Evidence map›Paper›PMID 32438306›Full record

ArticleNeoplasia (New York, N.Y.)2020

Stemness regulation of the adrenal mixed corticomedullary tumorigenesis-a case-control study.

Hsin-Ying Clair Chiou, He-Jiun Jiang, Sheau-Fang Yang, Kung-Kai Kuo, Pi-Chen Lin, Pi-Jung Hsiao

Open access · goldAbstract readCase Reports
In one paragraph

Article in Neoplasia (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 27% 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, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Mixed corticomedullary tumor of the adrenal gland.Frontiers in endocrinology · 2022
    Review
  5. 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

6 authors at 2 institutions in 1 country.

Hsin-Ying Clair ChiouDivision of Endocrinology and Metabolism, Department of Internal Medicine, Kaohsiung Medical University Hospital, Taiwan.
He-Jiun JiangDivision of Endocrinology and Metabolism, Department of Internal Medicine, Kaohsiung Medical University Hospital, Taiwan.
Sheau-Fang YangDepartment of Pathology, School of Medicine, College of Medicine, Kaohsiung Medical University, Taiwan. Electronic address: sfyang@kmu.edu.tw.
Kung-Kai KuoHepatobiliary Division, Department of Surgery, School of Medicine, College of Medicine, Kaohsiung Medical University, Taiwan.
Pi-Chen LinDivision of Endocrinology and Metabolism, Department of Internal Medicine, Kaohsiung Medical University Hospital, Taiwan. Electronic address: 890063@kmuh.org.tw.
Pi-Jung HsiaoDivision of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Taiwan. Electronic address: pjhsiao@cc.kmu.edu.
Kaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mixed corticomedullary tumor is an adrenal tumor intermixed with cortical and medullary cells. It is extremely rare with unclear tumorigenesis. We reported a 32-year-old female, manifested with typical Cushing's syndrome and hypertension, to be diagnosed with right huge adrenal mixed corticomedullary tumor (8.8 cm). Right adrenalectomy was done to document the tumor intimately admixed with adrenal cortical adenoma and pheochromocytoma by biochemistry and immunohistochemistry. A case-control study was designed to explore the tumorigenesis of mixed corticomedullary tumor by whole exome sequencing. Expression of the stemness markers was controlled by a tissue array of 80 adrenal tumors. Overall, 1559 identical variants coexisted in parts of adrenal cortical adenoma and pheochromocytoma, which mainly (85.8%) originated from germline mutations. These enriched mutations were engaged in stemness control, coherent with substantial expression of the stemness markers (SOX2, CD44 and OCT4) in both parts. The differential stemness expressions were demonstrated in other adrenal tumors as well. The germline mutations were also enriched in signaling involving cancer proliferation, hypoxia inducible factor-1, focal adhesion and extracellular matrix receptor interaction. Somatic mutations affecting mitogen-activated protein kinase signaling, glycolysis and the citrate cycle were found in some tumor elements. This is the first study to verify the rare mixed corticomedullary tumor by molecular and genetic evidence to link with its phenotype. Germline mutations involving the stemness regulation and cancer proliferative signaling may drive intermixed tumor formation. Somatic mutations related to glycolysis and the citrate cycle may contribute to greater tumor outgrowth.

Indexed as

MutationNeoplasms, Complex and MixedAdrenal Gland NeoplasmsAdrenal MedullaAdultCase-Control StudiesFemaleGene Expression Regulation, NeoplasticGlycolysisHumansMaleMiddle AgedMutation RateNeoplastic Stem CellsWhole Genome SequencingAdrenocortical adenomaMixed corticomedullary tumor (MCT)PheochromocytomaStemnessWhole exome sequencing (WES)

Identifiers

PMID32438306
PMCPMC7240194
OpenAlexW3026212823

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.