Evidence map›Paper›PMID 28611469›Full record

ArticleThe Journal of antibiotics2017

Antimicrobial sulfonamides clear latent Kaposi sarcoma herpesvirus infection and impair MDM2-p53 complex formation.

Fabrizio Angius, Enrica Piras, Sabrina Uda, Clelia Madeddu, Roberto Serpe, Rachele Bigi, Wuguo Chen, Dirk P Dittmer, Raffaello Pompei, Angela Ingianni

Abstract readComparative Study
In one paragraph

Article in The Journal of antibiotics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2022
    Review
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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

10 authors at 2 institutions in 2 countries.

Fabrizio AngiusDepartment of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
Enrica PirasDepartment of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
Sabrina UdaDepartment of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
Clelia MadedduDepartment of Medical Sciences, 'Mario Aresu', University of Cagliari, Cagliari, Italy.
Roberto SerpeDepartment of Medical Sciences, 'Mario Aresu', University of Cagliari, Cagliari, Italy.
Rachele BigiDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Wuguo ChenDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Dirk P DittmerDepartment of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Raffaello PompeiDepartment of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
Angela IngianniDepartment of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
University of Cagliari · ITUniversity of North Carolina at Chapel Hill · US

Funding

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
NCI NIH HHS R01 CA163217NIDCR NIH HHS R01 DE018304
6 · The paper itself

Abstract

Kaposi sarcoma herpesvirus (KSHV), also known as human herpesvirus 8, is the causative agent of Kaposi sarcoma; this malignant angiosarcoma is usually treated with conventional antitumor agents that can control disease evolution, but do not clear the latent KSHV episome that binds to cellular DNA. Some commercial antibacterial sulfonamides were tested for the ability to suppress latent KSHV. Quantitative PCR (qPCR) and cytofluorometry assays were used for detecting both viral DNA and the latency factor LANA (latency-associated nuclear antigen) in BC3 cells, respectively. The capacity of sulfonamides to impair MDM2-p53 complex formation was detected by an enzyme-linked immunosorbent assay method. The analysis of variance was performed according to one-way analysis of variance with Fisher as a post hoc test. Here we show that sulfonamide antibiotics are able to suppress the KSHV latent state in permanently infected BC3 lymphoma cells and interfere with the formation of the MDM2-p53 complex that KSHV seemingly needs to support latency and to trigger tumor cell transformation. These findings detected a new molecular target for the activity of sulfonamides and offer a new potential perspective for treating KSHV-induced lymphoproliferative diseases.

Indexed as

Anti-Bacterial AgentsAntigens, ViralAntiviral AgentsCell Line, TumorCells, CulturedCell SurvivalCell Transformation, NeoplasticCell Transformation, ViralDNA, ViralHerpesvirus 8, HumanHumansHuman Umbilical Vein Endothelial CellsInhibitory Concentration 50Nuclear ProteinsProtein MultimerizationProto-Oncogene Proteins c-mdm2Anti-Bacterial AgentsAntigens, ViralAntiviral AgentsDNA, Virallatency-associated nuclear antigenMDM2 protein, humanNuclear ProteinsProto-Oncogene Proteins c-mdm2Recombinant Fusion ProteinsSulfaguanidineSulfamethoxazoleSulfanilamideSulfanilamidesSulfathiazoleSulfathiazolesSulfonamidesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28611469
PMCPMC6002838
OpenAlexW2624747694

What OpenQuestion holds

Textmetadata
LicenceTDM
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.