Evidence map›Paper›PMID 23889735›Full record

ArticleAlcoholism, clinical and experimental research2013

Alcohol exposure in utero increases susceptibility to prostate tumorigenesis in rat offspring.

Sengottuvelan Murugan, Changqing Zhang, Sepideh Mojtahedzadeh, Dipak K Sarkar

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
6.9field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Alcoholic Beverage Consumption and Chronic Diseases.International journal of environmental research and public health · 2016
    Review
  7. Article
  8. Article
  9. Article
  10. Cerebellar fastigial nuclear glutamatergic neurons regulate immune function via hypothalamic and sympathetic pathways.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015
    Article
  11. Review
  12. Environmental alterations of epigenetics prior to the birth.International review of neurobiology · 2014
    Review
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.

Sengottuvelan MuruganEndocrine Program, Department of Animal Sciences , Rutgers, The State University of New Jersey, New Brunswick, New Jersey.
Changqing Zhang
Sepideh Mojtahedzadeh
Dipak K Sarkar
Rutgers, The State University of New Jersey · US

Funding

ALCOHOL AND HYPERPROLACTINEMIAR01AA011591 · NIAAA · WASHINGTON STATE UNIVERSITY · PI SARKAR, DIPAK KUMAR · 1998 to 2022
$5.0M
Role of Opiates in Alcohol-Induced Neurotoxicity- Diversity supplementR37AA008757 · NIAAA · RUTGERS, THE STATE UNIV OF N.J. · PI SARKAR, DIPAK KUMAR · 2009 to 2018
$4.0M
NIAAA NIH HHS AA11591NIAAA NIH HHS R01 AA011591NIAAA NIH HHS R37 AA008757NIAAA NIH HHS R37AA08757
6 · The paper itself

Abstract

backgroundPrenatal alcohol exposure has been shown to increase offspring susceptibility to some chemical carcinogens. Whether prenatal exposure to alcohol makes the offspring more susceptible to the development of prostate cancer is not known. Therefore, we determined whether any functional abnormalities and increased cancer susceptibility exist in the prostate of fetal alcohol-exposed male rats during the adult period.

methodsPregnant rats were fed with a liquid diet containing alcohol (alcohol-fed [AF]), or pair-fed with isocaloric liquid diet (PF) or ad libitum fed with rat chow (ad lib-fed). Male offspring of these rats were given N-Nitroso-N-methylurea and testosterone to induce prostate neoplasia or left untreated. Around 6 to 8 months of age, the prostates of these animals were processed for determination of biochemical changes and histopathologies.

resultsProstates of noncarcinogen treated animals that were alcohol exposed during the prenatal period demonstrated inflammatory cell infiltration and epithelial atypia and increased number of proliferative cells in the ventral lobe of this gland, but the prostate of control animal showed normal cytoarchitecture. In addition, prenatal alcohol-exposed rats showed decreased levels of cell-cell adhesion marker and increased estrogenic activity in the ventral prostate. Prenatally ethanol (EtOH)-exposed rats, when treated with carcinogen and testosterone, showed histological evidence for high-grade prostatic intraepithelial neoplasia (PIN) primarily in the ventral prostate, whereas control animals showed only low-grade PIN. Prenatally EtOH-exposed rats treated with carcinogen and testosterone also showed increased number of proliferative cells and androgen receptor with concomitant decreased levels of tumor suppressor proteins in the ventral prostate.

conclusionsThese results suggest for the first time that prenatal EtOH exposures induce histophysiological changes in the prostate as well as it increases the susceptibility of the prostate to develop neoplasia during adulthood.

Indexed as

Prenatal Exposure Delayed EffectsAlcohol-Induced DisordersAnimalsAromataseCarcinogenesisCentral Nervous System DepressantsEstrogen Receptor alphaEthanolFemaleMalePregnancyProstateProstatic NeoplasmsRatsRats, Sprague-DawleyAromataseCentral Nervous System DepressantsEstrogen Receptor alphaEthanolAromataseEstrogen ReceptorFetal AlcoholProstate Cancers

Identifiers

PMID23889735
PMCPMC3812315
OpenAlexW2072846372

What OpenQuestion holds

Textmetadata
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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.