Evidence map›Paper›PMID 34696429›Full record

ReviewViruses2021

Genomic Signatures in HPV-Associated Tumors.

Suleman S Hussain, Devon Lundine, Jonathan E Leeman, Daniel S Higginson

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. HPV16 E6 oncoprotein promotes microhomology-mediated viral integration by increasing PolΘ protein expression.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Tumor Antigens beyond the Human Exome.International journal of molecular sciences · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

4 authors at 2 institutions in 1 country.

Suleman S HussainDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0003-1342-143X
Devon LundineDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0003-4845-3116
Jonathan E LeemanDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02189, USA.
Daniel S HigginsonDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0002-6686-7454
Memorial Sloan Kettering Cancer Center · USHarvard University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Comprehensive breakpoint analyses for simultaneous quantification of all DNA double strand break repair pathwaysR33CA236670 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI HIGGINSON, DANIEL · 2020 to 2020
$1.3M
NCI NIH HHS P30 CA008748NCI NIH HHS P30CA008748NCI NIH HHS R33 CA236670-01A1
6 · The paper itself

Abstract

Papillomaviruses dysregulate the G1/S cell cycle transition in order to promote DNA synthesis in S phase, which is a requirement for viral replication. The human papillomaviruses (HPV) E6 and E7 oncoproteins mediate degradation of the cell cycle regulators p53 and Rb, which are two of the most universally disrupted tumor-suppressor genes in all of cancer. The G1/S checkpoint is activated in normal cells to allow sufficient time for DNA repair in G1 before proceeding to replicate DNA and risk propagating unrepaired errors. The TP53 pathway suppresses a variety of such errors, including translocation, copy number alterations, and aneuploidy, which are thus found in HPV-associated tumors similarly to HPV-negative tumors with other mechanisms of TP53 disruption. However, E6 and E7 maintain a variety of other virus-host interactions that directly disrupt a growing list of other DNA repair and chromatin remodeling factors, implying HPV-specific repair deficiencies. In addition, HPV-associated squamous cell carcinomas tumors clinically respond differently to DNA damaging agents compared to their HPV negative counterparts. The focus of this review is to integrate three categories of observations: (1) pre-clinical understanding as to the effect of HPV on DNA repair, (2) genomic signatures of DNA repair in HPV-associated tumor genomes, and (3) clinical responses of HPV-associated tumors to DNA damaging agents. The goals are to try to explain why HPV-associated tumors respond so well to DNA damaging agents, identify missing pieces, and suggest clinical strategies could be used to further improve treatment of these cancers.

Indexed as

AlphapapillomavirusCarcinoma, Squamous CellCell CycleDNA RepairDNA, ViralFemaleGenomicsHumansNeoplasmsOncogene Proteins, ViralPapillomaviridaePapillomavirus E7 ProteinsPapillomavirus InfectionsRepressor ProteinsRetinoblastoma ProteinTumor Suppressor Protein p53DNA, ViralE6 protein, human papillomavirus type 1Oncogene Proteins, ViralPapillomavirus E7 ProteinsRepressor ProteinsRetinoblastoma ProteinTP53 protein, humanTumor Suppressor Protein p53alternative end-joiningDNA repairE6 E7 oncoproteinshuman papillomavirus

Identifiers

PMID34696429
PMCPMC8537705
OpenAlexW3203223682

What Socratic 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 Socratic graph.