Evidence map›Paper›PMID 32414619›Full record

ReviewBest practice & research. Clinical endocrinology & metabolism2020

Cushing syndrome: Old and new genes.

Christina Tatsi, Chelsi Flippo, Constantine A Stratakis

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Best practice & research. Clinical endocrinology & metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

5 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Genetic Basis of ACTH-Secreting Adenomas.International journal of molecular sciences · 2022
    Review
  3. Review
  4. Clinical Outcomes and Complications of Pituitary Blastoma.The Journal of clinical endocrinology and metabolism · 2021
    Observational
  5. [Hyperandrogenism, adrenal dysfunction, and hirsutism].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2020
    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

3 authors at 2 institutions in 1 country.

Christina TatsiSection on Genetics and Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Bethesda, 20892, MD, USA. Electronic address: christina.tatsi3@nih.gov.
Chelsi FlippoSection on Genetics and Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Bethesda, 20892, MD, USA. Electronic address: chelsi.flippo@nih.gov.
Constantine A StratakisSection on Genetics and Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Bethesda, 20892, MD, USA. Electronic address: stratakc@mail.nih.gov.
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Molecular Genetics Of Adrenocortical Tumors And Related DisordersZIAHD000642 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STRATAKIS, CONSTANTINE A. · 2009 to 2011
$9.6M
Molecular Genetics Of Adrenocortical Tumors And Related DisordersZ01HD000642 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STRATAKIS, CONSTANTINE A. · 1998 to 2008
$4.7M
Intramural NIH HHS Z01 HD000642Intramural NIH HHS Z99 HD999999Intramural NIH HHS ZIA HD000642
6 · The paper itself

Abstract

Cushing syndrome (CS) describes the signs and symptoms caused by exogenous or endogenous hypercortisolemia. Endogenous CS is caused by either ACTH-dependent sources (pituitary or ectopic) or ACTH-independent (adrenal) hypercortisolemia. Several genes are currently known to contribute to the pathogenesis of CS. Germline gene defects, such as MEN1, AIP, PRKAR1A and others, often present in patients with pituitary or adrenal involvement as part of a genetic syndrome. Somatic defects in genes, such as USP8, TP53, and others, are also involved in the development of pituitary or adrenal tumors in a large percentage of patients with CS, and give insight in pathways involved in pituitary or adrenal tumorigenesis.

Indexed as

DNA Mutational AnalysisAdrenal Gland NeoplasmsCarcinogenesisCushing SyndromeGenetic Association StudiesGenetic Predisposition to DiseaseGerm-Line MutationHumansPituitary NeoplasmsSignal TransductionadrenalCushinggenepituitarytumor

Identifiers

PMID32414619
PMCPMC7566855
OpenAlexW3015120707

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.