Evidence map›Paper›PMID 21084867›Full record

ReviewCancer biology & therapy2010

Tumor viruses and cancer biology: Modulating signaling pathways for therapeutic intervention.

Abhik Saha, Rajeev Kaul, Masanao Murakami, Erle S Robertson

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Cancer biology & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05714748 (A Phase I Study of mRNA Vaccine for Patients With EBV-positive Advanced Malignant Tumors), which is not on this map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.1field-weighted citation impact, top 4% 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.

NCT05714748 phase1active not recruitingnot on this mapstarted 2023, after this paper: background citation

A Phase I Study of mRNA Vaccine for Patients With EBV-positive Advanced Malignant Tumors

TypeinterventionalSponsorWest China HospitalRan2023 to 2025Enrolled19ConditionsMalignant TumorsArmsEBV mRNA vaccine
3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
  2. Review
  3. Recent progress in mRNA cancer vaccines.Human vaccines & immunotherapeutics · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Malignancy: An Adverse Effect of Immunosuppression.Handbook of experimental pharmacology · 2022
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Clinical metagenomics.Nature reviews. Genetics · 2019
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

4 authors at 3 institutions in 4 countries.

Abhik SahaDepartment of Microbiology and Tumor Virology, University of Pennsylvania School of Medicine, Philadelphia, USA.
Rajeev Kaul
Masanao Murakami
Erle S Robertson
Schlumberger (Ireland) · IEUniversity of Delhi · INUniversity of Pennsylvania · US

Funding

Mechanism of KSHV reactivationR01DE017338 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S · 2005 to 2007
$811k
NIDCR NIH HHS R01 DE017338
6 · The paper itself

Abstract

Tumor viruses have provided relatively simple genetic systems, which can be manipulated for understanding the molecular mechanisms of the cellular transformation process. A growing body of information in the tumor virology field provides several prospects for rationally targeted therapies. However, further research is needed to better understand the multiple mechanisms utilized by these viruses in cancer progression in order to develop therapeutic strategies. Initially viruses were believed to be associated with cancers as causative agents only in animals. It was almost half a century before the first human tumor virus, Epstein-Barr virus (EBV), was identified in 1964. Subsequently, several human tumor viruses have been identified including Kaposi sarcoma associated herpesvirus (KSHV), human Papillomaviruses (HPV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), Human T lymphotropic virus (HTLV-1) and recently identified Merkel cell Polyomavirus (MCPyV). Tumor viruses are sub-categorized as either DNA viruses, which include EBV, KSHV, HPV, HBV, and MCPyV, or RNA viruses such as HCV and HTLV-1. Tumor-viruses induce oncogenesis through manipulating an array of different cellular pathways. These viruses initiate a series of cellular events, which lead to immortalization and proliferation of the infected cells by disrupting the mitotic checkpoint upon infection of the host cell. This is often accomplished by functional inhibition or proteasomal degradation of many tumor suppressor proteins by virally encoded gene products. The virally infected cells can either be eliminated via cell-mediated apoptosis or persist in a state of chronic infection. Importantly, the chronic persistence of infection by tumor viruses can lead to oncogenesis. This review discusses the major human tumor associated viruses and their ability to modulate numerous cell signaling pathways, which can be targeted for potential therapeutic approaches.

Indexed as

Antineoplastic AgentsHumansNeoplasmsOncogenic VirusesSignal TransductionTumor Virus InfectionsAntineoplastic Agents

Identifiers

PMID21084867
PMCPMC5965687
OpenAlexW2087206540

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.