Exploring MYSM1 as a potential drug-target for cMYC-driven B cell lymphoma
cMYC is an important regulator of gene expression and abnormal increase in cMYC activity is a major cause of cancer. In recent work we demonstrated that cMYC works together with another protein MYSM1 in the regulation of gene expression in the blood and immune systems. Loss of MYSM1 therefore can protect mice from cancers of the blood and immune system. The molecular mechanisms involved in the MYSM1 and cMYC interaction will be analyzed in our proposed project. The long term goal is to determine whether inhibition of MYSM1 will also inhibit cMYC activity, and thus provide another potential treatment option.