Evidence map›Paper›PMID 24122795›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2014

Molecular pathways: SWI/SNF (BAF) complexes are frequently mutated in cancer--mechanisms and potential therapeutic insights.

Xiaofeng Wang, Jeffrey R Haswell, Charles W M Roberts

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
8.4field-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

98 citing papers in PubMed, 212 citations in OpenAlex.

  1. SWI/SNF Complex-Deficient Undifferentiated Carcinoma of the Pancreas: Clinicopathologic and Genomic Analysis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024
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  15. A comprehensive insights of cancer immunotherapy resistance.Medical oncology (Northwood, London, England) · 2025
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  20. Molecular pathology in diagnosis and prognostication of head and neck tumors.Virchows Archiv : an international journal of pathology · 2024
    Review

38 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

3 authors at 2 institutions in 1 country.

Xiaofeng WangAuthors' Affiliations: Department of Pediatric Oncology, Dana-Farber Cancer Institute; Division of Hematology/Oncology, Children's Hospital Boston; and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts.
Jeffrey R Haswell
Charles W M Roberts
Dana-Farber Cancer Institute · USHarvard University · 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

SWI/SNF chromatin remodeling complexes are pleomorphic multisubunit cellular machines that utilize the energy of ATP hydrolysis to modulate chromatin structure. The complexes interact with transcription factors at promoters and enhancers to modulate gene expression and contribute to lineage specification, differentiation, and development. Initial clues to a role in tumor suppression for SWI/SNF complexes came over a decade ago when the gene encoding the SMARCB1/SNF5 core subunit was found specifically inactivated in nearly all pediatric rhabdoid tumors. In the last three years, cancer-genome sequencing efforts have revealed an unexpectedly high mutation rate of SWI/SNF subunit genes, which are collectively mutated in 20% of all human cancers and approach the frequency of p53 mutations. Here, we provide a background on these newly recognized tumor suppressor complexes, discuss mechanisms implicated in the tumor suppressor activity, and highlight findings that may lead to potential therapeutic targets for SWI/SNF-mutant cancers.

Indexed as

AnimalsAntineoplastic AgentsChromosomal Proteins, Non-HistoneEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyMutationNeoplasmsProtein SubunitsSignal TransductionTranscription FactorsTumor Suppressor ProteinsAntineoplastic AgentsChromosomal Proteins, Non-HistoneProtein SubunitsSWI-SNF-B chromatin-remodeling complexTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID24122795
PMCPMC3947303
OpenAlexW2144195427

What OpenQuestion holds

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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.