Hamed is a PhD student at the University of Freiburg. He holds a masters degree in molecular medicine from the University of Tuebingen.

Rhabdomyosarcoma (RMS) is a highly aggressive type of cancer that arises from mesenchymal cells that have failed to fully differentiate into skeletal muscle. TP53 mutations in the germline and tumour genome have been linked to phenotypic differences. TP53 variants and oncogenic RAS are frequent aberrations in human RMS tissues. Hamed's research builds on the hypothesis that a transgenic RMS mouse expressing oncogenic KRAS (G12v) and conditionally active/inactive TP53TAM-ER may provide a unique platform to better comprehend the interaction of TP53 and MAPK signaling in RMS induction as well as malignancy.

In the future, Hamed will produce genetically-engineered mouse rhabdomyosarcomas, expressing oncogenic KRAS(G12v) and conditionally active/ inactive TP53TAM-ER may serve as a platform to understand the interaction of TP53 and MAPK signaling in rhabdomyosarcoma induction and malignancy.