Evidence map›Paper›PMID 21606321›Full record

ArticleCarcinogenesis2011

The role for estrogen receptor-alpha and prolactin receptor in sex-dependent DEN-induced liver tumorigenesis.

Robert M Bigsby, Andrea Caperell-Grant

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Clinicopathological and Prognostic Significance of Klotho and Estrogen Receptors Expression in Human Hepatocellular Carcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2021
    Article
  10. Article
  11. TrxR1, Gsr, and oxidative stress determine hepatocellular carcinoma malignancy.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Prolactin prevents hepatocellular carcinoma by restricting innate immune activation of c-Myc in mice.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  20. 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

2 authors at 2 institutions in 1 country.

Robert M BigsbyDepartment of Obstetrics and Gynecology, Indiana University School of Medicine, 975 West Walnut Street, Indianapolis, IN 46202-5121, USA. rbigsby@iupui.edu
Andrea Caperell-Grant
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Endocrine Regulation of Hepatocellular CarcinogenesisR21ES014367 · NIEHS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BIGSBY, ROBERT M · 2006 to 2007
$411k
NIEHS NIH HHS ES014367
6 · The paper itself

Abstract

Mice treated neonatally with diethylnitrosamine (DEN) develop liver tumors in a male-dominant manner, reflecting the male bias in human hepatocellular carcinoma. Evidence suggests that estrogen, androgen, prolactin (PRL) and growth hormone (GH) modify liver tumorigenesis. We determined the roles of estrogen receptor-α (ERα) and prolactin receptor (PRLR) using receptor null mice, ERαKO (C57Bl/6J) and PRLR-KO (129Ola-X-C57BL/6), in the neonatal-DEN model of liver tumorigenesis. In both mouse strains, females had reduced tumorigenesis compared with males (P < 0.01), regardless of ERα or PRLR status. Tumorigenesis was not affected by ovariectomy in C57Bl/6J mice but it was increased by ovariectomy in the mixed strain, 129Ola-X-C57BL/6, regardless of PRLR status. ERαKO males had 47% fewer tumors than ERα wild-type males (P < 0.01). On the other hand, estradiol treatment protected against tumorigenesis in males only in the presence of ERα. As evidenced by liver gene expression, lack of ERα did not alter the pattern of GH secretion in males but resulted in the male GH pattern in females. These observations indicate that ERα is not required for lower tumorigenesis in females, but it is required for the protective effects of exogenously delivered estradiol. Unexpectedly, the results indicate that ERα plays a role in promotion of liver tumors in males. In addition, it can be concluded that sex differences in liver tumorigenesis cannot be explained by the sexually dimorphic pattern of GH secretion. The results also rule out PRL as the mediator of the protective effect of the ovaries.

Indexed as

AnimalsDiethylnitrosamineEstradiolEstrogen Receptor alphaFemaleGene ExpressionGrowth HormoneHumansLiver Neoplasms, ExperimentalMaleMiceMice, Inbred C57BLMice, KnockoutOvariectomyProlactinReceptors, ProlactinDiethylnitrosamineEstradiolEstrogen Receptor alphaGrowth HormoneProlactinReceptors, Prolactin

Identifiers

PMID21606321
PMCPMC3149205
OpenAlexW2102125265

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.