While type-2 diabetes and breast cancer are separate diseases, poor metabolic health frequently occurs in women with breast cancer. Recent studies provide evidence that poor metabolic health (rather than high body mass index; BMI) - may be the more important driver of biologically aggressive breast cancers – particularly triple-negative breast cancers (ER-/PR-/Her2-wt; TNBC) and chemotherapy-resistant, HER2- luminal B breast cancer (ER+/PR-/Ki67>14 HER2-; LBBC). Key to the aggressive biology of both TNBC and LBBC are epithelial cell plasticity (reversible epithelial to mesenchymal transition; EMT-MET) and aberrant adoption of stem-cell programs. Cell plasticity and aberrant adoption of stem cell programs allow TNBC and LBBC to rapidly invade and metastasize and evade the cytotoxic impact of chemotherapy; many of these pathways are regulated by insulin.
The aim of this Research Topic is to explore the impact type-2 diabetes and poor metabolic health has on aggressive breast cancer biology.
We are accepting articles on the below, but not limited subjects, in the form of original research and review:
• Mechanistic articles on the impact of 1) insulin on activating EMT-MET and aberrant adoption of stem cell signaling pathways, 2) insulin and cholesterol on immune cell dysregulation, tissue inflammation, and cancer risk, and 3) insulin on epigenetic damage.
• Clinical articles on the impact of 1) poor metabolic health on aggressive breast cancer presentation and survival and 2) breast cancer treatment on poor metabolic health.
• Prevention: potential for re-purposing of diabetes drugs (metformin, SGL2 inhibitor, GLP1 agonist) for breast cancer prevention
While type-2 diabetes and breast cancer are separate diseases, poor metabolic health frequently occurs in women with breast cancer. Recent studies provide evidence that poor metabolic health (rather than high body mass index; BMI) - may be the more important driver of biologically aggressive breast cancers – particularly triple-negative breast cancers (ER-/PR-/Her2-wt; TNBC) and chemotherapy-resistant, HER2- luminal B breast cancer (ER+/PR-/Ki67>14 HER2-; LBBC). Key to the aggressive biology of both TNBC and LBBC are epithelial cell plasticity (reversible epithelial to mesenchymal transition; EMT-MET) and aberrant adoption of stem-cell programs. Cell plasticity and aberrant adoption of stem cell programs allow TNBC and LBBC to rapidly invade and metastasize and evade the cytotoxic impact of chemotherapy; many of these pathways are regulated by insulin.
The aim of this Research Topic is to explore the impact type-2 diabetes and poor metabolic health has on aggressive breast cancer biology.
We are accepting articles on the below, but not limited subjects, in the form of original research and review:
• Mechanistic articles on the impact of 1) insulin on activating EMT-MET and aberrant adoption of stem cell signaling pathways, 2) insulin and cholesterol on immune cell dysregulation, tissue inflammation, and cancer risk, and 3) insulin on epigenetic damage.
• Clinical articles on the impact of 1) poor metabolic health on aggressive breast cancer presentation and survival and 2) breast cancer treatment on poor metabolic health.
• Prevention: potential for re-purposing of diabetes drugs (metformin, SGL2 inhibitor, GLP1 agonist) for breast cancer prevention