Three junior investigators awarded Institutional Research Grants

Three junior investigators awarded Institutional Research Grants

 

National Cancer Research Month

The Arizona Cancer Center is joining the American Association for Cancer Research during May, National Cancer Research Month, to raise awareness of the importance of cancer research and the progress research institutions are making in critical areas of research and patient care. Learn more about research at the Arizona Cancer Center and consider supporting our research.

The American Cancer Society Institutional Research Grant program at the Arizona Cancer Center (ACS-IRG), currently led by Joyce Schroeder, PhD, supports the development of new investigators to conduct independent cancer research. The ACS-IRG has been competitively renewed at the Arizona Cancer Center for the past 28 years, and awardees have gone on to garner nearly $13 million dollars in external grant funding in the last 5 years alone.

Each year, the Scientific Review Committee, comprised of University of Arizona faculty, chooses recipients for these grants. The $80,000 grant distribution for 2011 will fund three junior investigators' research into the topics of colon cancer metastasis, tumor suppression of breast cancer, and the mapping and modeling of tumor heterogeneity.


Yao.jpgGuang Yao, PhD
Assistant Professor
Department of Molecular and Cellular Biology
“Understanding Life and Death Decisions of Individual Cells”

Cancer is notoriously difficult to treat, because we do not fully understand how individual cancer cells respond to treatments. Researchers have now worked out the map (signaling network) of major signaling molecules that dictate cellular responses. However, like one with a map may still get stuck on the road without knowing traffic patterns, researchers are currently hindered by the lack of knowledge on the dynamic properties of cell signaling network. As a first step to tackle this problem, we propose to construct a high-resolution observation system that will allow us to monitor the dynamic states of signaling networks in individual cells. In subsequent research, data collected from this experimental platform can be integrated into a computer model to achieve a global understanding of how cells respond to oncogenic signals and drug treatments, which could eventually help researchers to identify effective cancer therapeutics.

 

McDermott.jpgKimberly McDermott, PhD
Assistant Professor
Department of Cell Biology and Anatomy
“Mechanisms of Localization of BMPR2 to the Primary Cilium”

Cilia are an important part of normal cells and have often been compared to the cells antennae. The cilia project out from the surface of the cell to receive important signals from the surroundings. Proper reception of these signals is critical to maintaining normal function of the cell. We hypothesize that these antennae (cilia) are required to allow a cell to respond to a specific signals and in turn then communicate to the cell to begin to migration in a precise direction. Our  studies are designed to strengthen this hypothesis by better understanding how the BMP receptor (known as BMPR2) is localized to the primary cilium. Recent studies in human breast cancer tissue suggest that primary cilia may function to prevent tumor progression. These studies will provide valuable insight into the role of primary cilia in normal cell migration. Once we understand the normal we can begin to understand how this migration is abrogated to contribute to cancer cell metastasis.

 

Mercado-Pimentel.jpgMelania Mercado-Pimentel, PhD
Assistant Professor
Department of Pathology
“Deciphering S100P/RAGE signaling during epithelial-mesenchymal transition (EMT) in colon cancer metastasis”

Recent cancer studies have shown that epithelial-mesenchymal transition (EMT) is one of the first events in cancer metastasis and that chronic inflammation may be an inducer of EMT, the process by which a cell being a part of a cell layer or a tissue becomes migratory and invasive. Though EMT is a normal process during the development of an organism to form organs or different structures, it is considered aberrant when it leads to progression of diseases such as fibrosis and cancer. S100P and RAGE are molecules that play important roles in different cancer types such as colon, breast, pancreatic, lung, etc. RAGE plays a role in inflammation but its role in EMT has not been studied and our results show that S100P plays a role in EMT. The objective of my research is to determine if S100P and RAGE signaling constitute a link between inflammation and EMT during cancer progression leading to metastasis. Studying the mechanism by which these molecules drive EMT in cancer progression will reveal putative molecular targets for future treatments in preventing metastasis of several cancers.