
NCI NIH HHS R01 CA184984NCI NIH HHS R01 CA185404NIBIB NIH HHS T32 EB009383
6 · The paper itself

Abstract

Drug-insensitive tumor subpopulations remain a significant barrier to effective cancer treatment. Recent works suggest that within isogenic drug-sensitive cancer populations, subsets of cells can enter a 'persister' state allowing them to survive prolonged drug treatment. Such persisters are well-described in antibiotic-treated bacterial populations. In this review, we compare mechanisms of drug persistence in bacteria and cancer. Both bacterial and cancer persisters are associated with slow-growing phenotypes, are metabolically distinct from non-persisters, and depend on the activation of specific regulatory programs. Moreover, evidence suggests that bacterial and cancer persisters are an important reservoir for the emergence of drug-resistant mutants. The emerging parallels between persistence in bacteria and cancer can guide efforts to untangle mechanistic links between growth, metabolism, and cellular regulation, and reveal exploitable therapeutic vulnerabilities.

Identifiers

PMID30740553
PMCPMC6366840

What OpenQuestion holds

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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.