Evidence map›Paper›PMID 23514892›Full record

ArticleJournal of virology2013

Merkel cell polyomavirus large T antigen has growth-promoting and inhibitory activities.

Jingwei Cheng, Orit Rozenblatt-Rosen, Kelly G Paulson, Paul Nghiem, James A DeCaprio

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
6.7field-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

89 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
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  5. 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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  18. Unlicensed origin DNA melting by MCV and SV40 polyomavirus LT proteins is independent of ATP-dependent helicase activity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. Article
  20. Article

29 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

5 authors at 3 institutions in 1 country.

Jingwei ChengDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Orit Rozenblatt-Rosen
Kelly G Paulson
Paul Nghiem
James A DeCaprio
Brigham and Women's Hospital · USUniversity of Washington Medical Center · USHarvard University · US

Funding

VIRAL ONCOPROTEIN PERTURBATION OF RB/E2F PATHWAYP01CA050661 · NCI · DANA-FARBER CANCER INSTITUTE · PI HAHN, WILLIAM C. · 1989 to 2013
$35.8M
University of Washington Medical Scientist Training Program: MD/PhDT32GM007266 · NIGMS · UNIVERSITY OF WASHINGTON · PI HORWITZ, MARSHALL S. · 1985 to 2023
$30.4M
RB-RELATED PROTEINS IN SV4OT AND E1A TRANSFORMATIONR01CA063113 · NCI · DANA-FARBER CANCER INSTITUTE · PI DECAPRIO, JAMES A. · 1994 to 2018
$5.0M
Interaction Between SV40 Large T and P185 CullinR01CA093804 · NCI · DANA-FARBER CANCER INSTITUTE · PI DECAPRIO, JAMES A. · 2002 to 2011
$3.0M
Pathogenetic and prognostic studies for improved therapy of Merkel cell carcinomaK24CA139052 · NCI · UNIVERSITY OF WASHINGTON · PI NGHIEM, PAUL · 2009 to 2018
$1.8M
Humoral and cellular immunity in polyomavirus-linked Merkel cell carcinomaR01CA162522 · NCI · UNIVERSITY OF WASHINGTON · PI NGHIEM, PAUL · 2011 to 2015
$1.6M
NCI NIH HHS K24 CA139052NCI NIH HHS K24-CA139052NCI NIH HHS P01 CA050661NCI NIH HHS P01CA050661NCI NIH HHS R01 CA063113NCI NIH HHS R01 CA093804NCI NIH HHS R01 CA162522NCI NIH HHS R01CA162522NCI NIH HHS R01CA93804NIGMS NIH HHS T32 GM007266
6 · The paper itself

Abstract

Merkel cell carcinoma (MCC) is a rare and aggressive form of skin cancer. In at least 80% of all MCC, Merkel cell polyomavirus (MCPyV) DNA has undergone clonal integration into the host cell genome, and most tumors express the MCPyV large and small T antigens. In all cases of MCC reported to date, the integrated MCPyV genome has undergone mutations in the large T antigen. These mutations result in expression of a truncated large T antigen that retains the Rb binding or LXCXE motif but deletes the DNA binding and helicase domains. However, the transforming functions of full-length and truncated MCPyV large T antigen are unknown. We compared the transforming activities of full-length, truncated, and alternatively spliced 57kT forms of MCPyV large T antigen. MCPyV large T antigen could bind to Rb but was unable to bind to p53. Furthermore, MCPyV-truncated large T antigen was more effective than full-length and 57kT large T antigen in promoting the growth of human and mouse fibroblasts. In contrast, expression of the MCPyV large T antigen C-terminal 100 residues could inhibit the growth of several different cell types. These data imply that the deletion of the C terminus of MCPyV large T antigen found in MCC serves not only to disrupt viral replication but also results in the loss of a distinct growth-inhibitory function intrinsic to this region.

Indexed as

Amino Acid MotifsAnimalsAntigens, Polyomavirus TransformingCarcinoma, Merkel CellCell ProliferationCell Transformation, NeoplasticGrowth SubstancesHumansMerkel cell polyomavirusMiceSkin NeoplasmsTumor Virus InfectionsAntigens, Polyomavirus TransformingGrowth Substances

Identifiers

PMID23514892
PMCPMC3648111
OpenAlexW2111566951

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.