Evidence map›Paper›PMID 39518131›Full record

ReviewCancers2024

Molecular Mechanisms of Kaposi Sarcoma-Associated Herpesvirus (HHV8)-Related Lymphomagenesis.

Caroline J Yu, Blossom Damania

Abstract readReview
In one paragraph

Review in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
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

2 authors.

Caroline J YuDepartment of Microbiology & Immunology, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.ORCID 0000-0003-4801-0972
Blossom DamaniaDepartment of Microbiology & Immunology, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.ORCID 0000-0002-9205-1774

Funding

Vironomics and Biostatistics CoreP01CA019014 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, NANCY JOAN RAAB-TRAUB · 1985 to 2026
$43.8M
Training in Sexually Transmitted Infections and HIVT32AI007001 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SENA-SOBERANO, ARLENE C. · 1985 to 2025
$10.9M
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
Therapy for Non-Hodgkin lympomaR01CA291437 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA · 2024 to 2026
$2.2M
Targeting EBV-associated lymphomasU01CA294800 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA · 2024 to 2026
$1.9M
National Institutes of Health, USA CA019014, CA291437, CA294800, CA163217.NCI NIH HHS P01 CA019014NCI NIH HHS R01 CA163217NCI NIH HHS R01 CA291437NCI NIH HHS U01 CA294800NIAID NIH HHS T32 AI007001
6 · The paper itself

Abstract

Approximately 15-20% of cancers are caused by viruses. Kaposi sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8), is an oncogenic virus that is the etiologic agent of not only Kaposi sarcoma but also the lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD). KSHV can infect a broad tropism of cells, including B lymphocytes, wherein KSHV encodes specific viral proteins that can transform the cell. KSHV infection precedes the progression of PEL and MCD. KSHV establishes lifelong infection and has two phases of its lifecycle: latent and lytic. During the latent phase, viral genomes are maintained episomally with limited gene expression. Upon sporadic reactivation, the virus enters its replicative lytic phase to produce infectious virions. KSHV relies on its viral products to modulate host factors to evade immune detection or to co-opt their function for KSHV persistence. These manipulations dysregulate normal cell pathways to ensure cell survival and inhibit antiviral immune responses, which in turn, contribute to KSHV-associated malignancies. Here, we highlight the known molecular mechanisms of KSHV that promote lymphomagenesis and how these findings identify potential therapeutic targets for KSHV-associated lymphomas.

Indexed as

HHV8Kaposi sarcoma-associated herpesvirusKSHVlymphomalymphomagenesisviral oncogenesis

Identifiers

PMID39518131
PMCPMC11544871

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.