The genomes inside cancer cells nearly always contain genetic mutations or alternations in their DNA sequence. Now it is becoming more and more evident that changes in gene expression that don’t involve changing the DNA sequence itself —called “epigenetics”— are also important in cancer.
Molecular biologist Taiping Chen is trying to understand the mechanisms and importance of epigenetic changes during cancer initiation and progression, at the University of Texas MD Anderson Cancer Center, Science Park campus in Smithville. Chen was recruited in 2011, with the help of a Rising Stars Award from CPRIT, to the department of epigenetics and molecular carcinogenesis. He was a researcher at the Novartis Institutes for Biomedical Research in Cambridge, Mass.
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The genomes inside cancer cells nearly always contain genetic mutations or alternations in their DNA sequence. Now it is becoming more and more evident that changes in gene expression that don’t involve changing the DNA sequence itself —called “epigenetics”— are also important in cancer.
Molecular biologist Taiping Chen is trying to understand the mechanisms and importance of epigenetic changes during cancer initiation and progression, at the University of Texas MD Anderson Cancer Center, Science Park campus in Smithville. Chen was recruited in 2011, with the help of a Rising Stars Award from CPRIT, to the department of epigenetics and molecular carcinogenesis. He was a researcher at the Novartis Institutes for Biomedical Research in Cambridge, Mass.
Epigenetic modifications don’t involve altering the genetic sequence but do change the expression of the genome in terms of the proteins and other gene products the gene codes for. Unlike genetic changes, epigenetic modifications are reversible, and are becoming a new target for cancer therapeutics.
Chen is specifically studying the patterns of small chemical groups added to specific DNA bases, such as methyl groups added to the base cytosine. Methylation of DNA helps inhibit gene expression, and areas of a genome that are highly methylated are usually less active.
In cancer cells, the methylation pattern of the genome is abnormal, and overall tends to be lower than normal cells. But how methylation patterns are regulated in cancer and other diseases is not well understood.
Chen is studying the genes involved in adding and removing methyl groups to DNA, in order to understand how the methylation pattern is altered in cancer. He hopes that a better understanding of the process could eventually lead to clinical applications.
“For example, you could use this methylation change as a biomarker for cancer diagnosis,” he says, “and also for monitoring the effects of therapy.”
Eventually, he believes, altering DNA methylation could be used therapeutically to treat cancer. “These kinds of changes are reversible, and theoretically, you could correct it,” he says.
In comparison to his previous work in the pharmaceutical industry, Chen enjoys the intellectual freedom the academic environment allows him to follow his own research interests. “At Novartis, we did a lot of good work, but the research priorities change all the time,” he says. “They’re a drug company whose end-product is medicine, while in academia, our focus is on in-depth understanding of mechanisms—which, in the end, is really the basis of all successful drugs. And companies like Novartis rely heavily on academic research.”
Chen credits CPRIT for providing the seed funding he used to generate preliminary data, which helped him secure nearly $2.4 million in federal funding for his research, with two grants from the National Institutes of Health.
Chen received his bachelor of medicine degree from Xi’an Medical University in China prior to embarking on graduate study in the U.S. He received his master’s degree in biology from the University of Texas at El Paso, and then his Ph.D. in molecular and cell biology from McGill University in Montreal. He was a postdoctoral fellow at Harvard Medical School and Massachusetts General Hospital before joining Novartis in 2004.
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