Actin-related protein 5 antagonizes the interaction of Pbx/Meis with myogenic regulatory factors such as MyoD and MyoG, which is involved in the recruitment of the BRG1-based switch/sucrose nonfermentable chromatin remodeling complex required for myogenic gene activation.

The basic helix-loop-helix transcription factor, HES3, acts downstream of the PAX3-FOXO1 fusion oncogene to impair muscle differentiation and promote tumorigenesis in rhabdomyosarcoma, a childhood muscle cancer.

In fusion-positive rhabdomyosarcoma, CHD4 positively regulates super-enhancer-mediated gene expression by allowing a chromatin architecture at these cis-regulatory regions, which is permissive to the binding of the transcription factor PAX3-FOXO1.

Syngeneic tp53-null zebrafish develop a wide range of tumors that engraft into recipient animals with loss of Tp53 leading to increased metastasis in embryonal rhabdomyosarcoma (ERMS), likely accounting for increased aggression in TP53-inactivated human ERMS.

Zebrafish are an optimal model organism to study rare TP53 mutations whose functions are not readily understood.

The functional relevance of stem cell niche perturbation in sarcomagenesis is defined and the mouse model presented provides a rationale for the use of combination therapy for the treatment of genetically heterogeneous sarcomas.

MYF5 and MYOD regulate rhabdomyosaroma growth and tumor-propagating potential, acting more than as passive markers retained from the target cell-of-origin during transformation.

Inhibition of the lysine methyltransferase G9a blocks oncogenic phenotypes in embryonal rhabdomyosarcoma.

A zebrafish genetic model of Ewing sarcoma, a pediatric bone cancer, showed how molecules in the normal tissue can support tumor cells, and identified a therapeutic compound that slows tumor growth.

Unique integrate stress response sensors differentially trigger pro-survival versus pro-apoptotic responses in cells confronted with Hsp70 inhibitor-associated proteotoxic challenges.