Evidence map›Paper›PMID 26473186›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015

Invasive Bladder Cancer: Genomic Insights and Therapeutic Promise.

Jaegil Kim, Rehan Akbani, Chad J Creighton, Seth P Lerner, John N Weinstein, Gad Getz, David J Kwiatkowski

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
14.8field-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

74 citing papers in PubMed, 136 citations in OpenAlex.

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14 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

7 authors at 3 institutions in 1 country.

Jaegil KimThe Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts. dk@rics.bwh.harvard.edu jaegil@broadinstitute.org.
Rehan AkbaniUniversity of Texas MD Anderson Cancer Center, Houston, Texas.
Chad J CreightonBaylor College of Medicine, Houston, Texas.
Seth P LernerBaylor College of Medicine, Houston, Texas.
John N WeinsteinUniversity of Texas MD Anderson Cancer Center, Houston, Texas.
Gad GetzThe Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts. Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
David J KwiatkowskiThe Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts. Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. dk@rics.bwh.harvard.edu jaegil@broadinstitute.org.
Baylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · USMassachusetts General Hospital · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Integrative Pipeline for Analysis & Translational Application of TCGA Data (GDAC)U24CA143883 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI AKBANI, REHAN, MILLS, GORDON B. · 2009 to 2016
$10.6M
The BCM Tumor Genome Characterization CenterU24CA143843 · NCI · BAYLOR COLLEGE OF MEDICINE · PI GIBBS, RICHARD A, WHEELER, DAVID ANDREW · 2009 to 2013
$9.5M
Next-Generation Clustered Heat Maps for fluent, interactive exploration of omic data: Cloud Pilot SupplementU24CA199461 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BROOM, BRADLEY MCINTOSH, WEINSTEIN, JOHN N · 2015 to 2019
$2.7M
Genetic Predictors of Response to mTOR inhibitors in advanced Renal CancerR21CA191687 · NCI · DANA-FARBER CANCER INST · PI CHOUEIRI, TONI, KWIATKOWSKI, DAVID J. · 2015 to 2016
$421k
NCI NIH HHS CA143883NCI NIH HHS P01 CA120964NCI NIH HHS P01CA120964NCI NIH HHS P30 CA016672NCI NIH HHS P30CA016672NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCI NIH HHS R21 CA191687NCI NIH HHS U24 CA143843NCI NIH HHS U24CA143843NCI NIH HHS U24 CA143883NCI NIH HHS U24 CA199461PHS HHS RP130397
6 · The paper itself

Abstract

Invasive bladder cancer, for which there have been few therapeutic advances in the past 20 years, is a significant medical problem associated with metastatic disease and frequent mortality. Although previous studies had identified many genetic alterations in invasive bladder cancer, recent genome-wide studies have provided a more comprehensive view. Here, we review those recent findings and suggest therapeutic strategies. Bladder cancer has a high mutation rate, exceeded only by lung cancer and melanoma. About 65% of all mutations are due to APOBEC-mediated mutagenesis. There is a high frequency of mutations and/or genomic amplification or deletion events that affect many of the canonical signaling pathways involved in cancer development: cell cycle, receptor tyrosine kinase, RAS, and PI-3-kinase/mTOR. In addition, mutations in chromatin-modifying genes are unusually frequent in comparison with other cancers, and mutation or amplification of transcription factors is also common. Expression clustering analyses organize bladder cancers into four principal groups, which can be characterized as luminal, immune undifferentiated, luminal immune, and basal. The four groups show markedly different expression patterns for urothelial differentiation (keratins and uroplakins) and immunity genes (CD274 and CTLA4), among others. These observations suggest numerous therapeutic opportunities, including kinase inhibitors and antibody therapies for genes in the canonical signaling pathways, histone deacetylase inhibitors and novel molecules for chromatin gene mutations, and immune therapies, which should be targeted to specific patients based on genomic profiling of their cancers.

Indexed as

AnimalsAntineoplastic AgentsGenomicsHumansMutationSignal TransductionUrinary Bladder NeoplasmsAntineoplastic Agents

Identifiers

PMID26473186
PMCPMC4610178
OpenAlexW2196566976

What OpenQuestion holds

Textmetadata
LicenceTDM
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.