Evidence map›Paper›PMID 28325870›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

CRISPR-Cas9-guided oncogenic chromosomal translocations with conditional fusion protein expression in human mesenchymal cells.

Fabio Vanoli, Mark Tomishima, Weiran Feng, Khadija Lamribet, Loelia Babin, Erika Brunet, Maria Jasin

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.9field-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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Small round cell sarcomas.Nature reviews. Disease primers · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Rapid interrogation of cancer cell of origin through CRISPR editing.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  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

7 authors at 3 institutions in 2 countries.

Fabio VanoliDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Mark TomishimaDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Weiran FengDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Khadija LamribetGenome Dynamics of the Immune System, INSERM, UMR 1163, Imagine Institute, Paris, France.
Loelia BabinGenome Dynamics of the Immune System, INSERM, UMR 1163, Imagine Institute, Paris, France.
Erika BrunetGenome Dynamics of the Immune System, INSERM, UMR 1163, Imagine Institute, Paris, France.
Maria JasinDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065; m-jasin@ski.mskcc.org.
Memorial Sloan Kettering Cancer Center · USInstitut des Maladies Génétiques Imagine · FRInserm · FR

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
HOMOLOGY-DIRECTED DNA REPAIR PROTEINS BRCA2 AND RAD51 PARALOGS IN TUMOR-RELEVANT TISSUESR01CA185660 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA · 2014 to 2020
$2.7M
Homologous recombination mechanisms in mammalian cellsR35GM118175 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA · 2016 to 2020
$2.6M
NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA185660NIGMS NIH HHS R35 GM118175
6 · The paper itself

Abstract

Gene editing techniques have been extensively used to attempt to model recurrent genomic rearrangements found in tumor cells. These methods involve the induction of double-strand breaks at endogenous loci followed by the identification of breakpoint junctions within a population, which typically arise by nonhomologous end joining. The low frequency of these events, however, has hindered the cloning of cells with the desired rearrangement before oncogenic transformation. Here we present a strategy combining CRISPR-Cas9 technology and homology-directed repair to allow for the selection of human mesenchymal stem cells harboring the oncogenic translocation

Indexed as

Translocation, GeneticCRISPR-Cas SystemsDNA Breaks, Double-StrandedGene EditingHumansMesenchymal Stem CellsOncogene Proteins, FusionPromoter Regions, GeneticRNA-Binding Protein EWSWT1 ProteinsEWSR1 protein, humanOncogene Proteins, FusionRNA-Binding Protein EWSWT1 protein, humanWT1 Proteinschromosomal translocationCRISPR-Cas9DSRCTEWSR1–WT1homology-directed repair

Identifiers

PMID28325870
PMCPMC5389291
OpenAlexW2602745715

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.