Evidence map›Paper›PMID 20651980›Full record

ReviewNeoplasia (New York, N.Y.)2010

Tumor-initiating and -propagating cells: cells that we would like to identify and control.

Berit Bølge Tysnes

Abstract readReview
In one paragraph

Review in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Article
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  4. Review
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  11. EP4 as a Therapeutic Target for Aggressive Human Breast Cancer.International journal of molecular sciences · 2018
    Review
  12. Article
  13. Review
  14. 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

1 author.

Berit Bølge TysnesNorLux Neuro Oncology, Department of Biomedicine, University of Bergen, Bergen, Norway. berit.tysnes@biomed.uib.no

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identification of the cell types capable of initiating and sustaining growth of the neoplastic clone in vivo is a fundamental problem in cancer research. It is likely that tumor growth can be sustained both by rare cancer stem-like cells and selected aggressive clones and that the nature of the mutations, the cell of origin, and its environment will contribute to tumor propagation. Genomic instability, suggested as a driving force in tumorigenesis, may be induced by genetic and epigenetic changes. The feature of self-renewal in stem cells is shared with tumor cells, and deviant function of the stem cell regulatory networks may, in complex ways, contribute to malignant transformation and the establishment of a cancer stem cell-like phenotype. Understanding the nature of the more quiescent cancer stem-like cells and their niches has the potential to develop novel cancer therapeutic protocols including pharmacological targeting of self-renewal pathways. Drugs that target cancer-related inflammation may have the potential to reeducate a tumor-promoting microenvironment. Because most epigenetic modifications may be reversible, DNA methylation and histone deacetylase inhibitors can be used to induce reexpression of genes that have been silenced epigenetically. Design of therapies that eliminate cancer stem-like cells without eliminating normal stem cells will be important. Further insight into the mechanisms by which pluripotency transcription factors (e.g., OCT4, SOX2, and Nanog), polycomb repressive complexes and microRNA balance selfrenewal and differentiation will be essential for our understanding of both embryonic differentiation and human carcinogenesis and for the development of new treatment strategies.

Indexed as

Cell DifferentiationCell ProliferationCell SeparationCell Transformation, NeoplasticHumansInfectionsInflammationModels, BiologicalNeoplasm InvasivenessNeoplasmsNeoplastic Stem CellsRegeneration

Identifiers

PMID20651980
PMCPMC2907577

What OpenQuestion holds

Textmetadata
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.