Evidence map›Paper›PMID 26317490›Full record

ArticleInternational journal of cancer2016

Human papillomavirus capsids preferentially bind and infect tumor cells.

Rhonda C Kines, Rebecca J Cerio, Jeffrey N Roberts, Cynthia D Thompson, Elisabet de Los Pinos, Douglas R Lowy, John T Schiller

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Papillomavirus-like particles as vectors forMolecular therapy. Nucleic acids · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Virus-inspired strategies for cancer therapy.Seminars in cancer biology · 2022
    Review
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  12. Article
  13. Article
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  15. Article
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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 at 4 institutions in 1 country.

Rhonda C KinesAura Biosciences, Cambridge, MA.
Rebecca J CerioLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Jeffrey N RobertsLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Cynthia D ThompsonLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Elisabet de Los PinosAura Biosciences, Cambridge, MA.
Douglas R LowyLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
John T SchillerLaboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Center for Cancer Research · USNational Cancer Institute · USPulse Biosciences (United States) · USNational Institutes of Health · US

Funding

Understanding Papillomavirus Virion Proteins and VaccinesZIABC009052 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHILLER, JOHN T. · 2009 to 2025
$38.4M
Papillomavirus Virion Proteins and VaccinesZIABC010579 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LOWY, DOUGLAS R. · 2009 to 2025
$15.4M
Papillomavirus Virion Proteins and Vaccines Z01BC009052 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI SCHILLER, JOHN T. · 1996 to 2008
$3.3M
Intramural NIH HHS Z01 BC009052
6 · The paper itself

Abstract

We previously determined that human papillomavirus (HPV) virus-like particles (VLPs) and pseudovirions (PsV) did not, respectively, bind to or infect intact epithelium of the cervicovaginal tract. However, they strongly bound heparan sulfate proteoglycans (HSPG) on the basement membrane of disrupted epithelium and infected the keratinocytes that subsequently entered the disrupted site. We here report that HPV capsids (VLP and PsV) have the same restricted tropism for a wide variety of disrupted epithelial and mesothelial tissues, whereas intact tissues remain resistant to binding. However, the HPV capsids directly bind and infect most tumor-derived cell lines in vitro and have analogous tumor-specific properties in vivo, after local or intravenous injection, using orthotopic models for human ovarian and lung cancer, respectively. The pseudovirions also specifically infected implanted primary human ovarian tumors. Heparin and ι-carrageenan blocked binding and infection of all tumor lines tested, implying that tumor cell binding is HSPG-dependent. A survey using a panel of modified heparins indicates that N-sulfation and, to a lesser degree, O-6 sulfation of the surface HSPG on the tumors are important for HPV binding. Therefore, it appears that tumor cells consistently evolve HSPG modification patterns that mimic the pattern normally found on the basement membrane but not on the apical surfaces of normal epithelial or mesothelial cells. Consequently, appropriately modified HPV VLPs and/or PsV could be useful reagents to detect and potentially treat a remarkably broad spectrum of cancers.

Indexed as

AnimalsCapsidCell Line, TumorCell SeparationFemaleHeparan Sulfate ProteoglycansHuman papillomavirus 16HumansMiceNeoplasmsPapillomavirus InfectionsHeparan Sulfate Proteoglycansheparan sulfate proteoglycanshuman papillomavirustumor tropism

Identifiers

PMID26317490
PMCPMC4715788
OpenAlexW1875219743

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.