Pancreatic cancer is often identified in late stages, and thus is resistant to most available therapies. Scientists like Donghui Li, Ph.D., a professor in the Department of Gastrointestinal Medical Oncology at The University of Texas M. D. Anderson Cancer Center, are working to determine genetic profiles that can be used in identifying high-risk individuals for the purpose of prevention and early detection of this disease.

"Our study provides some preliminary data on one pattern of genetic variations that may be useful in determining risk," said Li, who is the lead author on the Clinical Cancer Research paper. "However, we still need to be cautious. As with any science, the key is replication, and the results of this study need to be confirmed by others."

Li and colleagues analyzed nine single nucleotide polymorphisms of seven DNA repair genes among 734 patients with pancreatic cancer and 780 people without cancer. DNA repair is the guardian of the genome. When DNA repair failed to fix the DNA damages caused by exogenous agents such as tobacco carcinogens or endogenous agents such as reactive oxygen species, there is an increased chance of getting cancer.

Researchers found that the presence of a homozygous mutant genotype of LIG3 G-39A was associated with a 77 percent reduction in the risk of pancreatic cancer. By contrast, the presence of the gene ATM D1853N was associated with a nearly threefold (255 percent) increased risk of pancreatic cancer.

Currently, there is no approved genetic screening tool for pancreatic cancer, Li said.

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Thus, DREAM turns out to be a genetic candidate for explaining old age dementia. Even a causal connection to Alzheimer's disease seems plausible. Studies published in mid 2008 suggest that the devastating condition may be related to Calcium regulation gone awry. The accumulation of amyloid plaques in brain cells, usually blamed for Alzheimer's, might be a consequence of the Calcium-imbalance rather than the culprit for the disease.

And Calcium regulation is also responsible for tuning the activity of the DREAM-gene. Calcium homeostasis may thus be the link between pain perception, learning and memory. This is supported by observations of patients suffering from chronic pain: very often their ability to memorize is strikingly reduced and they need a lot more time to learn than individuals without pain.

"It is absolutely fascinating that we found a gene which at the same time regulates pain, learning and old age memory function", says Josef Penninger, "and it is of great interest to the millions of people suffering from chronic pain that we follow up on these results."

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