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• W2317192448 abstract "The development of human breast cancer is a multi-step process leading from normal epithelium to fully transformed breast cancer. Early genetic changes result in hyperplasias which evolves into ductal carcinoma in situ (DCIS) and culminates as invasive ductal carcinoma. The transition from DCIS to invasive disease has been implicated as the key transition in breast cancer progression. Specific genomic, transcriptomic, and proteomic alterations responsible for this transition process have yet to been elucidated. HER2/Neu, a member of the EGFR family of receptor tyrosine kinases, is associated with poor clinical outcome. HER2/Neu overexpression/amplification is commonly seen (50–60%) in non-invasive lesions but is significantly less common (20–30%) in invasive and metastatic breast carcinoma. This indicates that HER2/Neu gives normal epithelium a proliferative advantage but additional genetic alterations are required for full malignant transformation. This idea is supported by the fact that transgenic mice that overexpress HER2/Neu develop spontaneous mammary tumors but only after a prolonged latency period. Recent forward genetic approaches use insertional mutagenesis to randomly integrate a strong promoter into the genome, activating downstream gene transcription that can lead to either gain or loss-of-function mutations based on the integration site. We used this insertional mutagenesis approach to induce anchorage-independent growth of isolated murine HER2/Neu over-expressing mammary epithelial cells. We identified HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1 (HACE1) as a putative breast tumor suppressor protein whose loss leads to the formation of anchorage-independent colonies. Loss of HACE1 expression is commonly seen in breast cancer patients [as well as other tumor types] supporting the role of HACE1 as a breast tumor suppressor gene. Knockdown of HACE1 in human mammary epithelial cells (HMECs) results in the acquisition of anchorage-independent growth. Moreover, knockdown of HACE1 in established breast cancer cell lines that express moderate levels of HACE1 results in enhanced cloniginicity. Therefore, we propose that the loss of HACE1 can potentially be used as a predictive marker for breast cancer progression. Additional studies investigating the mechanism of HACE1 action may also identify therapeutic targets that counteract HACE1 loss. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-04-06." @default.
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• W2317192448 date "2012-12-15" @default.
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• W2317192448 title "Abstract P1-04-06: Insertional mutagenesis identifies HACE1 as a HER2/Neu Cooperating Breast Cancer Tumor Suppressor Gene" @default.
• W2317192448 doi "https://doi.org/10.1158/0008-5472.sabcs12-p1-04-06" @default.
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