Identification of Molecular Targets in Triple-Negative Breast Cancer

抑制雌激素通路或靶向雌激素通路的分子靶向疗法 扩增的Her 2/Neu在乳腺癌的治疗中是有效的。那些肿瘤 不表达雌激素受体（ER）、孕激素受体（PR）或扩增的Her 2/Neu， 包括20%的乳腺癌患者的亚组没有从经验证的靶向治疗中获益。 治疗（即，抗雌激素疗法和赫赛汀），并且只能用 化疗这些三阴性肿瘤往往表现出预后不良的特征， 表达这些肿瘤的患者与那些 表达ER、PR和/或具有扩增的Her 2/Neu。在一项新的计划中，我们正在使用RNAi 功能基因组学方法中鉴定作为治疗靶点的激酶的技术 在三阴性乳腺癌细胞中。我们已经确定了一系列激酶， 下调，导致癌细胞死亡。正在进行的工作是表征这些激酶 进一步.

Molecularly targeted therapies that inhibit the estrogen pathway or that target amplified Her2/Neu are efficacious in the treatment of breast cancer. Patients whose tumors do not express estrogen receptor (ER), progesterone receptor (PR), or amplified Her2/Neu, a subset comprising 20% of breast cancer patients, do not benefit from the validated targeted therapies (i.e., anti-estrogen therapies and Herceptin) and can only be treated with chemotherapy. These triple-negative tumors tend to present with poor prognostic features and the patients who express these tumors have a poor outcome compared to those whose tumors express ER, PR, and/or have amplified Her2/Neu. In a new initiative, we are using RNAi technology in a functional genomic approach to identify kinases that are therapeutic targets in triple-negative breast cancer cells. We have identified a list of kinases that, when downregulated, lead to death in the cancer cells. Ongoing work is characterizing these kinases further.