Evidence map›Paper›PMID 24721247›Full record

ReviewSeminars in cancer biology2015

Cellular reprogramming in skin cancer.

Ihn Young Song, Allan Balmain

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Basosquamous carcinoma: epigenetic considerations in a case.Postepy dermatologii i alergologii · 2020
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Cancer Microenvironment: What Can We Learn from the Stem Cell Niche.International journal of molecular sciences · 2015
    Review
  12. Review
  13. Article
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.

Ihn Young SongHelen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158, USA.
Allan BalmainHelen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158, USA. Electronic address: abalmain@cc.ucsf.edu.

Funding

Identification of epithelial tumor susceptiility genesU01CA084244 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 1999 to 2013
$13.3M
Molecular and Cellular Mechanisms in CancerT32CA108462 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI · 2004 to 2024
$10.4M
Science Leadership and IntegrationU01CA141455 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 2009 to 2013
$3.2M
The role of the Kras4A isoform in epithelial carcinogenesisR01CA111834 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 2006 to 2016
$2.6M
NCI NIH HHS R01 CA111834NCI NIH HHS R01 CA111834-06A1NCI NIH HHS T32 CA108462NCI NIH HHS T32-CA108462-10NCI NIH HHS U01 CA084244NCI NIH HHS U01 CA141455NCI NIH HHS U01 CA84244
6 · The paper itself

Abstract

Early primitive stem cells have long been viewed as the cancer cells of origin (tumor initiating target cells) due to their intrinsic features of self-renewal and longevity. However, emerging evidence suggests a surprising capacity for normal committed cells to function as reserve stem cells upon reprogramming as a consequence of tissue damage resulting in inflammation and wound healing. This results in an alternative concept positing that tumors may originate from differentiated cells that can re-acquire stem cell properties due to genetic or epigenetic reprogramming. It is likely that both models are correct, and that a continuum of potential cells of origin exists, ranging from early primitive stem cells to committed progenitor or even terminally differentiated cells. A combination of the nature of the target cell and the specific types of gene mutations introduced determine tumor cell lineage, as well as potential for malignant conversion. Evidence from mouse skin models of carcinogenesis suggests that initiated cells at different stages within a stem cell hierarchy have varying degrees of requirement for reprogramming (e.g. inflammation stimuli), depending on their degree of differentiation. This article will present evidence in favor of these concepts that has been developed from studies of several mouse models of skin carcinogenesis.

Indexed as

Neoplastic Stem CellsAnimalsCarcinogenesisCell DifferentiationCell Transformation, NeoplasticCellular ReprogrammingHumansInflammationMiceOncogenesSkin NeoplasmsCell of originInflammationMalignant potentialp53ReprogrammingSkin cancerStem cell hierarchy

Identifiers

PMID24721247
PMCPMC4467683

What OpenQuestion holds

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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.