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Scientists identify new mechanisms for cancer cell mutations

By Ryan Maass
Scientists say cancer-promoting HRasV12 genes in cells influence the replication stress that results in cancer growth. Photo by skeeze/Pixabay.
Scientists say cancer-promoting HRasV12 genes in cells influence the replication stress that results in cancer growth. Photo by skeeze/Pixabay.

BIRMINGHAM, England, Oct. 11 (UPI) -- Abnormalities in a cell's transcription machinery are responsible for aggressive cancer mutations, new research by University of Birmingham scientists suggests.

University of Birmingham scientists say they have identified a previously unknown molecular mechanism that helps cancer spread throughout its host.

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It has long been understood that cancer spreads through genetic mutations that eventually form malignant tumors. Cells often become cancerous due to "replication stress," where DNA becomes damaged while it's duplicated. In their study, published in Nature Communications, University of Birmingham scientists trace this phenomenon to an increase in the activity of a cell's own transcription machinery.

During the study, the research team observed cells with an activated version of the cancer-promoting HRasV12, or "oncogene," experience a rapid increase in transcription rates.

"This research is the first to show conclusively that an oncogene-induced boost in gene expression is enough to interfere with DNA replication," lead researcher Dr. Eva Petermann said in a press release. "Our findings help to create a new unified view of the roles of transcription and replication in the process of cancer cell mutations."

The disrupted transcription process results in unusual RNA structures the authors referred to as "R-loops" within the DNA of the cell. These abnormalities were found to influence DNA damage and replication stress.

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Petermann says the findings open the door for further investigation into cancer and its causes, and can be used to develop more advanced drugs to fight the disease.

"This is a big step in basic cancer biology, and potentially opens up a whole new area of research into transcription proteins and replication stress," she added.

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