Evidence map›Paper›PMID 17121789›Full record

ArticleJournal of virology2007

Functional p53 signaling in Kaposi's sarcoma-associated herpesvirus lymphomas: implications for therapy.

Christin E Petre, Sang-Hoon Sin, Dirk P Dittmer

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

81 citing papers in PubMed, 122 citations in OpenAlex.

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  19. Epstein-Barr virus enhances genome maintenance of Kaposi sarcoma-associated herpesvirus.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. Article

21 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

3 authors at 2 institutions in 1 country.

Christin E PetreLineberger Comprehensive Cancer Center, Center for AIDS Research and Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
Sang-Hoon Sin
Dirk P Dittmer
Johns Hopkins University Center for AIDS ResearchUniversity of North Carolina at Chapel Hill · US

Funding

Integrated Training in Cancer Model SystemsT32CA009156 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1985 to 2020
$19.7M
ART Modulation of Viral Pathogenesis in Oral EpitheliaR01DE018304 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2007 to 2025
$6.9M
Targeted Therapies for HIV-Associated Kaposi Sarcoma and LymphomaR01CA163217 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, Dirk P Dittmer · 2011 to 2026
$5.5M
Regulation of the KSHV Latent PromoterR01CA109232 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2004 to 2014
$2.5M
NCI NIH HHS CA009156NCI NIH HHS CA109232NCI NIH HHS CA700580NCI NIH HHS R01 CA109232NCI NIH HHS R01 CA163217NCI NIH HHS T32 CA009156NIDCR NIH HHS R01 DE018304
6 · The paper itself

Abstract

The Kaposi's sarcoma-associated herpesvirus (KSHV/HHV8) is associated with Kaposi's sarcoma (KS) as well as primary effusion lymphomas (PEL). The expression of viral proteins capable of inactivating the p53 tumor suppressor protein has been implicated in KSHV oncogenesis. However, DNA-damaging drugs such as doxorubicin are clinically efficacious against PEL and KS, suggesting that p53 signaling remains intact despite the presence of KSHV. To investigate the functionality of p53 in PEL, we examined the response of a large number of PEL cell lines to doxorubicin. Two out of seven (29%) PEL cell lines harbored a mutant p53 allele (BCBL-1 and BCP-1) which led to doxorubicin resistance. In contrast, all other PEL containing wild-type p53 showed DNA damage-induced cell cycle arrest, p53 phosphorylation, and p53 target gene activation. These data imply that p53-mediated DNA damage signaling was intact. Supporting this finding, chemical inhibition of p53 signaling in PEL led to doxorubicin resistance, and chemical activation of p53 by the Hdm2 antagonist Nutlin-3 led to unimpaired induction of p53 target genes as well as growth inhibition and apoptosis.

Indexed as

Herpesvirus 8, HumanAnimalsCell Cycle ProteinsCell LineCell Transformation, ViralDNA DamageDoxorubicinDrug Resistance, NeoplasmGene ExpressionHerpesviridae InfectionsImidazolesLymphomaPhosphorylationPiperazinesProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Cell Cycle ProteinsDoxorubicinImidazolesMDM2 protein, humannutlin 3PiperazinesProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID17121789
PMCPMC1797584
OpenAlexW2129377621

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.