Evidence map›Paper›PMID 38730612›Full record

ReviewCancers2024

The Causes and Consequences of DNA Damage and Chromosomal Instability Induced by Human Papillomavirus.

Kathryn M Jones, Ava Bryan, Emily McCunn, Pate E Lantz, Hunter Blalock, Isabel C Ojeda, Kavi Mehta, Pippa F Cosper

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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

8 authors.

Kathryn M JonesDepartment of Human Oncology, University of Wisconsin, Madison, WI 53705, USA.ORCID 0000-0002-4525-2071
Ava BryanDepartment of Human Oncology, University of Wisconsin, Madison, WI 53705, USA.
Emily McCunnDepartment of Human Oncology, University of Wisconsin, Madison, WI 53705, USA.
Pate E LantzDepartment of Human Oncology, University of Wisconsin, Madison, WI 53705, USA.
Hunter BlalockDepartment of Human Oncology, University of Wisconsin, Madison, WI 53705, USA.
Isabel C OjedaDepartment of Human Oncology, University of Wisconsin, Madison, WI 53705, USA.
Kavi MehtaDepartment of Comparative Biosciences, University of Wisconsin, Madison, WI 53705, USA.ORCID 0000-0002-2582-073X
Pippa F CosperDepartment of Human Oncology, University of Wisconsin, Madison, WI 53705, USA.ORCID 0000-0003-3362-5587

Funding

Project 3: Modulation of the head and neck tumor immune microenvironment by targeting the TAM family of receptorsP50CA278595 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Irene M Ong · 2022 to 2026
$12.5M
Project 4: Role of Receptor Tyrosine Kinase AXL in HNSCC Therapy ResistanceP50DE026787 · NIDCR · UNIVERSITY OF WISCONSIN-MADISON · PI HARARI, PAUL M · 2016 to 2020
$10.8M
Chromosomal Instability as a Marker and Mechanism of Radiation ResponseK08CA256166 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI COSPER, PIPPA F · 2021 to 2025
$926k
NCI NIH HHS K08 CA256166NCI NIH HHS P50 CA278595NIDCR NIH HHS P50 DE026787NIH HHS 1K08CA256166-01A1
6 · The paper itself

Abstract

High-risk human papillomaviruses (HPVs) are the main cause of cervical, oropharyngeal, and anogenital cancers, which are all treated with definitive chemoradiation therapy when locally advanced. HPV proteins are known to exploit the host DNA damage response to enable viral replication and the epithelial differentiation protocol. This has far-reaching consequences for the host genome, as the DNA damage response is critical for the maintenance of genomic stability. HPV+ cells therefore have increased DNA damage, leading to widespread genomic instability, a hallmark of cancer, which can contribute to tumorigenesis. Following transformation, high-risk HPV oncoproteins induce chromosomal instability, or chromosome missegregation during mitosis, which is associated with a further increase in DNA damage, particularly due to micronuclei and double-strand break formation. Thus, HPV induces significant DNA damage and activation of the DNA damage response in multiple contexts, which likely affects radiation sensitivity and efficacy. Here, we review how HPV activates the DNA damage response, how it induces chromosome missegregation and micronuclei formation, and discuss how these factors may affect radiation response. Understanding how HPV affects the DNA damage response in the context of radiation therapy may help determine potential mechanisms to improve therapeutic response.

Indexed as

alternative end-joiningchromosomal instability (CIN)DNA damage responsehuman papillomavirus (HPV)mitosisradiation

Identifiers

PMID38730612
PMCPMC11083350

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.