Some of the Law Lab’s primary research interests revolves around cyclin-dependent kinases (Cdks) in mammary tumorigenesis and chromosomal instability, and Cdk regulation by the mTOR and TGFβ pathways. This research involves the use of novel models to understand how the activation of Cdks in the mammary gland causes tumor formation by dysregulation of cell proliferation and through genetic alterations that result from chromosomal instability. These models also provide systems for testing new therapeutic strategies, includinh non-ATP competitive Cdk inhibitors discovered in their laboratory and for targeting the upstream signaling pathways, such as the mTOR and TGFβ axes, that stimulate Cdk kinase activity.
The mechanisms promoting breast cancer invasion and metastasisE-cadherin are the primary barriers preventing the invasion and metastasis of human carcinomas; therefore, their functions must be abrogated in epithelial cancers in order for tumor dissemination to occur. E-cadherin expression can be blocked by epigenetic silencing, but the lab’s results indicate that the loss of the E-cadherin protein function is highly prevalent among the most aggressive breast cancers. The Law Lab has discovered that the protein, Cub Domain-Containing Protein 1 (CDCP1), which has been implicated in tumor invasion and metastasis, is a novel E-cadherin-associated protein. Ongoing studies focus on determining how CDCP1 controls cell-cell adhesion through its association with Cadherins, Catenins, cytoskeletal proteins, and Matrix Metalloproteinases.