Evidence map›Paper›PMID 32521509›Full record

ArticleiScience2020

Urothelial-to-Neural Plasticity Drives Progression to Small Cell Bladder Cancer.

Guoliang Yang, Jolanta Bondaruk, David Cogdell, Ziqiao Wang, Sangkyou Lee, June Goo Lee, Shizhen Zhang, Woonyoung Choi, Yan Wang, Yu Liang and 16 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  17. Differential NEUROD1, ASCL1, and POU2F3 Expression Defines Molecular Subsets of Bladder Small Cell/Neuroendocrine Carcinoma With Prognostic Implications.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024
    Article
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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

26 authors at 4 institutions in 1 country.

Guoliang YangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jolanta BondarukDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
David CogdellDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ziqiao WangDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Sangkyou LeeDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
June Goo LeeDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Shizhen ZhangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Woonyoung ChoiJohns Hopkins Greenberg Bladder Cancer Institute, Johns Hopkins University, Baltimore, MD, USA.
Yan WangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Yu LiangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Gang WangDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ying WangDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Hui YaoDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Vipulkumar DadhaniaDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jianjun GaoDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Christopher LogothetisDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Arlene Siefker-RadtkeDepartment of Genitourinary Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ashish KamatDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Colin DinneyDepartment of Urology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Dan TheodorescuSamuel Oschin Comprehensive Cancer Institute, Cedars-Sinai, Los Angeles, CA, USA.
Marek KimmelDepartment of Statistics, Rice University, Houston, TX, USA.
Peng WeiDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Charles C GuoDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: ccguo@mdanderson.org.
John N WeinsteinDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
David J McConkeyJohns Hopkins Greenberg Bladder Cancer Institute, Johns Hopkins University, Baltimore, MD, USA.
Bogdan CzerniakDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: bczernia@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USJohns Hopkins University · USCedars-Sinai Medical Center · USRice University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

We report a comprehensive molecular analysis of 34 cases of small cell carcinoma (SCC) and 84 cases of conventional urothelial carcinoma (UC), with The Cancer Genome Atlas cohort of 408 conventional UC bladder cancers used as the reference. SCCs showed mutational landscapes characterized by nearly uniform inactivation of TP53 and were dominated by Sanger mutation signature 3 associated with loss of BRCA1/2 function. SCCs were characterized by downregulation of luminal and basal markers and were referred to as double-negative. Transcriptome analyses indicated that SCCs displayed lineage plasticity driven by a urothelial-to-neural phenotypic switch with a dysregulated epithelial-to-mesenchymal transition network. SCCs were depleted of immune cells, and expressed high levels of the immune checkpoint receptor, adenosine receptor A2A (ADORA2A), which is a potent inhibitor of immune infiltration. Our observations have important implications for the prognostication and development of more effective therapies for this lethal bladder cancer variant.

Indexed as

Biological SciencesCancerCancer Systems BiologyGenomicsTranscriptomics

Identifiers

PMID32521509
PMCPMC7286965
OpenAlexW3031370779

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.