Targeting up‐regulated notch signaling in inflammatory breast cancer

TL;DRAbstract

Inflammatory breast cancer (IBC) is a type of human breast cancer with extremely high metastatic behavior due to the presence of florid lymphovascular tumor emboli present early in the disease's natural history. We have recapitulated this phenotype in a human xenograft model of IBC termed Mary‐X. In this xenograft, the tumor emboli (spheroids) are mediated by an intact and overexpressed E‐cadherin / alpha, beta‐catenin adhesion axis. These emboli resist the apoptosis‐inducing effects of chemotherapy and radiotherapy. When the tumor emboli are disadhered into single individual tumor cells by strategies which disrupt the E‐cadherin adhesion axis, both spontaneous apoptosis and chemotherapy / radiation‐induced apoptosis are dramatically enhanced. Because it remains to be determined whether selective targeting of E‐cadherin on tumor v normal cells can be achieved, we investigated other signaling pathways that are up‐regulated within the Mary‐X emboli that might be more amenable to selectiv

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