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Cigarette smoke can turn normal breast cells cancerous by blocking their ability to repair themselves, eventually triggering tumor development, University of Florida scientists report.

While some cells nonetheless rally and are able to fix their damaged DNA, many others become unable to access their own cellular first aid kit, according to findings from a UF study published today (Aug. 21) in the journal Oncogene. If they survive long enough to divide and multiply, they pass along their mutations, acquiring malignant properties.

Past research has been controversial. Tobacco smoke contains dozens of cancer-causing chemicals, but until more recently many studies found only weak correlations between smoking and breast cancer risk, or none at all. Those findings are increasingly being challenged by newer studies that are focusing on more than just single chemical components of tobacco, as past research often has done. In the UF study, researchers instead used a tar that contains all of the 4,000 chemicals found in cigarette smoke.

“Our study suggests the mechanism by which this may be happening,” said Satya Narayan, an associate professor of anatomy and cell biology at UF’s College of Medicine. “This is basically the important finding in our case: We are now describing how cigarette smoke condensate, which is a surrogate for cigarette smoke, can cause DNA damage and can block the DNA repair of a cell or compromise the DNA repair capacity of a cell. That can be detrimental for the cell and can lead to transformation or carcinogenesis.”

In their study, funded by the National Institutes of Health and the Miami-based Flight Attendant Medical Research Institute, UF researchers exposed normal breast epithelial cells to cigarette smoke condensate—a tar derived from a machine that literally “smokes” a cigarette in the laboratory—and found the cells acquired mutations characteristic of malignant cells.

The scientists say DNA repair appears to be compromised when chemical components of smoke activate a key gene. That gene interacts with an enzyme that plays a crucial role in repairing damaged DNA, preventing it from doing its job. The cell, despite its mutated form, can then multiply wildly.

A cell with damaged DNA has one of two fates, said Narayan, also a member of the UF Shands Cancer Center.