It is estimated that one in eight women in the United States will be diagnosed with breast cancer during their lifetime. Between 2011 and 2030, the incidence of breast cancer is expected to rise by more than 50%.1 According to the American Cancer Society, breast cancer rates in postmenopausal women are expected to rise as obesity rates continue to rise2. High-calorie diets have also been shown to increase the size and number of primary tumors4,5–6,7–8,9–10–11 in breast cancer models that are both genetically and chemically generated.
Neoadjuvant treatments that target the metabolism of breast cancer patients are becoming increasingly prominent. By far, the most popular antihyperglycemic strategy for cancer patients has been the biguanide metformin, an inhibitor of gluconeogenesis12,13,14 and the world’s most used diabetes drug. Breast cancer individuals with elevated levels of insulin in their blood may benefit from metabolism-targeting medications, which may then boost the efficacy of further chemotherapy treatments. A report on the findings was just released in the journal Communications in Biology.
Between 2011 and 2030, the prevalence of breast cancer is expected to rise by more than 50%. Increasing obesity rates in postmenopausal women have been linked to an increase in breast cancer occurrence and progression in these women. Metformin, an anti-diabetic medicine, has become increasingly popular in the treatment of breast cancer, with inconsistent results in clinical studies.
Dapagliflozin was examined as an option to metformin by Yale researchers using a new class of diabetes medication known as SGLT2 inhibitors. Studying the effects of dapagliflozin and chemotherapy on breast cancers was done in animal models. Mutation-specific results were made by them. For breast cancer models with mutations proximal of the insulin signaling system, dapagliflozin enhances chemotherapy’s ability to reduce tumor development, according to this study. Breast cancer models driven by mutations downstream of the insulin system or other driver mutations did not benefit from the combined therapy.