Evidence map›Paper›PMID 28190919›Full record

ReviewJournal of toxicologic pathology2017

Heterogeneity of tumor cells in terms of cancer-initiating cells.

Eiichi Morii

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of toxicologic pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. DDX51 gene promotes proliferation by activating Wnt/β-catenin signaling in breast cancer.International journal of clinical and experimental pathology · 2017
    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

1 author at 1 institution in 1 country.

Eiichi MoriiDepartment of Pathology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors derive from a single cell clone but consist of heterogeneous cell subpopulations with diverse features and functions. A limited number of subclones with a selective advantage can initiate tumors when inoculated into immunocompromised mice, and are called cancer-initiating cells (CICs). CICs can be isolated from the bulk of tumors on the basis of their characteristics, such as high reagent efflux, degradation of reactive oxygen species, and aldehyde dehydrogenase (ALDH) activity. Under normal conditions, new CICs are produced by existing CICs rather than non-CICs. However, under stress conditions, non-CICs can occasionally produce CICs, a phenomenon known as plasticity. The dynamic exchange between CICs and non-CICs may enable tumors to survive under unfavorable conditions. CICs are located in a small portion of tumors. This suggests that microenvironmental factors induce or inhibit the CIC phenotype, which might be regulated by intercellular signaling between tumor cells. This review describes isolation of CICs from tumor cell populations and the microenvironmental factors that regulate CIC phenotypes in uterine cancer and lymphoma.

Indexed as

aldehyde dehydrogenasecancer initiating cellsplasticity

Identifiers

PMID28190919
PMCPMC5293686
OpenAlexW2523509945

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.