Our joint groups at the University of Helsinki and UCSF have discovered that the MYC oncogene is associated with poor breast cancer patient outcomes and resistance to immunotherapies. MYCimmune project focuses on finding new improved treatments that selectively kill high-MYC tumor cells and improve response to immune treatments.

Metastasis, the spread of cancer throughout the body, remains the single greatest challenge that breast cancer patients face, because therapeutics directed against metastatic breast cancer often result in only partial and transient responses. One of the major challenges for improving such therapies is our inability to identify ways to selectively kill metastatic tumor cells. Immunotherapies that reactivate the patient’s immune cells to attack breast cancer cells have the potential to eliminate even large metastatic tumors, offering hope for long-term clinical benefit for patients. Unfortunately, typically less than 20% of patients with metastatic breast cancer will respond to current immunotherapies and recently approved combinations of chemotherapy and immune therapies only modestly extend patient survival.  

Our partnering labs have discovered that the MYC cancer gene is frequently overexpressed or activated in aggressive breast cancer subtypes, such as receptor triple-negative breast cancer (TNBC), ER+ luminal B tumors, or in the early stages of metastatic disease. Unfortunately, selective MYC-directed small molecule inhibitors have yet to be developed for clinical use. Nevertheless, the partnering investigators have discovered a variety of pathways, which when inhibited can preferentially kill MYC high cells, while sparing non-tumor cells – an approach known as synthetic lethality (SL).

Collaboration with patient groups in the US and Finland

The project is implemented in close collaboration with patient advocacy groups in the US and in Finland. In Finland, our partner is Breast Cancer Association Europa Donna Finland ry, led by Anu Niemi. In the US our advocate partners are Carole Baas, Vivian Lee, and Susan Samson. 

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