Evidence map›Paper›PMID 25779941›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015

Genomic landscape of human papillomavirus-associated cancers.

Maria Rusan, Yvonne Y Li, Peter S Hammerman

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 135 citations in OpenAlex.

  1. Trial
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  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Advances in cervical cancer: current insights and future directions.Cancer communications (London, England) · 2025
    Review
  14. Article
  15. Article
  16. Towards the elimination of infectious HPV: exploiting CRISPR/Cas innovations.Frontiers in cellular and infection microbiology · 2025
    Review
  17. Review
  18. Review
  19. Review
  20. Review

23 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Maria RusanDepartment of Clinical Medicine, Aarhus University, Denmark. Department of Otorhinolaryngology, Aarhus University, Denmark. Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts. Cancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Yvonne Y LiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts. Cancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Peter S HammermanDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts. Cancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts. phammerman@partners.org.
Dana-Farber Cancer Institute · USHarvard University · US

Funding

Genomic Discovery and Targeted Therapeutics in Squamous Cell Lung CancerK08CA163677 · NCI · DANA-FARBER CANCER INST · PI HAMMERMAN, PETER S · 2012 to 2016
$783k
NCI NIH HHS K08 CA163677NCI NIH HHS K08CA163677
6 · The paper itself

Abstract

Recent next-generation sequencing studies have generated a comprehensive overview of the genomic landscape of human papillomavirus (HPV)-associated cancers. This review summarizes these findings to provide insight into the tumor biology of these cancers and potential therapeutic opportunities for HPV-driven malignancies. In addition to the tumorigenic properties of the HPV oncoproteins, integration of HPV DNA into the host genome is suggested to be a driver of the neoplastic process. Integration may confer a growth and survival advantage via enhanced expression of viral oncoproteins, alteration of critical cellular genes, and changes in global promoter methylation and transcription. Alteration of cellular genes may lead to loss of function of tumor suppressor genes, enhanced oncogene expression, loss of function of DNA repair genes, or other vital cellular functions. Recurrent integrations in RAD51B, NR4A2, and TP63, leading to aberrant forms of these proteins, are observed in both HPV-positive head and neck squamous cell carcinoma (HNSCC) and cervical carcinoma. Additional genomic alterations, independent of integration events, include recurrent PIK3CA mutations (and aberrations in other members of the PI3K pathway), alterations in receptor tyrosine kinases (primarily FGFR2 and FGFR3 in HPV-positive HNSCC, and ERBB2 in cervical squamous cell carcinoma), and genes in pathways related to squamous cell differentiation and immune responses. A number of the alterations identified are potentially targetable, which may lead to advances in the treatment of HPV-associated cancers.

Indexed as

High-Throughput Nucleotide SequencingHumansNeoplasmsPapillomavirus Infections

Identifiers

PMID25779941
PMCPMC4417456
OpenAlexW2098158789

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.