The skin on the face is a competitive mix of mutant cells even if the individual doesn’t have skin cancer.
A group of scientists from Belgium and the United Kingdom examined “health” skin from four middle-aged people who were getting cosmetic surgery to tighten their eyelids. None of the participants had ever had skin cancer. Regardless, more than a quarter of their eyelids contained mutations associated with squamous cell carcinoma.
Unlike melanoma, squamous cell carcinoma is not deadly but can be inconvenient, painful and disfiguring.
The findings were published in the journal Science and could shed light on how skin cancers develop and aid in the search for drugs that could prevent or treat severe cases where surgery would be difficult.
Researchers believe that there are no exact statistics on these kinds of cancers but according to The American Cancer Society, there are about 700,000 cases of squamous cell skin cancer diagnosed each year in the U.S. and about 2.8 million cases of basal cell cancer, another common form of skin cancer.
An interesting part of the finding was that the mutated cells weren’t just sitting there. Many were growing in clusters which the researchers refer to as clones. Some of the clones are probably cleaned up by the body’s immune system, however some may become malignant later on.
Researchers expected to see some mutations in normal skin, but were surprised to see the amount of mutations were cell and the number of cells with mutations associated with cancer.
It does take more than one mutation to start the formation of skin cancer, unfortunately, scientists don’t know exactly how many mutations and which ones must accumulate in order to make a cell.
Mutations occur when DNA makes an error in copying itself as a cell divides. In skin, the mutation rate is accelerated by UV lights from the sun or tanning booths.
Many sophisticated cancer researchers take a Darwinian view that some of the mutations that crop up in cells instruct them to develop at a quicker pace, allowing groups of these cells to outcompete their slower growing neighbors.
The small study raises a number of interesting questions: How many of these mutations clones will die out or be killed by the immune system? How much does our risk go up from sun exposure decades ago?