Evidence map›Paper›PMID 33555144›Full record

ReviewEMBO molecular medicine2021

Non-genetic heterogeneity, altered cell fate and differentiation therapy.

Alexander C Lewis, Lev M Kats

Open access · goldAbstract readReview
In one paragraph

Review in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. Multilevel Mechanisms of Cancer Drug Resistance.International journal of molecular sciences · 2024
    Pooled it
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  8. Asian journal of pharmaceutical sciences · 2024
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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

2 authors at 2 institutions in 1 country.

Alexander C LewisThe Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.ORCID 0000-0002-6253-5823
Lev M KatsThe Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.ORCID 0000-0001-8742-8138
Peter MacCallum Cancer Centre · AUThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered capacity for self-renewal and differentiation is a hallmark of cancer, and many tumors are composed of cells with a developmentally immature phenotype. Among the malignancies where processes that govern cell fate decisions have been studied most extensively is acute myeloid leukemia (AML), a disease characterized by the presence of large numbers of "blasts" that resemble myeloid progenitors. Classically, the defining properties of AML cells were said to be aberrant self-renewal and a block of differentiation, and the term "differentiation therapy" was coined to describe drugs that promote the maturation of leukemic blasts. Notionally however, the simplistic view that such agents "unblock" differentiation is at odds with the cancer stem cell (CSC) hypothesis that posits that tumors are hierarchically organized and that CSCs, which underpin cancer growth, retain the capacity to progress to a developmentally more mature state. Herein, we will review recent developments that are providing unprecedented insights into non-genetic heterogeneity both at steady state and in response to treatment, and propose a new conceptual framework for therapies that aim to alter cell fate decisions in cancer.

Indexed as

Leukemia, Myeloid, AcuteCell DifferentiationHumansNeoplastic Stem CellsPhenotypecancercell fatedifferentiationdifferentiation therapyself-renewal

Identifiers

PMID33555144
PMCPMC7933953
OpenAlexW3126592607

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.