Melissa C Adriance

TL;DR: It is shown that the deletion of Muc1 expression from MMTV-Wnt-1 transgenic mice results in a significant increase in the time to mammary gland tumor onset, which indicates a potential mechanism for MUC1 promotion of invasive tumorigenesis in the breast through the modulation of β-catenin localization and subsequent cytoskeletal dynamics.

TL;DR: It is reported that multiparous MMTV-MUC1 transgenic mice stochastically develop unifocal mammary gland carcinomas late in life and is the first to determine that MUC1 overexpression promotes in vivo transformation of the mammary glands.

TL;DR: The MET mice appropriately mimic the human condition and are an excellent model with which to elucidate the native immune responses that develop during tumor progression and to develop effective antitumor vaccine strategies.

TL;DR: A seemingly indispensable interaction between β-catenin and epidermal growth factor receptor/c-Neu heterodimers in Wnt-1-mediated breast tumorigenesis that may indicate a fundamental signaling event in human metastatic progression is identified.

TL;DR: It is found that transient transfection of activated ErbB2 into human embryonic kidney 293/MUC1 cells resulted in the repression of MUC1 expression, which suggests that the activation of Erb B2, which only occurs in c-Neu tumors, selectively inhibits Muc1 expression.