Evidence map›Paper›PMID 27270441›Full record

ArticleOncogene2017

Molecular analysis of urothelial cancer cell lines for modeling tumor biology and drug response.

M L Nickerson, N Witte, K M Im, S Turan, C Owens, K Misner, S X Tsang, Z Cai, S Wu, M Dean and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 109 citations in OpenAlex.

  1. Trial
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  10. Interferon Epsilon: Properties and Functions.Current molecular medicine · 2025
    Review
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  13. Review
  14. Article
  15. Article
  16. Bladder cancer.Nature reviews. Disease primers · 2023
    Review
  17. Article
  18. Article
  19. Review
  20. Article

8 more citing papers are in PubMed but not listed here.

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

12 authors at 7 institutions in 2 countries.

M L NickersonCancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Frederick, MD, USA.
N WitteComputational Bioscience Program, University of Colorado, Aurora, CO, USA.
K M ImData Science for Genomics, LLC, Ellicott City, MD, USA.
S TuranCancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Frederick, MD, USA.
C OwensDepartment of Surgery (Urology), University of Colorado, Aurora, CO, USA.
K MisnerCancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Frederick, MD, USA.
S X TsangBGI-Shenzhen, Shenzhen, China.
Z CaiShenzhen Second People's Hospital, Shenzhen, China.
S WuShenzhen Second People's Hospital, Shenzhen, China.
M DeanCancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Frederick, MD, USA.
J C CostelloComputational Bioscience Program, University of Colorado, Aurora, CO, USA.
D TheodorescuDepartment of Surgery (Urology), University of Colorado, Aurora, CO, USA.
National Cancer Institute · USUniversity of Colorado Anschutz Medical Campus · USShenzhen Second People's Hospital · CNBGI Group (China) · CNID Genomics (United States) · USNational Institutes of Health · USUniversity of Colorado Cancer Center · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Computational Bioscience Program Training GrantT15LM009451 · NLM · UNIVERSITY OF COLORADO DENVER · PI Katherina Kechris-Mays, Arjun Krishnan · 2007 to 2026
$11.7M
Regulation and Targeting of CD24 in Bladder CancerR01CA075115 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI THEODORESCU, DAN · 2003 to 2024
$7.0M
Integrins in the Endothelial Response to Fluid Shear StressR01HL075092 · NHLBI · YALE UNIVERSITY · PI SCHWARTZ, MARTIN A · 2004 to 2019
$5.1M
Understanding the RhoGDI2 metastasis suppressor geneR01CA143971 · NCI · UNIVERSITY OF COLORADO DENVER · PI THEODORESCU, DAN · 2010 to 2020
$4.4M
MECHANISMS OF BLADDER CANCER INVANSIONR29CA075115 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI THEODORESCU, DAN · 1997 to 2001
$217k
NCI NIH HHS P30 CA046934NCI NIH HHS R01 CA075115NCI NIH HHS R01 CA143971NCI NIH HHS R29 CA075115NHLBI NIH HHS R01 HL075092NLM NIH HHS T15 LM009451
6 · The paper itself

Abstract

The utility of tumor-derived cell lines is dependent on their ability to recapitulate underlying genomic aberrations and primary tumor biology. Here, we sequenced the exomes of 25 bladder cancer (BCa) cell lines and compared mutations, copy number alterations (CNAs), gene expression and drug response to BCa patient profiles in The Cancer Genome Atlas (TCGA). We observed a mutation pattern associated with altered CpGs and APOBEC-family cytosine deaminases similar to mutation signatures derived from somatic alterations in muscle-invasive (MI) primary tumors, highlighting a major mechanism(s) contributing to cancer-associated alterations in the BCa cell line exomes. Non-silent sequence alterations were confirmed in 76 cancer-associated genes, including mutations that likely activate oncogenes TERT and PIK3CA, and alter chromatin-associated proteins (MLL3, ARID1A, CHD6 and KDM6A) and established BCa genes (TP53, RB1, CDKN2A and TSC1). We identified alterations in signaling pathways and proteins with related functions, including the PI3K/mTOR pathway, altered in 60% of lines; BRCA DNA repair, 44%; and SYNE1-SYNE2, 60%. Homozygous deletions of chromosome 9p21 are known to target the cell cycle regulators CDKN2A and CDKN2B. This loci was commonly lost in BCa cell lines and we show the deletions extended to the polyamine enzyme methylthioadenosine (MTA) phosphorylase (MTAP) in 36% of lines, transcription factor DMRTA1 (27%) and antiviral interferon epsilon (IFNE, 19%). Overall, the BCa cell line genomic aberrations were concordant with those found in BCa patient tumors. We used gene expression and copy number data to infer pathway activities for cell lines, then used the inferred pathway activities to build a predictive model of cisplatin response. When applied to platinum-treated patients gathered from TCGA, the model predicted treatment-specific response. Together, these data and analysis represent a valuable community resource to model basic tumor biology and to study the pharmacogenomics of BCa.

Indexed as

GenomicsModels, BiologicalAntineoplastic AgentsBiomarkersCell Line, TumorChromosome DeletionChromosome MappingChromosomes, Human, Pair 9Cluster AnalysisComputational BiologyDNA Copy Number VariationsDNA MethylationExomeHigh-Throughput Nucleotide SequencingHumansMutationAntineoplastic AgentsBiomarkersPhosphatidylinositol 3-KinasesTOR Serine-Threonine Kinases

Identifiers

PMID27270441
PMCPMC5140783
OpenAlexW2412836466

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.