Evidence map›Paper›PMID 28049147›Full record

ArticlemBio2017

Merkel Cell Polyomavirus Exhibits Dominant Control of the Tumor Genome and Transcriptome in Virus-Associated Merkel Cell Carcinoma.

Gabriel J Starrett, Christina Marcelus, Paul G Cantalupo, Joshua P Katz, Jingwei Cheng, Keiko Akagi, Manisha Thakuria, Guilherme Rabinowits, Linda C Wang, David E Symer and 3 more

Open access · goldAbstract read
In one paragraph

Article in mBio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 126 citations in OpenAlex.

  1. Trial
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  4. Pharmacologic reversion of Merkel cell carcinoma via CBP/p300 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2025
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16 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

13 authors at 5 institutions in 1 country.

Gabriel J StarrettDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, University of Minnesota, Minneapolis, Minnesota, USA.
Christina MarcelusDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Paul G CantalupoDepartment of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Joshua P KatzDepartment of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Jingwei ChengDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Keiko AkagiHuman Cancer Genetics Program, The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA.
Manisha ThakuriaDepartment of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Guilherme RabinowitsDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Linda C WangDepartment of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
David E SymerHuman Cancer Genetics Program, The Ohio State University Comprehensive Cancer Center, Columbus, Ohio, USA.
James M PipasDepartment of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Reuben S HarrisDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, University of Minnesota, Minneapolis, Minnesota, USA rsh@umn.edu james_decaprio@dfci.harvard.edu.
James A DeCaprioDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA rsh@umn.edu james_decaprio@dfci.harvard.edu.ORCID 0000-0002-0896-167X
Brigham and Women's Hospital · USUniversity of Pittsburgh · USCancer Genetics (United States) · USUniversity of Minnesota · USDana-Farber Cancer Institute · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Jennifer A. Woyach · 1985 to 2026
$132.3M
VIRAL ONCOPROTEIN PERTURBATION OF RB/E2F PATHWAYP01CA050661 · NCI · DANA-FARBER CANCER INSTITUTE · PI DECAPRIO, JAMES A. · 1989 to 2013
$35.8M
RB-RELATED PROTEINS IN SV4OT AND E1A TRANSFORMATIONR01CA063113 · NCI · DANA-FARBER CANCER INSTITUTE · PI DECAPRIO, JAMES A. · 1994 to 2018
$5.0M
Transforming Mechanisms of Merkel Cell Polyoma VirusR01CA173023 · NCI · DANA-FARBER CANCER INST · PI DECAPRIO, JAMES A. · 2013 to 2019
$2.3M
Dr. Keiko Akagi, A Bioinformatics Specialist in Cancer Genomics Research at OSU Comprehensive Cancer CenterR50CA211533 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI AKAGI, KEIKO · 2016 to 2020
$608k
(PQ2) HIV INFECTION, APOBEC UPREGULATION, AND CANCER MUTAGENESISR21CA206309 · NCI · UNIVERSITY OF MINNESOTA · PI HARRIS, REUBEN S · 2016 to 2017
$401k
Searching Environmental Metagenomes for Novel Infectious Cancer Agents (PQ12)R21CA170248 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PIPAS, JAMES M · 2012 to 2013
$355k
Howard Hughes Medical InstituteNCI NIH HHS P01 CA050661NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA063113NCI NIH HHS R01 CA173023NCI NIH HHS R21 CA170248NCI NIH HHS R21 CA206309NCI NIH HHS R50 CA211533
6 · The paper itself

Abstract

Merkel cell polyomavirus is the primary etiological agent of the aggressive skin cancer Merkel cell carcinoma (MCC). Recent studies have revealed that UV radiation is the primary mechanism for somatic mutagenesis in nonviral forms of MCC. Here, we analyze the whole transcriptomes and genomes of primary MCC tumors. Our study reveals that virus-associated tumors have minimally altered genomes compared to non-virus-associated tumors, which are dominated by UV-mediated mutations. Although virus-associated tumors contain relatively small mutation burdens, they exhibit a distinct mutation signature with observable transcriptionally biased kataegic events. In addition, viral integration sites overlap focal genome amplifications in virus-associated tumors, suggesting a potential mechanism for these events. Collectively, our studies indicate that Merkel cell polyomavirus is capable of hijacking cellular processes and driving tumorigenesis to the same severity as tens of thousands of somatic genome alterations. IMPORTANCE: A variety of mutagenic processes that shape the evolution of tumors are critical determinants of disease outcome. Here, we sequenced the entire genome of virus-positive and virus-negative primary Merkel cell carcinomas (MCCs), revealing distinct mutation spectra and corresponding expression profiles. Our studies highlight the strong effect that Merkel cell polyomavirus has on the divergent development of viral MCC compared to the somatic alterations that typically drive nonviral tumorigenesis. A more comprehensive understanding of the distinct mutagenic processes operative in viral and nonviral MCCs has implications for the effective treatment of these tumors.

Indexed as

Gene Expression RegulationHost-Pathogen InteractionsAgedAged, 80 and overCarcinogenesisCarcinoma, Merkel CellFemaleGene Expression ProfilingHumansMaleMerkel cell polyomavirusMiddle AgedVirus Integration

Identifiers

PMID28049147
PMCPMC5210499
OpenAlexW2566487375

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.