Evidence map›Paper›PMID 33524064›Full record

ArticlePloS one2021

Intrinsic growth heterogeneity of mouse leukemia cells underlies differential susceptibility to a growth-inhibiting anticancer drug.

Akihisa Seita, Hidenori Nakaoka, Reiko Okura, Yuichi Wakamoto

Abstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Stochasticity in mammalian cell growth rates drives cell-to-cell variability independently of cell size and divisions.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Article
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  7. Review
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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

4 authors.

Akihisa SeitaDepartment of Basic Science, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.
Hidenori NakaokaDepartment of Basic Science, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-8465-5853
Reiko OkuraDepartment of Basic Science, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.
Yuichi WakamotoDepartment of Basic Science, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-6233-0844

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cell populations consist of phenotypically heterogeneous cells. Growing evidence suggests that pre-existing phenotypic differences among cancer cells correlate with differential susceptibility to anticancer drugs and eventually lead to a relapse. Such phenotypic differences can arise not only externally driven by the environmental heterogeneity around individual cells but also internally by the intrinsic fluctuation of cells. However, the quantitative characteristics of intrinsic phenotypic heterogeneity emerging even under constant environments and their relevance to drug susceptibility remain elusive. Here we employed a microfluidic device, mammalian mother machine, for studying the intrinsic heterogeneity of growth dynamics of mouse lymphocytic leukemia cells (L1210) across tens of generations. The generation time of this cancer cell line had a distribution with a long tail and a heritability across generations. We determined that a minority of cell lineages exist in a slow-cycling state for multiple generations. These slow-cycling cell lineages had a higher chance of survival than the fast-cycling lineages under continuous exposure to the anticancer drug Mitomycin C. This result suggests that heritable heterogeneity in cancer cells' growth in a population influences their susceptibility to anticancer drugs.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmLeukemiaLeukemia, LymphoidMiceMicrofluidic Analytical TechniquesMitomycinNeoplasmsPhenotypeAntineoplastic AgentsMitomycin

Identifiers

PMID33524064
PMCPMC7850478

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Registered trials

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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.