Research Interests

The two most daunting obstacles in the clinical management of cancer are metastasis, or the spread of tumor cells from its origin to distant sites in the body, and resistance to chemotherapy and/or radiation, which are two primary means of treating the disease. Unfortunately, the molecular mechanisms that drive these central and elusive problems in oncology have remained poorly understood.

Our laboratory is focused on understanding how cancer cells acquire metastatic and treatment resistant phenotypes. Recent evidence suggests that these two traits are acquired during tumorigenesis by antagonistic forces encountered as tumors grow and interact with their environment. Key among these selective pressures include hypoxia, immune-mediated attack, and barriers imposed by surrounding stroma. Because the biology of these selective pressures can overlap with molecular mechanisms involved in metastasis and treatment resistance, genetic alterations that occur as a response to these pressures may predispose tumors to acquire a metastatic and/or treatment-resistant phenotype.

In order to better understand the basis for metastasis and treatment resistance, we utilize a multi-disciplinary approach towards both experimental and translational research goals. Hypothesis generation and testing relies on a systems biology paradigm that incorporates animal models, molecular biology, bioinformatics, and clinical observation with eventual testing. Using these methods we and colleagues have identified gene expression signatures that not only mark but also mediate cancer phenotypes such as aggressive organ-selective metastasis and resistance to DNA damaging agents (chemotherapy and radiation). Thus, gene signatures such as these point toward relevant biology that can be dissected and provide clinical tools for prognosis, prediction, and potential therapeutic targeting.

News and Announcements

We welcome applicants for postdoctoral research positions.

The Ludwig Fund gives $120 million to six leading cancer research institutions, including $20 million to the University of Chicago to focus on metastasis research, which will be the mission of the Ludwig Center for Metastasis Research, part of the future Gwen and Jules Knapp Center for Biomedical Discovery.

Select Research Publications

Khodarev, N. N., Minn, A. J., Efimova, E., Darga, T., Labay, E., Beckett, M., Mauceri, H. J., Roizman, B., and Weichselbaum, R. R. (2007). Stat1 regulates both cytotoxic and pro-survival functions in tumor cells. Cancer Res 67, 9214-9220.

Minn, A. J., Gupta, G. P., Padua, D., Bos, P., Nguyen, D. X., Nuyten, D., Kreike, B., Zhang, Y., Wang, Y., Ishwaran, H., et al. (2007). Lung metastasis genes couple breast tumor size and metastatic spread. Proc Natl Acad Sci U S A 104, 6740-6745.

Minn, A. J., Gupta, G. P., Siegel, P. M., Bos, P. D., Shu, W., Giri, D. D., Viale, A., Olshen, A. B., Gerald, W. L., and Massague, J. (2005). Genes that mediate breast cancer metastasis to lung. Nature 436, 518-524.

Minn, A. J., Kang, Y., Serganova, I., Gupta, G. P., Giri, D. D., Doubrovin, M., Ponomarev, V., Gerald, W. L., Blasberg, R., and Massague, J. (2005). Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors. J Clin Invest 115, 44-55.

Le, H. V., Minn, A. J., and Massague, J. (2005). Cyclin-dependent kinase inhibitors uncouple cell cycle progression from mitochondrial apoptotic functions in DNA-damaged cancer cells. J Biol Chem 280, 32018-32025.

Minn, A. J., Kettlun, C. S., Liang, H., Kelekar, A., Vander Heiden, M. G., Chang, B. S., Fesik, S. W., Fill, M., and Thompson, C. B. (1999). Bcl-xL regulates apoptosis by heterodimerization-dependent and -independent mechanisms. Embo J 18, 632-643.

Minn, A. J., Velez, P., Schendel, S. L., Liang, H., Muchmore, S. W., Fesik, S. W., Fill, M., and Thompson, C. B. (1997). Bcl-xL forms an ion channel in synthetic lipid membranes. Nature 385, 353-357.

Chang, B. S., Minn, A. J., Muchmore, S. W., Fesik, S. W., and Thompson, C. B. (1997). Identification of a novel regulatory domain in Bcl-X(L) and Bcl-2. Embo J 16, 968-977.

Sattler, M., Liang, H., Nettesheim, D., Meadows, R. P., Harlan, J. E., Eberstadt, M., Yoon, H. S., Shuker, S. B., Chang, B. S., Minn, A. J., et al. (1997). Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosis. Science 275, 983-986.

Minn, A. J., Boise, L. H., and Thompson, C. B. (1996). Expression of Bcl-xL and loss of p53 can cooperate to overcome a cell cycle checkpoint induced by mitotic spindle damage. Genes Dev 10, 2621-2631.

Minn, A. J., Boise, L. H., and Thompson, C. B. (1996). Bcl-xS anatagonizes the protective effects of Bcl-xL. J Biol Chem 271, 6306-6312.

Boise, L. H., Minn, A. J., Noel, P. J., June, C. H., Accavitti, M. A., Lindsten, T., and Thompson, C. B. (1995). CD28 costimulation can promote T cell survival by enhancing the expression of Bcl-XL. Immunity 3, 87-98.

Boise, L. H., Minn, A. J., June, C. H., Lindsten, T., and Thompson, C. B. (1995). Growth factors can enhance lymphocyte survival without committing the cell to undergo cell division. Proc Natl Acad Sci U S A 92, 5491-5495.

Minn, A. J., Rudin, C. M., Boise, L. H., and Thompson, C. B. (1995). Expression of bcl-xL can confer a multidrug resistance phenotype. Blood 86, 1903-1910.

Select Book Chapters

Minn, A. J., and Massague, J. (In press). Invasion and metastasis. In Cancer: Principles and Practice of Oncology, 8th Edition, V.T. DeVita, S. Hellman, and S.A. Rosenberg, eds. (Lippincott Williams & Wilkins).

The Andy Minn Oncology Lab

Research Interests

News and Announcements

Select Research Publications

Select Book Chapters