ArticleOncogene2011
Pharmacologic reversal of epigenetic silencing of the anticancer protein BRM: a novel targeted treatment strategy.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- BRM Promoter Polymorphisms and Survival of Advanced Non-Small Cell Lung Cancer Patients in the Princess Margaret Cohort and CCTG BR.24 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Trial
- The SWI/SNF Complex: A Frequently Mutated Chromatin Remodeling Complex in Cancer.Cancer treatment and research · 2023Article
- Tracking Down the Epigenetic Footprint of HCV-Induced Hepatocarcinogenesis.Journal of clinical medicine · 2021Review
- BRM: the core ATPase subunit of SWI/SNF chromatin-remodelling complex-a tumour suppressor or tumour-promoting factor?Epigenetics & chromatin · 2019Review
- Hypermethylation ofJournal of Cancer · 2019Article
- PRC2-mediated repression of SMARCA2 predicts EZH2 inhibitor activity in SWI/SNF mutant tumors.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- SMARCA4-deficient thoracic sarcoma: a distinctive clinicopathological entity with undifferentiated rhabdoid morphology and aggressive behavior.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- Article
- Review
- Concomitant loss of SMARCA2 and SMARCA4 expression in small cell carcinoma of the ovary, hypercalcemic type.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- Induction of functional Brm protein from Brm knockout mice.Oncoscience · 2015Article
- Modulation of Brahma expression by the mitogen-activated protein kinase/extracellular signal regulated kinase pathway is associated with changes in melanoma proliferation.Archives of biochemistry and biophysics · 2014Article
- Flavonoids from each of the six structural groups reactivate BRM, a possible cofactor for the anticancer effects of flavonoids.Carcinogenesis · 2014Article
- Article
- Oncogenic targeting of BRM drives malignancy through C/EBPβ-dependent induction of α5 integrin.Oncogene · 2014Article
- Two BRM promoter insertion polymorphisms increase the risk of early-stage upper aerodigestive tract cancers.Cancer medicine · 2014Article
- Article
- Beyond Mutations: Additional Mechanisms and Implications of SWI/SNF Complex Inactivation.Frontiers in oncology · 2014Review
- ATP-dependent chromatin remodeling complexes as novel targets for cancer therapy.Advances in cancer research · 2014Review
- Two novel BRM insertion promoter sequence variants are associated with loss of BRM expression and lung cancer risk.Oncogene · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Tumor suppressor genes and oncogenes are both commonly altered during carcinogenesis. For oncogenes and other genes that drive growth, targeting mutated or activated forms (such as the EGFR-Her2/Nneu pathway) has been shown to be an effective anti-cancer approach. Pharmacologically targeting tumor suppressor genes has not been as fruitful, as many tumor suppressor genes are irreversibly silenced through somatic mutation or entirely deleted during carcinogenesis, thereby making it difficult to restore gene function. BRM, a key SWI/SNF complex subunit and a putative tumor suppressor gene, is inactivated in 15-20% of many solid tumor types. Unlike other tumor suppressor genes, the loss of BRM has been shown to be a reversible epigenetic change, rather than an irreversible genetic alteration. Using a high throughput drug screen, we identified a number of compounds that could effectively restore BRM expression and function. Two of these compounds, RH (RH02032) and GK (GK0037), were found to be such reactivating agents. Both compounds led to robust re-expression of BRM, induced downstream expression of BRM-dependent genes and inhibited BRM-dependent growth across a wide range of BRM-deficient cancer cell lines of different origins. We therefore show, for the first time, that pharmacologic reversal of epigenetic changes of the SWI/SNF chromatic remodeling complex subunit, BRM, is a potentially viable and novel therapeutic approach.
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Registered trials
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.