Evidence map›Paper›PMID 20333244›Full record

ArticlePLoS computational biology2010

Tumor growth rate determines the timing of optimal chronomodulated treatment schedules.

Samuel Bernard, Branka Cajavec Bernard, Francis Lévi, Hanspeter Herzel

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Hypermetabolic state is associated with circadian rhythm disruption in mouse and human cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Circadian Rhythms, Disease and Chronotherapy.Journal of biological rhythms · 2021
    Review
  14. Review
  15. Synergies of Multiple Zeitgebers Tune Entrainment.Frontiers in network physiology · 2021
    Article
  16. Article
  17. Mathematical modeling of circadian rhythms.Wiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
  18. Article
  19. Systems Chronotherapeutics.Pharmacological reviews · 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 at 4 institutions in 3 countries.

Samuel BernardInstitute for Theoretical Biology, Humboldt University and Charité, Berlin, Germany. bernard@math.univ-lyon1.fr
Branka Cajavec Bernard
Francis Lévi
Hanspeter Herzel
Humboldt State University · USHumboldt-Universität zu Berlin · DEInserm · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In host and cancer tissues, drug metabolism and susceptibility to drugs vary in a circadian (24 h) manner. In particular, the efficacy of a cell cycle specific (CCS) cytotoxic agent is affected by the daily modulation of cell cycle activity in the target tissues. Anti-cancer chronotherapy, in which treatments are administered at a particular time each day, aims at exploiting these biological rhythms to reduce toxicity and improve efficacy of the treatment. The circadian status, which is the timing of physiological and behavioral activity relative to daily environmental cues, largely determines the best timing of treatments. However, the influence of variations in tumor kinetics has not been considered in determining appropriate treatment schedules. We used a simple model for cell populations under chronomodulated treatment to identify which biological parameters are important for the successful design of a chronotherapy strategy. We show that the duration of the phase of the cell cycle targeted by the treatment and the cell proliferation rate are crucial in determining the best times to administer CCS drugs. Thus, optimal treatment times depend not only on the circadian status of the patient but also on the cell cycle kinetics of the tumor. Then, we developed a theoretical analysis of treatment outcome (TATO) to relate the circadian status and cell cycle kinetic parameters to the treatment outcomes. We show that the best and the worst CCS drug administration schedules are those with 24 h intervals, implying that 24 h chronomodulated treatments can be ineffective or even harmful if administered at wrong circadian times. We show that for certain tumors, administration times at intervals different from 24 h may reduce these risks without compromising overall efficacy.

Indexed as

Drug ChronotherapyModels, BiologicalAntineoplastic AgentsCell CycleCircadian RhythmComputer SimulationHumansNeoplasmsOutcome Assessment, Health CareTreatment OutcomeAntineoplastic Agents

Identifiers

PMID20333244
PMCPMC2841621
OpenAlexW1968744698

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.