Gene Studies Reveal Cancer's Secrets

In addition, as the number of these SNPs increases, so does resistance to treatment and poorer survival, Wu said.

This information, along with other genetic and lifestyle risk factors, could be used to develop an ovarian cancer risk-prediction model, Wu said.

In a fourth study, researchers led by Dr. Gangning Liang, an associate professor of research in the department of urology at the University of Southern California, reported finding a DNA modification called a "methylation pattern," that may diagnosis bladder cancer and detect patients at risk for recurrence of the disease.

"Bladder cancer is the fifth most common cancer in men and the sixth most common in women," Liang said during the teleconference. "It is mainly found in smokers."

DNA methylation is a process in which genes can be either silenced or activated in cancer. For the study, researchers measured DNA methylation in 12 patients who did not have bladder cancer, 52 patients with non-invasive bladder tumors and 39 patients with invasive bladder tumors.

Comparing cancerous tissue with normal bladder tissue, they found 158 "hypermethylated" loci and 366 "hypomethylated" locations. In addition, they found 21 places that were hypermethylated in the normal-appearing bladder tissue in patients with bladder cancer.

These loci may be markers for identifying people at risk for bladder cancer, the researchers said.

In addition, the scientists found that non-invasive tumors had a distinct pattern of hypomethylation compared with invasive tumors. This finding supports the idea that two forms of bladder cancer develop along different paths.

Bladder cancer can easily recur, Liang noted. "It requires frequent and invasive monitoring. We think these results are clinically useful and have benefits for the patient, because we can detect these methylation changes in the patient's urine," he explained. "So, we can use a noninvasive method to monitor the patient and may also be able to screen for bladder cancer in high-risk populations, like smokers," he said.

In a final report, researchers led by Sunita Setlur, an instructor in pathology at Brigham and Women's Hospital and Harvard Medical School, found no association between the gene variant UGT2B17 and the risk of prostate cancer. Although this gene had been linked to the risk for prostate cancer in two earlier studies, this new study found no such association.

For the study, researchers looked at 269 men of whom 156 had prostate cancer. The researchers looked at the number of copies of the UGT2B7 gene and found that although deletion patterns for UGT2B17 and UGT2B28 genes were between 3.4 percent and 19.9, this did not increase the risk for prostate cancer.

"We did not see any association between polymorphism of UGT2B17 and UGT2B28 with cancer," Setlur said during Tuesday's teleconference.

More information

For more about cancer, visit the American Cancer Society.