Seitz and his research team performed genetic tests on 173 colon cancer patients and 788 healthy individuals. They discovered that individuals with the ADH1C*1 gene had a heightened risk of developing colorectal cancer – but only when they drank more a daily amount of 30 grams of alcohol (about 2 drinks).
The results of the research were published in the journal Alcoholism: Clinical and Experimental Research. It’s well known among researchers that long-term alcohol consumption increases the risk for many cancers, including those of the liver, breast, larynx, and esophagus. In fact, the American Cancer Society recommends drinking no more than one drink a day for women and two for men in order to lower overall cancer risk.
The Seitz group decided to focus their research on colon cancer in white people. When alcohol is consumed, it is broken down by the body into a nasty compound called acetaldehyde. In people with the ADH1C*1 gene present, the metabolic rate of this process occurs especially fast. So researchers predicated that, through research of individuals with two different genetic compositions, they could examine how colon-cancer risk might be impacted by the different speeds of conversion of ethyl alcohol into acetaldehyde.
Seitz notes that Acetaldehyde is a very toxic compound which alters and damages out DNA. The speed of the change from ethanol to acetaldehyde varies from individual to individual. So the theory was that if people have a gene which contributes to a faster metabolism to acetaldehyde, then more of it would be produced in a shorter period of time, allowing a greater amount to bind to our DNA. That would contribute to an increase in colon cancer risk. The message is very simple - if you are unaware of your genetic background, moderate your alcohol consumption. You can have 2 drinks, but you should be careful following that amount.
Emerging research out of UT Southwestern Medical Center says that there are at least 70 genetic mutations involved in the formation of colon cancer, far more than previously believed. Researchers are now suggesting a new approach to treating colon cancer that targets multiple genes and pathways simultaneously. Current cancer treatments typically target just one or two known cancer-driver genes, believing this would be beneficial to patients. While patients may get patients may see a reduction in tumor in transient tumor burden, the tumor growth eventually returns.
The UT Southwestern research contradicts previous thinking that only a few mutated genes are important in the development of cancerous tumors. According to Dr. Jerry Shay, professor of cell biology at UT Southwestern, the ways that patients have been treated up to now just go after just one target when we should be going after three to four different pathways simultaneously. Under the old model, scientists thought that there were 151 candidate genes and that mutations in just 8 to 15 of them would lead to the formation of cancer. There were 700 genes classified as passenger genes whose mutations were only incidental to cancer growth.
Shay concludes that those numbers are entirely incorrect and there are 65 candidate genes at least five passenger genes whose mutations play large roles in cancer development. Inactivating the function of any of these tumor-suppressing genes lead to a key mechanism in cancer development called anchorage-independent growth. This means that cells piled up on top of each other instead of aligning neatly. The next step for researchers is to determine more accurately which genes drive cancer growth and which are merely passengers.