Evidence map›Paper›PMID 16155595›Full record

ReviewOncogene2005

Viruses with deletions in antiapoptotic genes as potential oncolytic agents.

Ta-Chiang Liu, David Kirn

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Adenoviral vectors for prodrug activation-based gene therapy for cancer.Anti-cancer agents in medicinal chemistry · 2014
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. 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

2 authors.

Ta-Chiang LiuMolecular Neurosurgery Laboratory, Massachusetts General Hospital and Harvard Medical School, MA, USA. tachiangliu@yahoo.com
David Kirn

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Replication-selective oncolytic viruses have emerged as a new treatment platform for cancers. However, selectivity and potency need to be improved before virotherapy can become a standard treatment modality. In addition, mechanisms that can be incorporated to enable targeting a broad range of cancer types are highly desirable. Cancer cells are well known to have multiple blocks in apoptosis pathways. On the other hand, viruses have evolved to express numerous antiapoptotic genes to antagonize apoptosis induced upon infection. Viruses with deletions in antiapoptotic genes can therefore be complemented by antiapoptotic genetic changes in cancer cells for efficient replication and oncolysis. In this review, we summarize the recent development of this concept, the potential obstacles, and future directions for optimization.

Indexed as

Gene DeletionAnimalsApoptosisCaspase InhibitorsGenes, p53HumansInterferonsMutationNeoplasmsProtein KinasesVirusesCaspase InhibitorsInterferonsProtein Kinases

Identifiers

PMID16155595

What OpenQuestion holds

Textmetadata
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.