A5045364592- Cancer Immunotherapy and Biomarkers
- Cancer-related Molecular Pathways
- CAR-T cell therapy research
- Advanced Breast Cancer Therapies
- Immune cells in cancer
- Estrogen and related hormone effects
- Cancer Mechanisms and Therapy
- Cancer, Hypoxia, and Metabolism
- PI3K/AKT/mTOR signaling in cancer
- Research in Social Sciences
- Immunotherapy and Immune Responses
- Mast cells and histamine
- Metabolism, Diabetes, and Cancer
- Cytokine Signaling Pathways and Interactions
- Adenosine and Purinergic Signaling
- Mitochondrial Function and Pathology
University of Helsinki
2018-2024
Helsinki University Hospital
2022
Abstract Few patients with triple negative breast cancer (TNBC) benefit from immune checkpoint inhibitors complete and durable remissions being quite rare. Oncogenes can regulate tumor infiltration, however whether oncogenes dictate diminished response to immunotherapy these effects are reversible remains poorly understood. Here, we report that TNBCs elevated MYC expression resistant inhibitor therapy. Using mouse models patient data, show signaling is associated low cell PD-L1, overall...
Abstract Elevated MYC expression sensitizes tumor cells to apoptosis but the therapeutic potential of this mechanism remains unclear. We find, in a model MYC-driven breast cancer, that pharmacological activation AMPK strongly synergizes with BCL-2/BCL-X L inhibitors activate apoptosis. demonstrate translational an and co-targeting strategy ex vivo models MYC-high cancer. Metformin combined navitoclax or venetoclax efficiently inhibited growth, conferred survival benefits induced infiltration...
Abstract There is a compelling medical need for novel and safe treatment options patients with advanced difficult to treat breast cancer. Our previous findings have demonstrated that combination of metformin navitoclax (BCL-2/BCL-XL inhibitor) successfully prevents tumor growth in patient derived xenograft syngrafted mouse models aggressive MYC-driven This outcome due the synthetic lethal action these drugs tumors elevated MYC expression. Here, we explored combinations all clinically...
Abstract Oncogenic MYC is frequently overexpressed in breast cancer, and its overexpression associated with aggressiveness unfavorable prognosis of cancer. promotes tumor growth by stimulating cell cycle progression rewiring metabolism – creating cancer vulnerabilities that can be therapeutically targeted via synthetic lethal strategies. A large part our current understanding the biology related pathways based on findings various inducible systems, which demonstrate acute effects activation...
Elevated MYC levels sensitize tumor cells to apoptosis but the therapeutic potential of this mechanism remains unclear. We find, in a model MYC-driven breast cancer, that pharmacological activation AMPK dramatically synergizes with BCL-2/BCL-XL inhibitors activate MYC-dependent apoptosis. demonstrate translational an and BCL- 2/BCL-XL co-targeting strategy ex vivo models MYC-high cancer. Metformin combined either navitoclax or venetoclax efficiently inhibits growth, confers survival benefits...
Abstract Elevated MYC levels sensitize tumor cells to apoptosis but the therapeutic potential of this mechanism remains unclear. We find, in a model MYC-driven breast cancer, that pharmacological activation AMPK dramatically synergizes with BCL-2/BCL-XL inhibitors activate MYC-dependent apoptosis. demonstrate translational an and BCL- 2/BCL-XL co-targeting strategy ex vivo models MYC-high cancer. Metformin combined either navitoclax or venetoclax efficiently inhibits growth, confers survival...