Evidence map›Paper›PMID 26385761›Full record

ArticleThe Journal of general virology2015

Merkel cell polyomavirus T antigens promote cell proliferation and inflammatory cytokine gene expression.

Kathleen F Richards, Anna Guastafierro, Masahiro Shuda, Tuna Toptan, Patrick S Moore, Yuan Chang

Open access · greenAbstract read
In one paragraph

Article in The Journal of general virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 44 citations in OpenAlex.

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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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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

6 authors at 1 institution in 1 country.

Kathleen F RichardsCancer Virology Program, University of Pittsburgh, Pittsburgh, PA, USA.
Anna GuastafierroCancer Virology Program, University of Pittsburgh, Pittsburgh, PA, USA.
Masahiro ShudaCancer Virology Program, University of Pittsburgh, Pittsburgh, PA, USA.
Tuna ToptanCancer Virology Program, University of Pittsburgh, Pittsburgh, PA, USA.
Patrick S MooreCancer Virology Program, University of Pittsburgh, Pittsburgh, PA, USA.
Yuan ChangCancer Virology Program, University of Pittsburgh, Pittsburgh, PA, USA.
UPMC Hillman Cancer Center · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
Role of a New Polyomavirus in Merkel Cell CarcinomaR01CA136806 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MOORE, PATRICK S. · 2009 to 2015
$3.0M
Protein Biomarkers for a New Human Polyomavirus in AIDS-related MalignanciesR01CA136363 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MOORE, PATRICK S. · 2008 to 2015
$2.3M
Transcriptomic and Proteomic Approaches to Discovering Viral Causes for Human HemR01CA170354 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHANG, YUAN · 2012 to 2015
$1.3M
Training Program in Skin Biology and CancerT32CA175294 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KIRKWOOD, JOHN MUNN · 2014 to 2018
$973k
NCI NIH HHS CA12197305NCI NIH HHS CA136363NCI NIH HHS CA170354NCI NIH HHS CA175294NCI NIH HHS P30 CA047904NCI NIH HHS P30CA047904NCI NIH HHS R01 CA136363NCI NIH HHS R01 CA136806NCI NIH HHS R01CA136806NCI NIH HHS R01 CA170354NCI NIH HHS T32 CA175294
6 · The paper itself

Abstract

Merkel cell polyomavirus (MCV) is clonally integrated in over 80 % of Merkel cell carcinomas and mediates tumour development through the expression of viral oncoproteins, the large T (LT) and small T antigens (sT). Viral integration is associated with signature mutations in the T-antigen locus that result in deletions of C-terminal replicative functions of the LT antigen. Despite these truncations, the LT LXCXE retinoblastoma (Rb) pocket protein family binding domain is retained, and the entire sT isoform is maintained intact. To investigate the ability of MCV oncoproteins to regulate host gene expression, we performed microarray analysis on cells stably expressing tumour-derived LT, tumour-derived LT along with sT, and tumour-derived LT with a mutated Rb interaction domain. Gene expression alterations in the presence of tumour-derived LT could be classified into three main groups: genes that are involved in the cell cycle (specifically the G1/S transition), genes involved in DNA replication and genes involved in cellular movement. The LXCXE mutant LT largely reversed gene expression alterations detected with the WT tumour-derived LT, while co-expression of sT did not significantly affect these patterns of gene expression. LXCXE-dependent upregulation of cyclin E and CDK2 correlated with increased proliferation in tumour-derived LT-expressing cells. Tumour-derived LT and tumour-derived LT plus sT increased expression of multiple cytokines and chemokines, which resulted in elevated levels of secreted IL-8. We concluded that, in human fibroblasts, the LXCXE motif of tumour-derived LT enhances cellular proliferation and upregulates cell cycle and immune signalling gene transcription.

Indexed as

Antigens, Viral, TumorCell ProliferationCells, CulturedCytokinesDNA RepairDNA ReplicationFibroblastsGene Expression RegulationHumansInflammationMerkel cell polyomavirusSignal TransductionTranscription, GeneticUp-RegulationAntigens, Viral, TumorCytokines

Identifiers

PMID26385761
PMCPMC4804762
OpenAlexW2099942611

What OpenQuestion holds

Textmetadata
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.