Evidence map›Paper›PMID 26919034›Full record

ArticleGenesis (New York, N.Y. : 2000)2016

Foxa1 is essential for mammary duct formation.

Yi Liu, Yongbing Zhao, Benjamin Skerry, Xiao Wang, Christelle Colin-Cassin, Derek C Radisky, Klaus H Kaestner, Zhaoyu Li

Abstract read
In one paragraph

Article in Genesis (New York, N.Y. : 2000), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Deletion ofAmerican journal of cancer research · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Pathobiology of the 129:Stat1Breast cancer research : BCR · 2017
    Article
  14. 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

8 authors at 3 institutions in 1 country.

Yi LiuDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida.
Yongbing ZhaoDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida.
Benjamin SkerryDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida.
Xiao WangDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida.
Christelle Colin-CassinDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida.
Derek C RadiskyDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida.
Klaus H KaestnerDepartment of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Zhaoyu LiDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida.
Mayo Clinic in Florida · USJacksonville College · USUniversity of Pennsylvania · US

Funding

Comparative Genomics Study of Foxa/ER Targets in Liver Cancer and Breast CancerR00CA168983 · NCI · MAYO CLINIC JACKSONVILLE · PI LI, ZHAOYU · 2013 to 2015
$725k
NCI NIH HHS R00 CA168983
6 · The paper itself

Abstract

The transcription factor forkhead box protein A1 (FOXA1) plays a critical role in the proliferation of human breast cancer cells, particularly estrogen receptor alpha (ERα)-positive luminal breast cancer cells. However, genetic studies of the requirement for Foxa1 in mammary tumor formation in mice have been hampered by the lack of a conditional gene ablation. We examined three mouse models of mammary-specific ablation of Foxa1 in ductal epithelial cells to identify the best system for complete and mammary-specific ablation of Foxa1. We found that MMTV-Cre and MMTV-rtTA;Tet-On-Cre led to partial deletion of Foxa1 and attenuated mammary duct formation, whereas Krt14-Cre led to complete ablation of Foxa1 and abolished mammary duct formation, in Foxa1(loxP/loxP) mice. These results demonstrate that Foxa1 is essential for mammary duct formation, and reveal a series of mouse models in which mammary expression of Foxa1 can be attenuated or completely blocked. Our study also suggests a potentially powerful model for complete ablation of Foxa1 in mammary epithelial cells using Krt14-driven Cre expression in an inducible manner, such as Krt14-rtTA;Tet-On-Cre. This model system will facilitate further in vivo functional studies of Foxa1 or other factors in mammary gland development and tumor formation and progression. genesis 54:277-285, 2016. © 2016 Wiley Periodicals, Inc.

Indexed as

AnimalsCell ProliferationEpithelial CellsFemaleHepatocyte Nuclear Factor 3-alphaHumansIntegrasesKeratin-14Mammary Glands, AnimalMiceMice, TransgenicCre recombinaseFoxa1 protein, mouseHepatocyte Nuclear Factor 3-alphaIntegrasesKeratin-14Krt14 protein, mouseKrt14mammary glandMMTVtransgenic mice

Identifiers

PMID26919034
PMCPMC5419034
OpenAlexW2283791146

What OpenQuestion holds

Textmetadata
LicenceTDM
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.