Johanna Reed

E-mail: eckl0033@umn.edu

Year entered: 2007

Thesis Advisor: Kaylee Schwertfeger

Degree received:
B.S., Genetics, Cell Biology and Development, University of Minnesota, 2007

Honors and Awards:

• Graduate School Block Fellowship, Fall Semester 2007
• Milne-Brandenburg MICaB Travel Award 2009

Thesis research:

According to the American Cancer Society, over 180,000 women are diagnosed with invasive breast cancer in the United States each year. It is now evident that alterations within both tumor cells and the microenvironment contribute to breast cancer. Recent studies have suggested that inflammation is an important component of breast cancer progression. Therefore, understanding how inflammatory factors, such as chemokines, are involved in invasion and metastasis will aid in the development of novel therapies targeting specific components of the mammary tumor microenvironment. Our studies focus on the pro-inflammatory chemokine CXCL1, which is known to contribute to the development and progression of melanoma and bladder carcinoma. However, the role of CXCL1 in the context of breast cancer remains unknown. We hypothesize that CXCL1 mediates mammary tumorigenesis by acting on both the tumor cells to promote migration and invasion and the microenvironment to promote inflammation. To test this hypothesis, different breast cancer cell lines are used to determine the effects of secreted CXCL1 on characteristics of transformed cells in vitro. Preliminary data showed that higher levels of CXCL1 are secreted in estrogen receptor negative cell lines, known to be more aggressive and invasive, in comparison to those that are estrogen receptor positive. In addition, a transgenic mouse model of mammary tumorigenesis that expresses inducible fibroblast growth factor receptor 1 (iFGFR1) will also be used to characterize the effects of secreted CXCL1 within a controlled inflammatory environment in vivo. This is an important model because it allows us to study early stages of mammary tumorigenesis in addition to FGFR1 which is upregulated in 10% of all human breast tumors. The ability of CXCL1 to contribute to breast cancer progression may provide a new target against which novel therapies and early detection methods can be designed in order to better combat this disease.

Publications:

• McDonnell, M., Md. J. Abedin, M. Melendez, T. Platikanova, J. Ecklund, K. Ahmed, and A. Kelekar. 2008. Phosphorylation of murine caspase-9 by the protein kinases casein kinase 2 regulates its cleavage by caspase-8. Journal of Biological Chemistry 283(29): 20149-20158.

• Reed, J., R. Leon, M. Hall, and K. Schwertfeger. 2009. Interleukin-1beta and fibroblast growth factor receptor 1 cooperate to induce cyclooxygenase-2 during early mammary tumorigenesis. Breast Cancer Research 11:R21