Evidence map›Paper›PMID 33537004›Full record

ArticleFrontiers in endocrinology2020

Regulation of the EGFR Pathway by HSP90 Is Involved in the Pathogenesis of Cushing's Disease.

Yue Shen, Chenxing Ji, Xuemin Jian, Juan Zhou, Qilin Zhang, Nidan Qiao, Yichao Zhang, Xuefei Shou, Xiang Zhou, Zengyi Ma

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. 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

10 authors at 4 institutions in 1 country.

Yue ShenDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Chenxing JiDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Xuemin JianShanghai Jiao Tong University School of Medicine, Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), and the Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University, Shanghai, China.
Juan ZhouShanghai Jiao Tong University School of Medicine, Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), and the Collaborative Innovation Center for Brain Science, Shanghai Jiao Tong University, Shanghai, China.
Qilin ZhangDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Nidan QiaoDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Yichao ZhangDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Xuefei ShouDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Xiang ZhouDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Zengyi MaDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Neurosurgical Institute of Fudan University, Shanghai Clinical Medical Center of Neurosurgery, Shanghai Key Laboratory of Brain Function Restoration and Neural Regeneration, Shanghai, China.
Shanghai Cancer Institute · CNHuashan Hospital · CNShanghai Jiao Tong University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: To investigate the role of heat-shock protein Hsp90 in adrenocorticotropic hormone (ACTH)-secreting cells, and to explore the potential clinical application of an inhibitor of Hsp90, 17-N-allylamino-17-demethoxygeldanamycin(17-AAG) in corticotropinomas [also known as "Cushing's disease" (CD)]. Methods: Culture of mouse pituitary tumor [AtT-20/D16v-F2 (ATCC Results: 17-AAG suppressed the viability and proliferation, and promoted the apoptosis, of AtT-20/D16v-F2 cells. 17-AAG suppressed the synthesis and secretion of ACTH in AtT-20/D16v-F2 cells and down-regulated POMC transcription. 17-AAG acted in a similar pattern upon treatment with human pituitary ACTH-secreting tumor cells. Inhibition by 17-AAG was stronger in human pituitary ACTH-secreting tumor cells carrying the ubiquitin-specific protease-8 ( Conclusions: The HSP90 inhibitor 17-AAG reduced the viability and secretory function of human pituitary ACTH-secreting tumor cells, and tumor cells carrying the

Indexed as

ACTH-Secreting Pituitary AdenomaAdenomaAdultAnimalsApoptosisBenzoquinonesCell ProliferationErbB ReceptorsGene Expression RegulationHSP90 Heat-Shock ProteinsHumansLactams, MacrocyclicMiceMiddle AgedPituitary ACTH HypersecretionTumor Cells, CulturedBenzoquinonesErbB ReceptorsHSP90 Heat-Shock ProteinsLactams, Macrocyclictanespimycin17-N-allylamino-17-demethoxygeldanamycin/tanespimycinCushing’s diseaseepidermal growth factor receptorHsp90pathogenesis

Identifiers

PMID33537004
PMCPMC7848029
OpenAlexW3121373903

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.