Evidence map›Paper›PMID 26462293›Full record

ArticleMolecular therapy oncolytics

Designing Herpes Viruses as Oncolytics.

Cole Peters, Samuel D Rabkin

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
8.4field-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

70 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Oncolytic viruses: advanced strategies in cancer therapy.Signal transduction and targeted therapy · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Oncolytic α-herpesvirus and myeloid-tropic cytomegalovirus cooperatively enhance systemic antitumor responses.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  18. Article
  19. Review
  20. Review

10 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

2 authors at 1 institution in 1 country.

Cole PetersProgram in Virology, Harvard Medical School, Boston, MA, and Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston MA.
Samuel D RabkinProgram in Virology, Harvard Medical School, Boston, MA, and Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston MA.
Massachusetts General Hospital · US

Funding

GENETICALLY ENGINEERED VIRUSES FOR BRAIN TUMOR THERAPYR01NS032677 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MARTUZA, ROBERT L · 1994 to 2022
$9.0M
Targeting Tumorigenic Pathways in Glioblastoma with Oncolytic HSVR01CA160762 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI RABKIN, SAMUEL DAVID · 2012 to 2023
$3.7M
Genetically Engineered Viruses for Prostate Cancer TherapyR01CA102139 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI MARTUZA, ROBERT L · 2004 to 2014
$3.3M
Oncolytic Herpes Simplex Virus Interactions with Glioblastoma Stem CellsF31CA192453 · NCI · HARVARD MEDICAL SCHOOL · PI PETERS, COLE WINSTEAD DYLAN · 2015 to 2017
$83k
NCI NIH HHS F31 CA192453NCI NIH HHS R01 CA102139NCI NIH HHS R01 CA160762NINDS NIH HHS R01 NS032677
6 · The paper itself

Abstract

Oncolytic herpes simplex virus (oHSV) was one of the first genetically-engineered oncolytic viruses. Because herpes simplex virus (HSV) is a natural human pathogen that can cause serious disease, it is incumbent that it be genetically-engineered or significantly attenuated for safety. Here we present a detailed explanation of the functions of HSV-1 genes frequently mutated to endow oncolytic activity. These genes are non-essential for growth in tissue culture cells but are important for growth in post-mitotic cells, interfering with intrinsic antiviral and innate immune responses or causing pathology, functions dispensable for replication in cancer cells. Understanding the function of these genes leads to informed creation of new oHSVs with better therapeutic efficacy. Virus infection and replication can also be directed to cancer cells through tumor-selective receptor binding and transcriptional- or post-transcriptional miRNA-targeting, respectively. In addition to the direct effects of oHSV on infected cancer cells and tumors, oHSV can be 'armed' with transgenes that are: reporters, to track virus replication and spread; cytotoxic, to kill uninfected tumor cells; immune modulatory, to stimulate anti-tumor immunity; or tumor microenvironment altering, to enhance virus spread or to inhibit tumor growth. In addition to HSV-1, other alphaherpesviruses are also discussed for their oncolytic activity.

Identifiers

PMID26462293
PMCPMC4599707
OpenAlexW2428390281

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.