It’s not difficult to find someone who has had their life adversely affected by cancer. A major reason why cancer is so devastating is due to its ability to metastasize, or spread to previously healthy parts of the body. New evidence suggests that our very own DNA might facilitate the spread of cancerous cells.
Luck of the Draw
Published in the journal Nature Medicine, this study focused specifically on a common form of skin cancer called melanoma. The potentially troublesome gene in question is known as APOE, which can be found in every single cell in the body. The lead author of the study, Sohail Tavazoie, had conducted earlier research indicating that APOE could enable the spread of melanoma.
However, the guilt of APOE in this matter was not an open and shut case. The human body actually carries one of three versions of the gene, known as ApoE2, ApoE3, and ApoE4. Given this fact, the authors speculated that the spread of melanoma could depend on just exactly which variant of this gene a person has.
Of Mice and Men
To put this theory to the test, the authors conducted an experiment involving groups of laboratory mice. These rodents were separated based on which one of the three APOE genes they possessed. The mice that fared the best during this trial were those with the ApoE4 gene. Among this group, cancerous tumors exhibited the least amount of both growth and metastasization.
The team then turned their attention to human subjects. As with their rodent counterparts, humans with the ApoE4 gene variant experienced the best documented outcomes, outliving cancer patients with different forms of the gene. Conversely, those with the ApoE2 gene generally tended to be the first to succumb to cancer.
For both humans and mice, the data revealed that subjects with the ApoE4 gene could benefit from specific types of treatment. Specifically, therapies designed to bolster the immune system were found to yield the best results.
In light of the study’s findings, Tavazoie contends that a new approach should be adopted for those who may be genetically vulnerable to cancer. “We need to find those patients whose genetics put them at risk for poor survival and determine what therapies work best for them,” stated Tavazoie.