New research has confirmed the role of a group of virus-fighting genes in the development of cancer.
Our understanding of the biological processes that cause cancer is limited. UV light and smoking are two well-understood cancer-causing processes. Exposure to either of these processes causes distinguishable patterns of genetic damage, or 'signatures', on the genome that can lead to cancer. All cancer-causing processes leave their own distinct imprint or signature, on the genomes of cancer cells.
Bile Duct Cancer
Bile duct cancer occurs either within the liver or the point where the bile ducts emerge from the liver or outside the liver.
Advertisement
The APOBEC family of genes control enzymes that are believed to have evolved in humans to fight off viral infections. Scientists have speculated that these enzymes are responsible for a very distinct signature of mutations that is present in approximately half of all cancer types. Therefore, understanding the cancer-causing process behind this common genetic signature is pivotal for disease control and prevention.
The team studied the genomes of breast cancers in patients with a specific inherited deletion in two of these APOBEC genes. They found that these cancer genomes had a much greater prevalence of the distinct mutational signature that is thought to be driven by the APOBEC family of genes.
![Lifetime Risk Calculator for Cancers]( "Lifetime Risk Calculator for Cancers")
What are your chances for developing some common cancers in your lifetime - find out now.
"The increased frequency of this common cancer signature in breast cancer patients with APOBEC gene abnormalities supports our theory that these enzymes play a role in generating this mutational signature," says Dr Serena Nik-Zainal, first author from the Wellcome Trust Sanger Institute.
This genetic deletion is found on chromosome 22 where the APOBEC genes, APOBEC3A and APOBEC3B, sit next to each other. Women with this genetic deletion have previously been reported to be more susceptible to breast cancer.
The team examined 923 samples of breast cancer from women from across the world and found more than 140 people with either one or two copies of the deletion on each chromosome. Breast cancer in women with the deletion had a much greater quantity of mutations of this particular genetic signature.
However, the mutational activity of the APOBEC genes appears to be a double-edged sword. This genetic deletion is much more prevalent in some populations than others: it is found in only 8 per cent of Europeans, but is present in 93 per cent of the population of Oceania. Although this deletion increases risk of cancer development, it also seems to provide a currently unknown advantage in populations where it is more common.
"In addition to this APOBEC mediated process, there appear to be many more cancer-causing mutational processes, the underlying nature of which has yet to be understood," says Professor Sir Mike Stratton, lead author and Director of the Sanger Institute. "Working out what these mutational processes are will have profound implications in the future for how we prevent and treat cancer."
Source: Eurekalert
Lifetime Risk Calculator for Cancers
What are your chances for developing some common cancers in your lifetime - find out now.
Advertisement
"The increased frequency of this common cancer signature in breast cancer patients with APOBEC gene abnormalities supports our theory that these enzymes play a role in generating this mutational signature," says Dr Serena Nik-Zainal, first author from the Wellcome Trust Sanger Institute.
This genetic deletion is found on chromosome 22 where the APOBEC genes, APOBEC3A and APOBEC3B, sit next to each other. Women with this genetic deletion have previously been reported to be more susceptible to breast cancer.
The team examined 923 samples of breast cancer from women from across the world and found more than 140 people with either one or two copies of the deletion on each chromosome. Breast cancer in women with the deletion had a much greater quantity of mutations of this particular genetic signature.
However, the mutational activity of the APOBEC genes appears to be a double-edged sword. This genetic deletion is much more prevalent in some populations than others: it is found in only 8 per cent of Europeans, but is present in 93 per cent of the population of Oceania. Although this deletion increases risk of cancer development, it also seems to provide a currently unknown advantage in populations where it is more common.
"In addition to this APOBEC mediated process, there appear to be many more cancer-causing mutational processes, the underlying nature of which has yet to be understood," says Professor Sir Mike Stratton, lead author and Director of the Sanger Institute. "Working out what these mutational processes are will have profound implications in the future for how we prevent and treat cancer."
Source: Eurekalert
Quiz on Cancer
Cancer, is the second most leading cause of death worldwide. Cancer is not just one disease but many diseases. There are more than 100 different types of cancer. Take this quiz on and test how much you know about cancer.
Advertisement
 Cancer Prevention thro' Lifestyle ChangesDid u know that simple changes in lifestyle could lower your cancer risks? Find out how! | Advertisement
|
Advertisement
Recommended Readings
Latest Cancer News
More affected relatives, higher lung cancer risk; participants with affected mothers or siblings faced increased risk.
Colorectal cancer can be lowered by up to 7% by increasing dietary consumption of folate rich foods like spinach, broccoli or taking folate supplements.
The effects and mechanisms of microRNA-451a (miR-451a), which hinders the progression of gemcitabine-resistant biliary tract cancers, are under study.
The blood test pinpointed 13 proteins capable of distinguishing between early and late stages of pancreatic cancer.
A fatty acid present in dairy products, beef, and lamb called trans-vaccenic acid enhances immune cells' capacity to combat cancers.