Evidence map›Paper›PMID 18420736›Full record

ArticleEndocrinology2008

Tissue-specific actions of the Ept1, Ept2, Ept6, and Ept9 genetic determinants of responsiveness to estrogens in the female rat.

Scott G Kurz, Kimberly K Hansen, Mac T McLaughlin, Vijay Shivaswamy, Beverly S Schaffer, Karen A Gould, Rodney D McComb, Jane L Meza, James D Shull

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Mapping Mammary Tumor Traits in the Rat.Methods in molecular biology (Clifton, N.J.) · 2019
    Review
  4. Review
  5. Genetic variation in sensitivity to estrogens and breast cancer risk.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. The role of genetics in estrogen responses: a critical piece of an intricate puzzle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Review
  11. Article
  12. Ept7 influences estrogen action in the pituitary gland and body weight of rats.Mammalian genome : official journal of the International Mammalian Genome Society · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. 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

9 authors at 1 institution in 1 country.

Scott G KurzDepartment of Genetics, Cell Biology and Anatomy, 6005 Durham Research Center, 985805 Nebraska Medical Center, Omaha, Nebraska 68198-5805, USA.
Kimberly K Hansen
Mac T McLaughlin
Vijay Shivaswamy
Beverly S Schaffer
Karen A Gould
Rodney D McComb
Jane L Meza
James D Shull
University of Nebraska Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
GENETIC SUSCEPTIBILITY TO ESTROGEN INDUCED MAMMARY CAR01CA077876 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SHULL, JAMES D · 1998 to 2012
$4.4M
ESTROGENS, DIETARY ENERGY AND PITUITARY TUMORIGENESISR01CA068529 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SHULL, JAMES D · 1995 to 2002
$924k
NCI NIH HHS P30 CA036727NCI NIH HHS P30-CA36727NCI NIH HHS R01 CA077876NCI NIH HHS R01-CA68529NCI NIH HHS R01-CA77876
6 · The paper itself

Abstract

Ept1, Ept2, Ept6, and Ept9 are quantitative trait loci mapped in crosses between the ACI and Copenhagen (COP) rat strains as genetic determinants of responsiveness of the pituitary gland to estrogens. We have developed four congenic rat strains, each of which carries, on the genetic background of the ACI rat strain, alleles from the COP rat strain that span one of these quantitative trait loci. Relative to the female ACI rats, female ACI.COP-Ept1 rats exhibited reduced responsiveness to 17beta-estradiol (E2) in the pituitary gland, as evidenced by quantification of pituitary mass and circulating prolactin, and in the mammary gland, as evidenced by reduced susceptibility to E2-induced mammary cancer. The ACI.COP-Ept2 rat strain exhibited reduced responsiveness to E2 in the pituitary gland but did not differ from the ACI strain in regard to susceptibility to E2-induced mammary cancer. Interestingly, female Ept2 congenic rats exhibited increased responsiveness to E2 in the thymus, as evidenced by enhanced thymic atrophy. The ACI.COP-Ept6 rat strain exhibited increased responsiveness to E2 in the pituitary gland, which was associated with a qualitative phenotype suggestive of enhanced pituitary vascularization. The ACI.COP-Ept9 rat strain exhibited reduced responsiveness to E2 in the anterior pituitary gland, relative to the ACI rat strain. Neither Ept6 nor Ept9 impacted responsiveness to E2 in the mammary gland or thymus. These data indicate that each of these Ept genetic determinants of estrogen action is unique in regard to the tissues in which it exerts its effects and/or the direction of its effect on estrogen responsiveness.

Indexed as

AnimalsAnimals, CongenicAtrophyDrug ResistanceEstrogensFemaleGenetic MarkersGenetic Predisposition to DiseaseIncidenceMammary Neoplasms, AnimalOrgan SizeOrgan SpecificityPituitary GlandProlactinQuantitative Trait LociRatsEstrogensGenetic MarkersProlactin

Identifiers

PMID18420736
PMCPMC2488241
OpenAlexW2020236150

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.