Evidence map›Paper›PMID 30214683›Full record

ArticleOncotarget2018

Differential signaling pathway activation in 7,12-dimethylbenz[a] anthracene (DMBA)-treated mammary stem/progenitor cells from species with varying mammary cancer incidence.

Melissa M Ledet, Meghan Oswald, Robyn Anderson, Gerlinde R Van de Walle

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Using Organoids to Tap Mammary Gland Diversity for Novel Insight.Journal of mammary gland biology and neoplasia · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Development and Pathology of the Equine Mammary Gland.Journal of mammary gland biology and neoplasia · 2021
    Review
  9. Review
  10. 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

4 authors at 1 institution in 1 country.

Melissa M LedetBaker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca 14853, NY, USA.
Meghan OswaldBaker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca 14853, NY, USA.
Robyn AndersonBaker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca 14853, NY, USA.
Gerlinde R Van de WalleBaker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca 14853, NY, USA.
Cornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A natural variation exists in the susceptibility to mammary cancer among wild and domestic mammalian species. Mammary stem/progenitor cells (MaSC) represent a primary target cell for transformation; however, little is known about the intrinsic response of these cells to carcinogenic insults. Polycyclic aromatic hydrocarbons (PAH), such as 7,12-dimethylbenz[a]anthracene (DMBA), are abundantly present in the environment and have been linked to the development of mammary cancer in humans and rodents. We treated MaSC from equine (mammary cancer-resistant) and canine (mammary cancer-susceptible) species with DMBA and assessed cytochrome P450 metabolic activity, DNA damage and viability. Our notable findings were that MaSC from both species showed DNA damage following DMBA treatment; however, equine MaSC initiated cell death whereas canine MaSC repaired this DNA damage. Follow-up studies, based on genome-wide transcriptome analyses, revealed that DMBA induced activation of both the intrinsic and extrinsic apoptotic pathways in equine, but not canine, MaSC. Based on these findings, we propose a hypothetical model in which undergoing apoptosis in response to an oncogenic event might contribute to a lower incidence of mammary cancer in certain mammalian species. Such a mechanism would allow for the elimination of DNA-damaged MaSC, and hence, reduce the risk of potential tumor-initiating mutations in these cells.

Indexed as

apoptosisDMBADNA damagemammary cancermammary stem/progenitor cells

Identifiers

PMID30214683
PMCPMC6132353
OpenAlexW2889017188

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.