Evidence map›Paper›PMID 32049575›Full record

ArticleMolecular biology of the cell2020

The effects of proliferation status and cell cycle phase on the responses of single cells to chemotherapy.

Adrián E Granada, Alba Jiménez, Jacob Stewart-Ornstein, Nils Blüthgen, Simone Reber, Ashwini Jambhekar, Galit Lahav

Open access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in Molecular biology of the cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Ethyl acetate extract ofResearch in pharmaceutical sciences · 2026
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  9. Leveraging chromatin packing domains to target chemoevasion in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

7 authors at 3 institutions in 2 countries.

Adrián E GranadaIRI Life Sciences, Humboldt University Berlin, 10115 Berlin, Germany.
Alba JiménezDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115.
Jacob Stewart-OrnsteinDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115.
Nils BlüthgenIRI Life Sciences, Humboldt University Berlin, 10115 Berlin, Germany.
Simone ReberIRI Life Sciences, Humboldt University Berlin, 10115 Berlin, Germany.
Ashwini JambhekarDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115.
Galit LahavDepartment of Systems Biology, Harvard Medical School, Boston, MA 02115.
Harvard University · USBerliner Hochschule für Technik · DEGerman Cancer Research Center · DE

Funding

Dynamics of Signaling Pathways: Mechanism and FunctionR01GM083303 · NIGMS · HARVARD MEDICAL SCHOOL · PI LAHAV, GALIT · 2008 to 2020
$5.2M
Dynamics of Cellular Senescence in Single CellsR01GM116864 · NIGMS · HARVARD MEDICAL SCHOOL · PI LAHAV, GALIT · 2017 to 2020
$1.6M
Defining and manipulating quiescence associated DNA damage resistance in single cellsR00CA207727 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STEWART-ORNSTEIN, JACOB · 2019 to 2021
$735k
NCI NIH HHS R00 CA207727NIGMS NIH HHS R01 GM083303NIGMS NIH HHS R01 GM116864
6 · The paper itself

Abstract

DNA-damaging chemotherapeutics are widely used in cancer treatments, but for solid tumors they often leave a residual tumor-cell population. Here we investigated how cellular states might affect the response of individual cells in a clonal population to cisplatin, a DNA-damaging chemotherapeutic agent. Using a live-cell reporter of cell cycle phase and long-term imaging, we monitored single-cell proliferation before, at the time of, and after treatment. We found that in response to cisplatin, cells either arrested or died, and the ratio of these outcomes depended on the dose. While we found that the cell cycle phase at the time of cisplatin addition was not predictive of outcome, the proliferative history of the cell was: highly proliferative cells were more likely to arrest than to die, whereas slowly proliferating cells showed a higher probability of death. Information theory analysis revealed that the dose of cisplatin had the greatest influence on the cells' decisions to arrest or die, and that the proliferation status interacted with the cisplatin dose to further guide this decision. These results show an unexpected effect of proliferation status in regulating responses to cisplatin and suggest that slowly proliferating cells within tumors may be acutely vulnerable to chemotherapy.

Indexed as

Antineoplastic Agents, AlkylatingBone NeoplasmsCell CycleCell Line, TumorCell ProliferationCisplatinDNA DamageDose-Response Relationship, DrugHumansIntravital MicroscopyMitotic IndexNormal DistributionOsteosarcomaTime-Lapse ImagingAntineoplastic Agents, AlkylatingCisplatin

Identifiers

PMID32049575
PMCPMC7185964
OpenAlexW3005803699

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.