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    Cancer as Cure

    Summer 2013

    Richard Harth

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    Jialing Xiang

    For certain forms of cancer, two wrongs can make a right. That is the surprising discovery revealed in new research by IIT Associate Professor of Biology Jialing Xiang.

    Xiang’s latest investigations deal with the biological mechanisms designed to prevent the growth of tumor cells. One of the most important weapons in the body’s cancer-fighting arsenal is a specialized tumor suppressor gene known as Bax, which codes for an anti-cancer protein.

    “Tumor suppressors like Bax are the cells’ police force,” Xiang says. When abnormal cells appear, the Bax protein attacks their power source, the mitochondria, terminating the diseased cells. This process of programmed cell death is known as apoptosis.

    If something goes awry with the Bax gene, however, the suppressor’s tumor-fighting abilities are disabled. It has long been assumed that cancer patients who have a mutated Bax tumor protein due to a faulty Bax gene have a poor disease prognosis. But Xiang’s research suggests the picture is more complex.

    As Xiang explains, there are two common processes that can disrupt the Bax gene, rendering its protective capability null and void. The first is a mutation in a specific coding region of the gene known as a microsatellite. Such regions carry multiple repeats of one of DNA’s four nucleotides—A, T, C, or G.

    The multiple repeats found in microsatellite regions can sometimes confuse the gene production system that first transcribes the DNA sequence into RNA and then translates it into Bax protein. For example, eight Gs might mistakenly get transcribed as seven Gs—or perhaps nine. If these mistakes are not repaired in time, it will lead to a silencing of Bax expression, leaving the body vulnerable to tumor growth.

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