Abstract: The present invention is based, in part, on the novel discovery of the architecture and assembly pathway of three different classes of mammalian SWI/SNF complexes, compositions comprising the isolated modified SWI/SNF complexes, and methods of screening for modulators of the function and/or stability of same.

Abstract: The present invention is directed to compositions comprising modified SMARCB1 and uses thereof.

Abstract: The present invention provides compositions and methods for treating cancers with canonical BAF (cBAF) complex perturbations (e.g. synovial sarcoma or malignant rhabdoid tumor) using an agent that inhibits the formation, activity, and/or stability of the ncBAF complex.

Abstract: Methods for identifying and treating cancer patients likely to respond to topoisomerase inhibitors or likely to fail to respond to topoisomerase inhibitors are provided. The methods take advantage of the newly discovered role of BAF complexes in decatenation of DNA by topoisomerase IIa. Cancer cells are frequently at least partly defective in BAF complex activity. Such cells are targeted for therapy using certain topoisomerase IIa inhibitors according to the disclosed methods of treatment. Therapy of such cells using other topoisomerase inhibitors should be avoided.

Abstract: The present invention includes compound and methods that are useful in treating certain cancers, such as synovial sarcomas.

Abstract: The present invention is based, in part, on the novel discovery of the interaction between EWS-FLI1 and BAF complexes, and methods of modulating same to treat cancer, including Ewing Sarcoma.

Abstract: Methods and compositions are provided for treating human synovial sarcoma (SS). Also provided are screens to identify therapeutics for the treatment of synovial sarcoma. These methods, compositions, and screens are based on the discovery that promoting the assembly of wild type BAF (also called mSWI/SNF) complexes in SS cells by increasing levels of wild type SS18 and/or decreasing levels of SS18-SSX fusion protein leads to the cessation of proliferation of malignant cells in synovial sarcoma.

Abstract: The present invention includes compound and methods that are useful in treating certain cancers, such as synovial sarcomas.

Abstract: The present invention provides methods of screening for compounds that interfere with interaction between ERG. ETV1, ETV4 or ETV5 and mSWI/SNF (BAF) chromatin remodeling complex proteins. Included are methods of screening for compounds that interfere with interaction between ERG, ETV1, ETV4 or ETV5 and BAF155. Methods of treating prostate cancer with compounds that interfere with interaction between ERG, ETV1, ETV4 or ETV5 and mSWI/SNF (BAF) chromatin remodeling complex proteins are also provided.

Abstract: Methods useful in the treatment of synovial sarcoma are provided. The methods comprise administering to a subject suffering from synovial sarcoma a compound as disclosed herein. Also provided are novel compounds having therapeutic effects on subjects suffering from synovial sarcoma and pharmaceutical compositions comprising the compounds. The compounds were identified by screening for agents that promote the assembly of wild-type BAF (also called mSWI/SNF) complexes in modified SS cells.

Abstract: Methods of inducibly targeting a chromatin effector to a genomic locus are provided. Aspects of the methods include employing a chemical inducer of proximity (CIP) system. Aspects of the invention further include methods of screening candidate agents that modulate chromatin-mediated transcription control and methods of inducibly modulating expression of a coding sequence from genomic locus. Also provided are compositions, e.g., cells, reagents and kits, etc., that find use in methods of the invention.

Abstract: Methods and compositions are provided for treating human synovial sarcoma (SS). Also provided are screens to identify therapeutics for the treatment of synovial sarcoma. These methods, compositions, and screens are based on the discovery that promoting the assembly of wild type BAF (also called mSWI/SNF) complexes in SS cells by increasing levels of wild type SS18 and/or decreasing levels of SS18-SSX fusion protein leads to the cessation of proliferation of malignant cells in synovial sarcoma.

Abstract: Methods and compositions are provided for treating human synovial sarcoma (SS). Also provided are screens to identify therapeutics for the treatment of synovial sarcoma. These methods, compositions, and screens are based on the discovery that promoting the assembly of wild type BAF (also called mSWI/SNF) complexes in SS cells by increasing levels of wild type SS18 and/or decreasing levels of SS18-SSX fusion protein leads to the cessation of proliferation of malignant cells in synovial sarcoma.

Abstract: Methods and compositions are provided for treating human synovial sarcoma (SS). Also provided are screens to identify therapeutics for the treatment of synovial sarcoma. These methods, compositions, and screens are based on the discovery that promoting the assembly of wild type BAF (also called mSWI/SNF) complexes in SS cells by increasing levels of wild type SS18 and/or decreasing levels of SS18-SSX fusion protein leads to the cessation of proliferation of malignant cells in synovial sarcoma.

Abstract: Methods for identifying and treating cancer patients likely to respond to topoisomerase inhibitors or likely to fail to respond to topoisomerase inhibitors are provided. The methods take advantage of the newly discovered role of BAF complexes in decatenation of DNA by topoisomerase IIa. Cancer cells are frequently at least partly defective in BAF complex activity. Such cells are targeted for therapy using certain topoisomerase IIa inhibitors according to the disclosed methods of treatment. Therapy of such cells using other topoisomerase inhibitors should be avoided.

Abstract: Methods and compositions are provided for treating human synovial sarcoma (SS). Also provided are screens to identify therapeutics for the treatment of synovial sarcoma. These methods, compositions, and screens are based on the discovery that promoting the assembly of wild type BAF (also called mSWI/SNF) complexes in SS cells by increasing levels of wild type SS18 and/or decreasing levels of SS18-SSX fusion protein leads to the cessation of proliferation of malignant cells in synovial sarcoma.