Inhibition of STAG1 using ASOs for treatment of STAG2-deficient cancers
The cohesin complex is one of the most frequently mutated protein complexes in cancer. Cohesin mutations are associated with poor survival and there are no therapies that selectively target cohesin-mutant cancers. STAG2 is the most frequently mutated cohesin subunit in AML and is also recurrently mutated in solid tumors. The Adelman lab has developed antisense oligonucleotides (ASOs) that target a genetic vulnerability of STAG2-mutant cancers.
The Harvard team identified STAG1 as a selective genetic dependency of STAG2-mutant cancers using a genome-wide CRISPR screen. The team developed ASOs that potently inhibit STAG1 expression and cause selective lethality in STAG2-deficient AML cells.
The ASOs have potential for therapeutic applications in treating STAG2-mutant cancers, including AML, glioblastoma, breast cancer, melanoma, and Ewing sarcoma.
The cohesin complex is one of the most frequently mutated protein complexes in cancer. Cohesin mutations are associated with poor survival and there are no therapies that selectively target cohesin-mutant cancers. STAG2 is the most frequently mutated cohesin subunit in AML and is also recurrently mutated in solid tumors. The Adelman lab has developed antisense oligonucleotides (ASOs) that target a genetic vulnerability of STAG2-mutant cancers.
The Harvard team identified STAG1 as a selective genetic dependency of STAG2-mutant cancers using a genome-wide CRISPR screen. The team developed ASOs that potently inhibit STAG1 expression and cause selective lethality in STAG2-deficient AML cells.
The ASOs have potential for therapeutic applications in treating STAG2-mutant cancers, including AML, glioblastoma, breast cancer, melanoma, and Ewing sarcoma.
Intellectual Property Status: Patent(s) Pending
Case Number: 8876