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

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

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.

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.

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.

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.

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.

Familial cancer clustering was significantly higher in US minority populations compared to those of US European origin, suggesting renewed need for a focus on family cancer predisposition in US Latinos, Blacks, and Asian/Pacific Islanders.

G9a regulates chromatin-bound b-catenin enabling cell-intrinsic control of WNT signaling-mediated cell fate decisions.