Evidence map›Paper›PMID 26840090›Full record

ReviewOncotarget2016

CRISPR/Cas9 and cancer targets: future possibilities and present challenges.

Martyn K White, Kamel Khalili

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 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
5.0field-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.

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, 59 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Targeting Cancer with CRISPR/Cas9-Based Therapy.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Human genetic variation alters CRISPR-Cas9 on- and off-targeting specificity at therapeutically implicated loci.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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 at 1 institution in 1 country.

Martyn K WhiteDepartment of Neuroscience, Center for Neurovirology and Comprehensive Neuroaids Center, Temple University School of Medicine, Philadelphia, PA, USA.
Kamel KhaliliDepartment of Neuroscience, Center for Neurovirology and Comprehensive Neuroaids Center, Temple University School of Medicine, Philadelphia, PA, USA.
Temple University · US

Funding

Viral Gene Editing and Bioinformatics Core for Institution # 269291P30MH092177 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI Ilker Kudret Sariyer · 2011 to 2026
$24.9M
Cytokine regulation of JC virus latency and reactivationR01AI077460 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI WHITE, MARTYN K · 2008 to 2016
$3.2M
RNA-mediated excision of the HIV-1 genome from latently infected cells in CNSR01NS087971 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI HU, WENHUI, KHALILI, KAMEL · 2014 to 2016
$1.2M
NIAID NIH HHS R01 AI077460NIMH NIH HHS P30 MH092177NINDS NIH HHS R01 NS087971
6 · The paper itself

Abstract

All cancers have multiple mutations that can largely be grouped into certain classes depending on the function of the gene in which they lie and these include oncogenic changes that enhance cellular proliferation, loss of function of tumor suppressors that regulate cell growth potential and induction of metabolic enzymes that confer resistance to chemotherapeutic agents. Thus the ability to correct such mutations is an important goal in cancer treatment. Recent research has led to the developments of reagents which specifically target nucleotide sequences within the cellular genome and these have a huge potential for expanding our anticancer armamentarium. One such a reagent is the clustered regulatory interspaced short palindromic repeat (CRISPR)-associated 9 (Cas9) system, a powerful, highly specific and adaptable tool that provides unparalleled control for editing the cellular genome. In this short review, we discuss the potential of CRISPR/Cas9 against human cancers and the current difficulties in translating this for novel therapeutic approaches.

Indexed as

AnimalsClustered Regularly Interspaced Short Palindromic RepeatsGenetic TherapyHumansMutationNeoplasmscancer genome manipulationCRISPR/Cas9gene correctiongene therapyoncogene disruption

Identifiers

PMID26840090
PMCPMC4914286
OpenAlexW2258620013

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.