7.341 DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer, Fall 2007
Author(s)Reinhardt, Hans Christian; van Vugt, Marcel A.
DNA Damage Checkpoints: The Emergency Brake on the Road to Cancer
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The DNA contained in human cells is under constant attack by both exogenous and endogenous agents that can damage one of its three billion base pairs. To cope with this permanent exposure to DNA-damaging agents, such as the sun's radiation or by-products of our normal metabolism, powerful DNA damage checkpoints have evolved that allow organisms to survive this constant assault on their genomes. In this class we will analyze classical and recent papers from the primary research literature to gain a profound understanding of checkpoints that act as powerful emergency brakes to prevent cancer. We will consider basic principles of cell proliferation and molecular details of the DNA damage response. We will discuss the methods and model organisms typically used in this field as well as how an understanding of checkpoint mechanisms translates into the development of treatments for human cancer. This course will not stop at discussing literature. We will take it one step further and analyze real data in an MIT Biology laboratory. This course is one of many Advanced Undergraduate Seminars offered by the Biology Department at MIT. These seminars are tailored for students with an interest in using primary research literature to discuss and learn about current biological research in a highly interactive setting. Many instructors of the Advanced Undergraduate Seminars are postdoctoral scientists with a strong interest in teaching.
DNA, damage checkpoints, cancer, cells, human cells, exogenous, endogenous, checkpoints, gene, signaling, cancer biology, cancer prevention, primary sources, discussion, DNA damage, molecular, enzyme, cell cycle, extracellular cues, growth factors, Cdk regulation, cyclin-dependent kinase, p53, tumor suppressor, apoptosis, signaling, MDC1, H2AX, Rad50, Fluorescence activated cell sorter, Chk1, mutant