So what's the origin of cancer? An Indian-origin professor at the UC San Diego Jacobs School of Engineering is all set to find out; this and the answers to the origin on a lot more diseases.
Nanoengineering professor Gaurav Arya has developed engineering tools and computer simulations that provide new insights into biology.
AdvertisementPublished in Proceedings of the National Academy of Sciences (PNAS), a research article says that this work has been carried out in collaboration with researchers from Penn State University, University of Massachusetts, and New York University.
The report states that the researchers have used innovative approaches to deduce the internal structure of chromatin, a key player in DNA regulation.
Chromatin is a complex combination of DNA and proteins that makes up chromosomes, but its internal structure is not known-a mystery that has baffled scientists for more than three decades.
The function of chromatin is to package DNA into a smaller volume to fit in the cell. It also plays an important role in the regulation of genetic processes like DNA replication, transcription, recombination, and repair because all these processes depend critically on the accessibility of the DNA, which is directly controlled by chromatin.
A loosely folded chromatin fibre allows easy access to DNA sequences while a tightly folded fiber prevents or inhibits such access.
Arya and his colleagues believe that this newfound discovery may help improve the scientific understanding of how chromatin folds and unfolds to regulate gene activities, as well as understand the origin of genetic diseases like cancer.
They point out that lots of diseases, including cancer, are directly linked to abnormal regulation of chromatin.
"When we talk about cancer and its link to abnormal gene regulation, we have to ask the question why are these genes misfiring? In the end, it boils down to the protein machinery that makes up and regulates chromatin. You could have mutations in the oncogenic or tumor suppressor genes that lead to cancer or you could have abnormalities in the proteins that regulate chromatin around these genes leading to cancer," Arya said.
He revealed that the next step for his team would be to study the mechanisms by which chromatin is regulated, and how those lead to genes being switched "on" and "off," genes being repaired in response to mutations, and genes being replicated during cell division.
He believes that a molecular-level understanding of such mechanisms could lead to the development of better drugs that will directly target the chromatin around abnormally regulated genes to correct their activity.
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