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Dr. William G. Kaelin's laboratory at DFCI (see Research) studies mechanisms behind VHL disease. Over time, cells can accumulate damage to DNA. If the DNA is a blueprint for making a protein (in other words, the DNA constitutes a gene), the behavior of the cell might be altered. If a particular combination of genes becomes altered, the cell will become malignant or cancerous. Some genes help to prevent malignant behavior and are therefore referred to as tumor suppressor genes. These genes contribute to cancer when they are inactivated or completely lost as a result of DNA damage (mutations). Other genes, known as proto-oncogenes, can promote cancer if they acquire new properties as a result of mutations (at which point they are called oncogenes). Most common cancers involve both inactivation of specific tumor suppressor genes and activation of certain proto-oncogenes.
Dr. Kaelin's laboratory studies tumor suppressor genes and, in particular, the normal functions of the proteins they encode. The long-term goal of this work is to lay the foundation for the development of new anticancer therapies that are based on the functions of specific tumor suppressor proteins. For example, it might be possible to develop a drug that would mimic the behavior of a particular tumor suppressor protein, inactivating a specific enzyme involved in cell growth. Or alternatively, it might be possible to design strategies for killing only those cells in which a particular tumor suppressor protein has been inactivated, thus sparing normal cells.
At Dana Farber Cancer Institute in Dr. Daniel George's laboratory biomarkers of disease progression are studied along with new drug development in prostate and kidney cancer. His research focuses on growth factors involved in disease progression and angiogenesis.
Read about related research at the BWH Brain Tumor Laboratory.
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