Evidence map›Paper›PMID 30224344›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2019

Divergent Biological Response to Neoadjuvant Chemotherapy in Muscle-invasive Bladder Cancer.

Roland Seiler, Ewan A Gibb, Natalie Q Wang, Htoo Zarni Oo, Hung-Ming Lam, Kim E van Kessel, Charlotte S Voskuilen, Brian Winters, Nicholas Erho, Mandeep M Takhar and 13 more

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing 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

64 citing papers in PubMed.

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  4. Bioinformatics analysis and clinical validation identifyTranslational andrology and urology · 2026
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4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors.

Roland Seiler *Department of Urologic Sciences, University of British Columbia, Vancouver, British Columbia, Canada. r_seiler@gmx.ch.ORCID 0000-0002-3529-2088
Ewan A Gibb *GenomeDx Biosciences, Inc., Vancouver, British Columbia, Canada.
Natalie Q WangGenomeDx Biosciences, Inc., Vancouver, British Columbia, Canada.
Htoo Zarni OoDepartment of Urologic Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Hung-Ming LamDepartment of Urology, University of Washington School of Medicine, Seattle, Washington.
Kim E van KesselDepartment of Pathology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands.
Charlotte S VoskuilenDivision of Urology, Department of Surgical Oncology, Netherlands Cancer Institute - Antoni van Leeuwenhoek Hospital, Amsterdam, the Netherlands.ORCID 0000-0002-6507-118X
Brian WintersDepartment of Urology, University of Washington School of Medicine, Seattle, Washington.
Nicholas ErhoGenomeDx Biosciences, Inc., Vancouver, British Columbia, Canada.
Mandeep M TakharGenomeDx Biosciences, Inc., Vancouver, British Columbia, Canada.
James DouglasDepartment of Urology, University Hospital of Southampton, Hampshire, United Kingdom.
Funda Vakar-LopezDepartment of Urology, University of Washington School of Medicine, Seattle, Washington.
Simon J CrabbDepartment of Medical Oncology, University Hospital of Southampton, Hampshire, United Kingdom.ORCID 0000-0003-3521-9064
Bas W G van RhijnDivision of Urology, Department of Surgical Oncology, Netherlands Cancer Institute - Antoni van Leeuwenhoek Hospital, Amsterdam, the Netherlands.
Elisabeth E Fransen van de PutteDivision of Urology, Department of Surgical Oncology, Netherlands Cancer Institute - Antoni van Leeuwenhoek Hospital, Amsterdam, the Netherlands.
Ellen C ZwarthoffDepartment of Pathology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands.
George N ThalmannDepartment of Urology, University Hospital Bern, Bern, Switzerland.
Elai DavicioniGenomeDx Biosciences, Inc., Vancouver, British Columbia, Canada.ORCID 0000-0001-9136-099X
Joost L BoormansDepartment of Urology, Erasmus MC Cancer Institute, Rotterdam, the Netherlands.
Marc Dall'EraUC Davis Comprehensive Cancer Center, Sacramento, California.
Michiel S van der HeijdenDepartment of Medical Oncology, University Hospital of Southampton, Hampshire, United Kingdom.
Jonathan L WrightDepartment of Urology, University of Washington School of Medicine, Seattle, Washington.
Peter C BlackDepartment of Urologic Sciences, University of British Columbia, Vancouver, British Columbia, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAfter cisplatin-based neoadjuvant chemotherapy (NAC), 60% of patients with muscle-invasive bladder cancer (MIBC) still have residual invasive disease at radical cystectomy. The NAC-induced biological alterations in these cisplatin-resistant tumors remain largely unstudied. EXPERIMENTAL

designRadical cystectomy samples were available for gene expression analysis from 133 patients with residual invasive disease after cisplatin-based NAC, of whom 116 had matched pre-NAC samples. Unsupervised consensus clustering (CC) was performed and the consensus clusters were investigated for their biological and clinical characteristics. Hematoxylin & Eosin and IHC on tissue microarrays were used to confirm tissue sampling and gene expression analysis.

resultsEstablished molecular subtyping models proved to be inconsistent in their classification of the post-NAC samples. Unsupervised CC revealed four distinct consensus clusters. The CC1-Basal and CC2-Luminal subtypes expressed genes consistent with a basal and a luminal phenotype, respectively, and were similar to the corresponding established pretreatment molecular subtypes. The CC3-Immune subtype had the highest immune activity, including T-cell infiltration and checkpoint molecule expression, but lacked both basal and luminal markers. The CC4-Scar-like subtype expressed genes associated with wound healing/scarring, although the proportion of tumor cell content in this subtype did not differ from the other subtypes. Patients with CC4-Scar-like tumors had the most favorable prognosis.

conclusionsThis study expands our knowledge on MIBC not responding to cisplatin by suggesting molecular subtypes to understand the biology of these tumors. Although these molecular subtypes imply consequences for adjuvant treatments, this ultimately needs to be tested in clinical trials.

Indexed as

AgedBiomarkers, TumorCisplatinCystectomyFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoadjuvant TherapyNeoplasm ProteinsUrinary Bladder NeoplasmsBiomarkers, TumorCisplatinNeoplasm Proteins

Identifiers

What OpenQuestion holds

Textmetadata
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.