Evidence map›Paper›PMID 22105164›Full record

ArticleThe Journal of clinical investigation2011

A new medical therapy for Cushing disease?

Fredric E Wondisford

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Somatic USP8 Gene Mutations Are a Common Cause of Pediatric Cushing Disease.The Journal of clinical endocrinology and metabolism · 2017
    Article
  3. Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Fredric E WondisfordDepartment of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. fwondisford@jhmi.edu
Johns Hopkins University · US

Funding

Diabetes Research and Training CenterP60DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WONDISFORD, FREDRIC E. · 2008 to 2012
$9.1M
Transcriptional coactivators and hepatic glucose productionR01DK063349 · NIDDK · UNIVERSITY OF CHICAGO · PI WONDISFORD, FREDRIC E. · 2002 to 2017
$5.0M
THYROID HORMONE ACTION IN THE PITUITARYR01DK049126 · NIDDK · UNIVERSITY OF CHICAGO · PI WONDISFORD, FREDRIC E. · 1995 to 2016
$3.8M
NIDDK NIH HHS P60 DK079637NIDDK NIH HHS P60 DK79637NIDDK NIH HHS R01 DK049126NIDDK NIH HHS R01 DK063349NIDDK NIH HHS R01DK49126NIDDK NIH HHS R01DK63349
6 · The paper itself

Abstract

Members of the ErbB family of cell surface tyrosine kinase receptors are important targets for cancer treatment because they frequently contribute to the pathogenesis of malignancy. In this issue of the JCI, Fukuoka et al. generate data that suggest that using a tyrosine kinase inhibitor (TKI) against epidermal growth factor receptor (EGFR; also known as ErbB1) may be a novel approach for treating patients with hypercortisolemia due to pituitary corticotroph adenomas (Cushing disease). While surgical resection remains the cornerstone of treatment for individuals with such tumors, this study suggests that TKIs could perhaps be used to reduce tumor size prior to surgery or to treat recurrent disease after surgery.

Indexed as

Molecular Targeted TherapyACTH-Secreting Pituitary AdenomaAdenomaAnimalsErbB ReceptorsGefitinibHumansProtein Kinase InhibitorsQuinazolinesErbB ReceptorsGefitinibProtein Kinase InhibitorsQuinazolines

Identifiers

PMID22105164
PMCPMC3226342
OpenAlexW2058611701

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.