Evidence map›Paper›PMID 19261630›Full record

ReviewVeterinary pathology2009

Review paper: origin and molecular pathology of adrenocortical neoplasms.

M Bielinska, H Parviainen, S Kiiveri, M Heikinheimo, D B Wilson

Open access · bronzeAbstract readReview
In one paragraph

Review in Veterinary pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. GLI1Molecular and cellular endocrinology · 2017
    Article
  9. Endocrinopathy and Aging in Ferrets.Veterinary pathology · 2016
    Review
  10. GATA factors in endocrine neoplasia.Molecular and cellular endocrinology · 2016
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Molecular markers of adrenocortical tumors.Journal of surgical oncology · 2012
    Review
  18. Article
  19. Article
  20. Animal models of adrenocortical tumorigenesis.Molecular and cellular endocrinology · 2012
    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

5 authors at 2 institutions in 2 countries.

M BielinskaBox 8208, Washington University School of Medicine, 660 S. Euclid Ave, St. Louis, MO 63110, USA. wilson_d@wustl.edu
H Parviainen
S Kiiveri
M Heikinheimo
D B Wilson
University of Helsinki · FIInstitute for Biomedicine · IT

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Regulation of Steroidogenic Cell Differentiation in the MouseR01DK075618 · NIDDK · WASHINGTON UNIVERSITY · PI WILSON, DAVID B · 2007 to 2011
$1.4M
NIDDK NIH HHS DK075618NIDDK NIH HHS DK52574NIDDK NIH HHS P30 DK052574NIDDK NIH HHS R01 DK075618
6 · The paper itself

Abstract

Neoplastic adrenocortical lesions are common in humans and several species of domestic animals. Although there are unanswered questions about the origin and evolution of adrenocortical neoplasms, analysis of human tumor specimens and animal models indicates that adrenocortical tumorigenesis involves both genetic and epigenetic alterations. Chromosomal changes accumulate during tumor progression, and aberrant telomere function is one of the key mechanisms underlying chromosome instability during this process. Epigenetic changes serve to expand the size of the uncommitted adrenal progenitor population, modulate their phenotypic plasticity (i.e., responsiveness to extracellular signals), and increase the likelihood of subsequent genetic alterations. Analyses of heritable and spontaneous types of human adrenocortical tumors documented alterations in either cell surface receptors or their downstream effectors that impact neoplastic transformation. Many of the mutations associated with benign human adrenocortical tumors result in dysregulated cyclic adenosine monophosphate signaling, whereas key factors and/or signaling pathways associated with adrenocortical carcinomas include dysregulated expression of the IGF2 gene cluster, activation of the Wnt/beta-catenin pathway, and inactivation of the p53 tumor suppressor. A better understanding of the factors and signaling pathways involved in adrenal tumorigenesis is necessary to develop targeted pharmacologic and genetic therapies.

Indexed as

Adrenal CortexAdrenal Cortex NeoplasmsAnimalsCattleCricetinaeFerretsGoatsHumansMice

Identifiers

PMID19261630
PMCPMC2811968
OpenAlexW2148501348

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.