Evidence map›Paper›PMID 24853101›Full record

ReviewCancer genetics2014

Mechanisms by which SMARCB1 loss drives rhabdoid tumor growth.

Kimberly H Kim, Charles W M Roberts

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

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27 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.

Kimberly H KimDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Division of Hematology/Oncology, Children's Hospital, Boston, MA, USA; Department of Pediatrics, Harvard Medical School, Boston, MA, USA; Broad Institute of Harvard and Massachusetts Institute of Technology, Boston, MA, USA.
Charles W M RobertsDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Division of Hematology/Oncology, Children's Hospital, Boston, MA, USA; Department of Pediatrics, Harvard Medical School, Boston, MA, USA; Broad Institute of Harvard and Massachusetts Institute of Technology, Boston, MA, USA. Electronic address: Charles_Roberts@dfci.harvard.edu.
Boston Children's Hospital · US

Funding

Systems Analysis of Cancer Pathways in Mouse ModelsU01CA105423 · NCI · DANA-FARBER CANCER INSTITUTE · PI ORKIN, STUART H · 2004 to 2013
$8.4M
THE FUNCTION OF SNF5 (SMARCB1), AN EPIGENETIC TUMOR SUPPRESSORR01CA113794 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 2005 to 2026
$7.8M
Role of the SWI/SNF complex in tumor suppressionR01CA172152 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 2013 to 2026
$5.1M
NCI NIH HHS R01 CA113794NCI NIH HHS R01CA113794NCI NIH HHS R01 CA172152NCI NIH HHS R01CA172152NCI NIH HHS U01 CA105423
6 · The paper itself

Abstract

SMARCB1 (INI1/SNF5/BAF47), a core subunit of the SWI/SNF (BAF) chromatin-remodeling complex, is inactivated in the large majority of rhabdoid tumors, and germline heterozygous SMARCB1 mutations form the basis for rhabdoid predisposition syndrome. Mouse models validated Smarcb1 as a bona fide tumor suppressor, as Smarcb1 inactivation in mice results in 100% of the animals rapidly developing cancer. SMARCB1 was the first subunit of the SWI/SNF complex found mutated in cancer. More recently, at least seven other genes encoding SWI/SNF subunits have been identified as recurrently mutated in cancer. Collectively, 20% of all human cancers contain a SWI/SNF mutation. Consequently, investigation of the mechanisms by which SMARCB1 mutation causes cancer has relevance not only for rhabdoid tumors, but also potentially for the wide variety of SWI/SNF mutant cancers. Here we discuss normal functions of SMARCB1 and the SWI/SNF complex as well as mechanistic and potentially therapeutic insights that have emerged.

Indexed as

AnimalsChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneCyclin D1Cyclin-Dependent Kinase 4DNA-Binding ProteinsEnzyme ActivationHumansMiceMutationNucleosomesRhabdoid TumorSMARCB1 ProteinTranscription FactorsTumor Suppressor ProteinsCDK4 protein, humanChromosomal Proteins, Non-HistoneCyclin D1Cyclin-Dependent Kinase 4DNA-Binding ProteinsNucleosomesSMARCB1 ProteinSMARCB1 protein, humanSWI-SNF-B chromatin-remodeling complexTranscription FactorsTumor Suppressor Proteinschromatin-remodeling complexRhabdoid tumorSMARCB1SNF5SWI/SNF

Identifiers

PMID24853101
PMCPMC4195815
OpenAlexW2122722975

What OpenQuestion holds

Textmetadata
LicenceTDM
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.