Evidence map›Paper›PMID 31871154›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer.

Sheng Rong Ng, William M Rideout, Elliot H Akama-Garren, Arjun Bhutkar, Kim L Mercer, Jason M Schenkel, Roderick T Bronson, Tyler Jacks

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.6field-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

46 citing papers in PubMed, 79 citations in OpenAlex.

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  10. Nonviral CRISPR/Cas9 mutagenesis for streamlined generation of mouse lung cancer models.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

8 authors at 4 institutions in 1 country.

Sheng Rong NgDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
William M RideoutDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Elliot H Akama-GarrenDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Arjun BhutkarDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Kim L MercerDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.ORCID 0000-0002-8525-483X
Jason M SchenkelDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Roderick T BronsonDepartment of Pathology, Tufts University School of Veterinary Medicine, North Grafton, MA 01536.
Tyler JacksDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139; tjacks@mit.edu.
Massachusetts Institute of Technology · USHoward Hughes Medical Institute · USBrigham and Women's Hospital · USTufts University · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014051NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is a highly aggressive subtype of lung cancer that remains among the most lethal of solid tumor malignancies. Recent genomic sequencing studies have identified many recurrently mutated genes in human SCLC tumors. However, the functional roles of most of these genes remain to be validated. Here, we have adapted the CRISPR-Cas9 system to a well-established murine model of SCLC to rapidly model loss-of-function mutations in candidate genes identified from SCLC sequencing studies. We show that loss of the gene

Indexed as

Gene Expression Regulation, NeoplasticGenes, Tumor SuppressorAnimalsApoptosisCell LineCell ProliferationCRISPR-Cas SystemsDisease Models, AnimalDisease ProgressionFeasibility StudiesGene EditingHumansLoss of Function MutationLungLung NeoplasmsMiceRbl1 protein, mouseRbl2 protein, mouseRetinoblastoma-Like Protein p107Retinoblastoma-Like Protein p130Trp53 protein, mouseTumor Suppressor Protein p53CRISPRGEMMp107small cell lung cancer

Identifiers

PMID31871154
PMCPMC6955235
OpenAlexW2997345748

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.