Evidence map›Paper›PMID 27801609›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Persistence to anti-cancer treatments in the stationary to proliferating transition.

Sivan Pearl Mizrahi, Orit Gefen, Itamar Simon, Nathalie Q Balaban

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Cellular quiescence in budding yeast.Yeast (Chichester, England) · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Drug persistence - from antibiotics to cancer therapies.Current opinion in systems biology · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Persistent bacterial infections and persister cells.Nature reviews. Microbiology · 2017
    Review
  20. 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

4 authors.

Sivan Pearl Mizrahia Racah Institute of Physics, Edmond J. Safra Campus, The Hebrew University , Jerusalem , Israel.
Orit Gefena Racah Institute of Physics, Edmond J. Safra Campus, The Hebrew University , Jerusalem , Israel.
Itamar Simonb Department of Microbiology and Molecular Genetics , IMRIC, The Hebrew University Hadassah Medical School , Jerusalem , Israel.
Nathalie Q Balabana Racah Institute of Physics, Edmond J. Safra Campus, The Hebrew University , Jerusalem , Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heterogeneous responses of clonal cancer cells to treatment is understood to be caused by several factors, including stochasticity, cell-cycle dynamics, and different micro-environments. In a tumor, cancer cells may encounter fluctuating conditions and transit from a stationary culture to a proliferating state, for example this may occur following treatment. Here, we undertake a quantitative evaluation of the response of single cancerous lymphoblasts (L1210 cells) to various treatments administered during this transition. Additionally, we developed an experimental system, a "Mammalian Mother Machine," that tracks the fate of thousands of mammalian cells over several generations under transient exposure to chemotherapeutic drugs. Using our developed system, we were able to follow the same cell under repeated treatments and continuously track many generations. We found that the dynamics of the transition between stationary and proliferative states are highly variable and affect the response to drug treatment. Using cell-cycle markers, we were able to isolate a subpopulation of persister cells with distinctly higher than average survival probability. The higher survival rate encountered with cell-cycle phase specific drugs was associated with a significantly longer time-till-division, and was reduced by a non cell-cycle specific drug. Our results suggest that the variability of transition times from the stationary to the proliferating state may be an obstacle hampering the effectiveness of drugs and should be taken into account when designing treatment regimens.

Indexed as

Antineoplastic AgentsBiomarkersCell LineCell Line, TumorCell ProliferationCell SurvivalCytarabineDrug Resistance, NeoplasmFluorescenceG1 PhaseHumansNeoplasmsResting Phase, Cell CycleUbiquitinAntineoplastic AgentsBiomarkersCytarabineUbiquitincell-cyclechemotherapymicrofluidicspersistenceproliferatingquiescencestationary

Identifiers

PMID27801609
PMCPMC5224467

What OpenQuestion holds

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LicenceCC BY-NC
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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.