Evidence map›Paper›PMID 21765473›Full record

ArticleOncogene2012

c-Kit is required for growth and survival of the cells of origin of Brca1-mutation-associated breast cancer.

J L Regan, H Kendrick, F-A Magnay, V Vafaizadeh, B Groner, M J Smalley

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. The molecular chronology of mammary epithelial cell fate switching.bioRxiv : the preprint server for biology · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. New C3H KitScientific reports · 2022
    Article
  14. Article
  15. Ductal keratin 15NPJ breast cancer · 2022
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

J L ReganBreakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London, UK.
H Kendrick
F-A Magnay
V Vafaizadeh
B Groner
M J Smalley
Breast Cancer Now · GBGeorg Speyer Haus · DEInstitute of Cancer Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BRCA1 mutation-associated breast cancer originates in oestrogen receptor-alpha-negative (ER(-)) progenitors in the mammary luminal epithelium. These cells also express high levels of the Kit gene and a recent study demonstrated a correlation between Brca1 loss and Kit over-expression in the mammary epithelium. However, the functional significance of c-Kit expression in the mammary gland is unknown. To address this, c-Kit(-) and c-Kit(+) mammary epithelial subsets were isolated by flow cytometry, characterised for expression of lineage-specific cell markers and functionally analysed by in vitro colony forming and in vivo transplantation assays. The results confirm that the majority of luminal ER(-) progenitors are c-Kit(+), but also that most stem cells and the differentiated cell populations are c-Kit(-). A subset of c-Kit(+) cells with high proliferative potential was found in the luminal ER(+) population, however, suggesting the existence of a distinct luminal ER(+) progenitor cell type. Analysis of mouse Brca1 mammary tumours demonstrated that they expressed Kit and its downstream effector Lyn at levels comparable to the most strongly c-Kit(+) luminal ER(-) progenitors. Consistent with c-Kit being a progenitor cell marker, in vitro three-dimensional differentiation of c-Kit(+) cells resulted in a loss of c-Kit expression, whereas c-Kit over-expression prevented normal differentiation in vivo. Furthermore, c-Kit was a functional marker of proliferative potential, as c-Kit inhibition by short hairpin knockdown prevented normal epithelial growth and caused cells to undergo apoptosis. Therefore, c-Kit defines distinct progenitor populations in the mammary epithelium and is critical for mammary progenitor survival and proliferation. Importantly, c-Kit is only the second mammary epithelial stem/progenitor marker to be shown to have a functional role in the mammary epithelium and the first marker to be shown to be required for progenitor cell function. The c-Kit signalling network has potential as a target for therapy and/or prevention in BRCA1-associated breast cancer.

Indexed as

Cell ProliferationMutationAnimalsApoptosisBRCA1 ProteinBreast NeoplasmsCell DifferentiationCells, CulturedCell SurvivalEpithelial CellsEstrogen Receptor alphaFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMammary Glands, AnimalBRCA1 ProteinEstrogen Receptor alphaProto-Oncogene Proteins c-kit

Identifiers

PMID21765473
OpenAlexW2062336370

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.