A recombinant protein may block two pathways used by triple-negative cancer cells to grow and spread.

Approximately 10–20% of all breast cancers are identified as triple-negative, which means the cancer cells do not possess estrogen or progesterone receptors or produce excess HER2 protein. As a result, cancer growth cannot be inhibited with hormonal therapies or treatments that target HER2 protein receptors, which makes treating them difficult.

Various groups have been seeking new options for the treatment of triple-negative breast cancer. Princeton University researchers recently reported positive results with their candidate drug Tinag11. The drug is based on a recombinant protein believed to block two pathways (used by triple-negative cancer cells to grow and spread) by inhibiting the epidermal growth factor receptor (EGFR) gene, which when mutated is known to accelerate tumor growth. 

Tinag11 is different from other EGFR inhibitors on the market, which cancer cells can bypass, according to Princeton molecular biology professor and lead author Yibin Kang. It is inspired by a naturally occurring protein that inhibits the protein focal adhesion kinase, preventing it from inhibiting integrins, which if allowed to function regulate the ability of cancer cells to migrate and develop into tumors. 

During the research, mouse and human tumor cells engineered to produce high levels of the protein formed slow-growing tumors with reduced likelihood of metastasizing. Mice with mammary tumors treated with Tinag11 experienced inhibited cancer growth and lung metastasis with no side effects. Notably, the drug even worked when given to mice after metastases had already formed.