Ten Basic Questions and Answers about Skin Cancers
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| Skin Cancers |
1. What are they?
Like other forms of cancer, skin cancers are groups of cells that have lost a part of the genetic fine-tuning that controls their activities. This shows particularly in their new ability to reproduce more rapidly. Skin cancers develop in the outermost protective cell layer of the skin called the epidermis but sometimes they do not stay put. It is when the cells leave the epidermis and spread to other parts of the body that the problem becomes a very serious (malignant) one.
2. What kinds are there?
There are three kinds. Skin cancers are quite easy to classify because each of the three kinds comes from a certain type of normal cell in the epidermis. Squamous cell carcinomas (SCCs) are altered, flattened (squamous) cells in the outer layers of the epidermis; basal cell carcinomas (BCCs) come from changed cells of the innermost (basal) layer; and malignant melanomas (MMs) are changed pigment cells that sit in among the basal cells. The first two kinds are similar to one another and are often lumped together as non-melanoma skin cancers (NMSCs).
3. What triggers skin cancers?
Ultraviolet light is by far the most common trigger of all three kinds of skin cancers. Exposure of the skin to ultraviolet (UV) radiation results in penetration of the outermost layers of the skin and results in transfer of energy within cells of the deeper layers. In most cases it is critical exposure to the UV light in sunlight that is responsible, but too much exposure to artificial sources of UV can also start skin cancers. NMSCs are caused by a specific (mid-wave type of UV (UVB), but appears that MMs can be started by both UVB and long-wave UV (UVA).
4. How do they get started?
Effects of UV on skin cells have been studies in great detail. Skin cancers start as a result of changes (mutations in the DNA of genes that signal when and how often a cell can divide and how DNA errors can be fixed. Mutations at one or more points in a complicated network of these genes and their products set the process in motion. UVB causes these mutations by direct hits on the DNA that lead to characteristic changes in the chemical structure of the bases that code for a specific message. UVA activates molecules called photosensitisers that are transported to the DNA and may cause mutations.
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| Skin Cancer Treatment |
5. How do they develop into skin tumors?
Once damaged and not repaired, a gene normally involved in the control of cell division no longer exerts control. As a result, the cell containing that gene is transformed into what can then be called a cancer cell. Usually, cancer cells divide rapidly to produce large numbers of cells which are clones of the original cell but with changed chromosome numbers and structure. One or more clones of cancer cells, normal skin cells and blood vessels may combine to form a swelling called a tumor. All three types of skin cancers form tumors that show a lot of variety in size, shape and color.
6. How do skin tumors become deadly?
Skin tumors contained in their growth and not invading surrounding normal tissue are called benign, meaning they are not harmful. Expanding tumors can invade nearby tissues and interfere with normal functions. However, a primary invasive skin tumor becomes possibly deadly when cancer cells detach, migrate through the walls of blood vessels and arrive at other parts of the body. The tumor is then malignant and the spread is called metastasis. Located in new organs, the skin cancer cells can divide rapidly to form secondary tumors that may disrupt organ function and cause death.
7. When do they become deadly?
Benign skin cancers may remain permanently in that state throughout the rest of life or they may eventually become malignant. In some cases, however, a primary tumor may become malignant relatively quickly. MM is the leading cause of death from skin disorders and is more likely to progress rapidly than NMSC. Both NMSC and MM affect adults of all ages and increase in incidence with age. Death from NMSC, however, is strongly concentrated among elderly people. MM, on the other hand, is often fatal at young ages in fact the average age at death from MM is younger than that of most other kinds of cancers.
8. Who is at risk?
Many risk factors have been associated with relationship between human skin cancer and exposure to sunlight. Most skin cancers appear to be sporadic but all three kinds show familial susceptibility so there is a genetic component. People with light-colored skin, fair hair and blue eyes are more likely to develop skin cancers after excessive exposure to sunlight than are darker-skinned people. Outside workers and people with outdoor recreational lifestyles, with chromic exposure to sunlight are more prone to developing NMSCs than inside workers but this does not seem to be so for MM.
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| Types of Skin Cancer |
9. How are skin cancers cured?
By far the best treatment for skin cancers is their removal before they reach the malignant stage, and international efforts are focused on early diagnosis. Early stages of NMSCs are destroyed by freezing with a very fine jet of liquid nitrogen or by surgical removal. Metastatic stages of NMSCs can be treated with improved anti-cancer drugs and/or ionizing radiation but cure rates are not high. Surgical removal or pre-MM tumors is almost totally effective but there is currently no cure for MM, although some promising gene therapies and vaccines are being developed and tested in clinical trials.
10. How are they prevented?
The best prevention measure for skin cancers is to avoid excessive exposure to sunlight. Many programs are underway around the world, encouraging the use of sun-protective clothing and a sun-avoidance lifestyle. However, beaches are still jammed with people who rely on sunscreens to prevent the damaging effects of UV in sunlight, including skin cancers, while giving them a "safe" tan. There are doubts about how effective the use of sunscreen products are in the prevention of skin cancers and much more research is needed on this important question.
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