Evidence map›Paper›PMID 30671724›Full record

ArticlePathology oncology research : POR2019

Correlations between Histological and Array Comparative Genomic Hybridization Characterizations of Wilms Tumor.

Ming-Ru Chiang, Chi-Wen Kuo, Wen-Chung Wang, Tai-Cheng Hou, Chen-Yun Kuo, Meng-Yao Lu, Yen-Chein Lai

Abstract read
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In one paragraph

Article in Pathology oncology research : POR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.5field-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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Genomic landscape and potential therapeutic targets in alpha-fetoprotein-producing gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
    Article
  4. Article
  5. Article
  6. 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

7 authors at 4 institutions in 1 country.

Ming-Ru ChiangDepartment of Pediatrics, Jen-Ai Hospital, 483 Dong Rong Road, Taichung, 412, Taiwan.
Chi-Wen KuoDepartment of Pharmacy, Jen-Ai Hospital, 483 Dong Rong Road, Taichung, 412, Taiwan.
Wen-Chung WangDepartment of Obstetrics and Gynecology, Jen-Ai Hospital, 483 Dong Rong Road, Taichung, 412, Taiwan.
Tai-Cheng HouDepartment of Pathology, Jen-Ai Hospital, 483 Dong Rong Road, Taichung, 412, Taiwan.
Chen-Yun KuoDepartment of Pathology, Jen-Ai Hospital, 483 Dong Rong Road, Taichung, 412, Taiwan.
Meng-Yao LuDepartment of Pediatrics, National Taiwan University Hospital, 8 Chung-Shan South Road, Taipei, 100, Taiwan.
Yen-Chein LaiDepartment of Medical Laboratory and Biotechnology, Chung Shan Medical University, No.110, Sec 1, Chien Kuo North Road, Taichung, 402, Taiwan. yenchein@csmu.edu.tw.ORCID http://orcid.org/0000-0001-9072-5272
Jen-Ai Hospital · TWChina Medical University · TWChung Shan Medical University · TWNational Taiwan University Hospital · TW

Funding

Chung Shan Medical University-Jen-Ai Hospital CSMU-JAH-106-02
6 · The paper itself

Abstract

Wilms tumor, or nephroblastoma, is the most common pediatric renal malignancy. Its diagnosis is principally based on histology. Several genetic loci have been shown to be associated with Wilms tumor formation, including WT1, WT2, FWT1, FWT2, CTNNB1, WTX, and TP53. Other loci, such as 1p, 2q, 7p, 9q, 12q, 14q, 16q, 17p, and 22, have also been implicated in the etiology of Wilms tumor. The aim of this study is to elucidate the molecular pathogenesis of this tumor. In the present study, we analyzed the histological appearance and copy number aberrations using array comparative genomic hybridization of six Wilms tumors without somatic mutation in the WT1 gene. Many chromosomal aberrations on array comparative genomic hybridization analysis revealed that the genetics of Wilms tumors are extremely complex. Amplifications and deletions of large DNA fragments were observed in some samples. Amplifications of NDUFV1, ZIC2, SIX1, NR2F2, MIR1469, SOX9, JAG1, MIR6870, and GNAS were found in all six Wilms tumors. Moreover, amplifications of five genes were identified in the Wilms tumors of stromal type and amplifications of at least 10 genes were identified in the Wilms tumors of epithelial type. Our results indicated that amplifications of nine genes are the essential events in the tumorigenesis of Wilms tumor, which may inform its clinical and therapeutic management. In addition, mixed type Wilms tumor may be the heterogeneous group able to be classified using genetic results of epithelial and stromal components based on immunohistochemistry.

Indexed as

Chromosome AberrationsBiomarkers, TumorComparative Genomic HybridizationFemaleFollow-Up StudiesHumansImmunohistochemistryKidney NeoplasmsMaleMutationPrognosisWilms TumorBiomarkers, TumorArray comparative genomic hybridizationMolecular pathogenesisNephroblastomaWilms tumor

Identifiers

PMID30671724
OpenAlexW2911881099

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.