Evidence map›Paper›PMID 25485495›Full record

ArticleCell cycle (Georgetown, Tex.)2014

The metabolically-modulated stem cell niche: a dynamic scenario regulating cancer cell phenotype and resistance to therapy.

Elisabetta Rovida, Silvia Peppicelli, Silvia Bono, Francesca Bianchini, Ignazia Tusa, Giulia Cheloni, Ilaria Marzi, Maria Grazia Cipolleschi, Lido Calorini, Persio Dello Sbarba

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  9. Article
  10. Stem Cell Niche Microenvironment: Review.Bioengineering (Basel, Switzerland) · 2021
    Review
  11. Hypoxia, endoplasmic reticulum stress and chemoresistance: dangerous liaisons.Journal of experimental & clinical cancer research : CR · 2021
    Review
  12. Review
  13. Article
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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

10 authors at 2 institutions in 1 country.

Elisabetta Rovidaa Dipartimento di Scienze Biomediche Sperimentali e Cliniche "Mario Serio" ; Università degli Studi di Firenze & Istituto Toscano Tumori ; Firenze , Italy.
Silvia Peppicelli
Silvia Bono
Francesca Bianchini
Ignazia Tusa
Giulia Cheloni
Ilaria Marzi
Maria Grazia Cipolleschi
Lido Calorini
Persio Dello Sbarba
Mario Negri Institute for Pharmacological Research · ITUniversity of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This Perspective addresses the interactions of cancer stem cells (CSC) with environment which result in the modulation of CSC metabolism, and thereby of CSC phenotype and resistance to therapy. We considered first as a model disease chronic myeloid leukemia (CML), which is triggered by a well-identified oncogenetic protein (BCR/Abl) and brilliantly treated with tyrosine kinase inhibitors (TKi). However, TKi are extremely effective in inducing remission of disease, but unable, in most cases, to prevent relapse. We demonstrated that the interference with cell metabolism (oxygen/glucose shortage) enriches cells exhibiting the leukemia stem cell (LSC) phenotype and, at the same time, suppresses BCR/Abl protein expression. These LSC are therefore refractory to the TKi Imatinib-mesylate, pointing to cell metabolism as an important factor controlling the onset of TKi-resistant minimal residual disease (MRD) of CML and the related relapse. Studies of solid neoplasias brought another player into the control of MRD, low tissue pH, which often parallels cancer growth and progression. Thus, a 3-party scenario emerged for the regulation of CSC/LSC maintenance, MRD induction and disease relapse: the "hypoxic" versus the "ischemic" vs. the "acidic" environment. As these environments are unlikely constrained within rigid borders, we named this model the "metabolically-modulated stem cell niche."

Indexed as

Drug Resistance, NeoplasmFusion Proteins, bcr-ablHumansNeoplastic Stem CellsStem Cell NicheFusion Proteins, bcr-ablacidityBCR/Ablcancer stem cellchronic myeloid leukemiahypoxiaischemialeukemia progenitor cellleukemia stem cellminimal residual diseaseneoplastic progressionresistance to imatinib-mesylatestem cell niche

Identifiers

PMID25485495
PMCPMC4612663
OpenAlexW2055786461

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.