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- W4229020741 abstract "Summary Breast cancer (BC) prognosis and outcome are adversely affected by increased body weight, obesity, and the obesity-associated type 2 diabetes. Hyperinsulinemia, common in the obese state, has been associated with higher risk of death and recurrence in BC. Up to 80% of breast cancers overexpress the insulin receptor (INSR), which correlates with worse prognosis. To directly probe the role of insulin signaling in mammary tumorigenesis, we generated the MMTV-driven polyoma middle T (PyMT) and ErbB2/Her2 BC mouse models, respectively, with coordinate mammary epithelium restricted deletion of the INSR . In both models, deletion of either one or both copies of the INSR in the mammary gland led to a marked delay in tumor onset and burden, including in mice fed to mimic conditions of human obesity. Phenotypic characterization and longitudinal monitoring of mouse tumours, and ex vivo analysis of mammary cells from the generated mouse models revealed that tumor initiation, rather than progression and metastasis, were impacted by INSR deletion. Mechanistically, INSR deficiency in non-transformed mammary epithelial cells led to diminished bioenergetic fitness. The similarity of phenotypes elicited by the deletion of one or both copies of INSR indicates that there is a dose-dependent threshold for the contribution of INSR to mammary tumorigenesis." @default.
- W4229020741 created "2022-05-08" @default.
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- W4229020741 date "2022-05-06" @default.
- W4229020741 modified "2023-10-14" @default.
- W4229020741 title "Insulin Receptor Loss Impairs Mammary Tumorigenesis in Mice" @default.
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- W4229020741 doi "https://doi.org/10.1101/2022.05.06.490906" @default.
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