Evidence map›Paper›PMID 41734070›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

Human oncogenic herpesvirus latency proteins activate NEK2 to promote chromosomal instability and tumorigenesis.

Dipayan Bose, Nian Ma, Rajnish Kumar Singh, Ramakrishna Vangala, Atharva Torne, Kiran Chunduru, Erle S Robertson

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

Dipayan BoseDepartments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.
Nian MaDepartments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.
Rajnish Kumar SinghDepartments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.
Ramakrishna VangalaDepartments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.
Atharva TorneDepartments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.ORCID 0009-0006-1692-8913
Kiran ChunduruDepartments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.ORCID 0000-0001-5823-7252
Erle S RobertsonDepartments of Otorhinolaryngology-Head and Neck Surgery, and Microbiology, The Tumor Virology Program, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.ORCID 0000-0002-6088-2979

Funding

Tumor suppressor reprogramming by EBV through post-translational modificationR01CA268998 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2022 to 2025
$2.6M
Epigenetic Regulation of KSHV Genome ReplicationR01CA244074 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2019 to 2023
$2.5M
HHS | NIH | National Cancer Institute (NCI) R01-CA244074HHS | NIH | National Cancer Institute (NCI) R01-CA268998NCI NIH HHS R01 CA244074NCI NIH HHS R01 CA268998
6 · The paper itself

Abstract

Never in mitosis A (NIMA)-related kinase 2 (NEK2) is a serine/threonine kinase that plays a crucial role in cell cycle regulation and is frequently induced across multiple cancer types, where its elevated levels are associated with poor prognosis. Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), both known to drive various malignancies, were observed to induce NEK2 expression during both primary infection and latent phases of infection. Increased NEK2 expression contributes to chromosomal instability by promoting nondisjunction, leading to a rise in aneuploid cell populations and fostering uncontrolled cell proliferation. Mechanistically, EBV latent protein EBNA2 and KSHV latent antigen LANA were identified as principal regulators of NEK2 upregulation, acting through modulation of RBP-Jκ activities at the NEK2 promoter region. Additionally, we demonstrated that targeting NEK2 impaired EBV- and KSHV-mediated tumor progression, highlighting its potential as a critical driver of virus-induced oncogenesis and a promising therapeutic target.

Indexed as

CarcinogenesisChromosomal InstabilityEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanHerpesvirus 8, HumanNIMA-Related KinasesVirus LatencyAnimalsAntigens, ViralHumansNuclear ProteinsViral ProteinsAntigens, ViralEBNA-2 protein, Human herpesvirus 4Epstein-Barr Virus Nuclear Antigenslatency-associated nuclear antigenNEK2 protein, humanNIMA-Related KinasesNuclear ProteinsViral Proteinscellular kinaseschromosomal nondisjunctionEBVKSHVnever in mitosis A-related kinase

Identifiers

PMID41734070
PMCPMC12956877

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.