Evidence map›Paper›PMID 30755618›Full record

ArticleNature communications2019

Whole-genome sequencing identifies ADGRG6 enhancer mutations and FRS2 duplications as angiogenesis-related drivers in bladder cancer.

Song Wu, Tong Ou, Nianzeng Xing, Jiang Lu, Shengqing Wan, Changxi Wang, Xi Zhang, Feiya Yang, Yi Huang, Zhiming Cai

Abstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
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

56 citing papers in PubMed.

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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.

Song WuUrology Institute of Shenzhen University, The Third Affiliated Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, China. wusong@szu.edu.cn.
Tong OuUrology Institute of Shenzhen University, The Third Affiliated Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, China.
Nianzeng XingDepartment of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100000, China.
Jiang LuUrology Institute of Shenzhen University, The Third Affiliated Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, China.
Shengqing WanShenzhen Following Precision Medical Research Institute, Luohu Hospital Group, Shenzhen, 518000, China.
Changxi WangUrology Institute of Shenzhen University, The Third Affiliated Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, China.
Xi ZhangUrology Institute of Shenzhen University, The Third Affiliated Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, China.
Feiya YangDepartment of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100000, China.
Yi HuangUrology Institute of Shenzhen University, The Third Affiliated Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, China.
Zhiming CaiUrology Institute of Shenzhen University, The Third Affiliated Hospital of Shenzhen University, Shenzhen University, Shenzhen, 518000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder cancer is one of the most common and highly vascularized cancers. To better understand its genomic structure and underlying etiology, we conduct whole-genome and targeted sequencing in urothelial bladder carcinomas (UBCs, the most common type of bladder cancer). Recurrent mutations in noncoding regions affecting gene regulatory elements and structural variations (SVs) leading to gene disruptions are prevalent. Notably, we find recurrent ADGRG6 enhancer mutations and FRS2 duplications which are associated with higher protein expression in the tumor and poor prognosis. Functional assays demonstrate that depletion of ADGRG6 or FRS2 expression in UBC cells compromise their abilities to recruit endothelial cells and induce tube formation. Moreover, pathway assessment reveals recurrent alterations in multiple angiogenesis-related genes. These results illustrate a multidimensional genomic landscape that highlights noncoding mutations and SVs in UBC tumorigenesis, and suggest ADGRG6 and FRS2 as novel pathological angiogenesis regulators that would facilitate vascular-targeted therapies for UBC.

Indexed as

MutationAdaptor Proteins, Signal TransducingCell Line, TumorDNA Mutational AnalysisExomeGene DosageGenetic Predisposition to DiseaseHumansMembrane ProteinsNeovascularization, PathologicReceptors, G-Protein-CoupledRegulatory Sequences, Nucleic AcidUrinary Bladder NeoplasmsWhole Genome SequencingAdaptor Proteins, Signal TransducingFRS2 protein, humanMembrane ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID30755618
PMCPMC6372626

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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.