The Role of Gap Junction Proteins in cytoskeletal rearrangements in B-lymphocytes

B-cell lymphomas are the most common type of blood cancer, accounting for 80-90 percent of non-Hodgkin’s lymphomas. Because lymphoma cancer cells can so readily spread from the blood stream to other tissues in the body, it is also a highly fatal form of disease. The key to preventing the spread of B-lymphomas is to prevent the proliferation and migration of these cancerous cells. To that end, an understanding of the underlying cellular processes is essential to the development of effective therapies. Recently, the Gap junction protein connexin43 (Cx43), was shown to cause neuronal migration in the brain. This novel role for gap junctions has led to speculation that Cx43 may be important for the migration of other cell types. Further, Cx43 expression on B-cells is important for hematopoiesis in the bone marrow, however the function of Cx43 on mature, circulating B-cells has remained elusive. Letitia Falk’s research involves a systematic dissection of the role of different protein domains of Cx43. Additionally, she is investigating the migration of B-lymphoid tumour cells expressing wild type and mutated forms of Cx43 in mouse models of tumour metastasis. These experiments will provide insight into processes that underlie normal lymphocyte development as well as the regulatory processes involved in the metastasis of B-cell leukemias, lymphomas and myelomas. Understanding in this area has the potential to aid in the development of novel anti-cancer therapeutics for the treatment of lymphoma cancers.