Make no mistake about it, cutaneous malignant melanoma (CMM) is not caused by exposure to ultraviolet radiation (UVR). Rather, the normal, natural and involuntary reaction to UVR exposure results in a signal sent by keratinocytes to the melanocytes, telling them to produce melanin that will be oxidized by UVA wavelengths to create a protective cap (i.e., a tan) that will protect the keratinocyte cells’ DNA from damage. But, if the UVR exposure is so intense or lasts so long that the existing melanocytes are not able to keep up with the demand for melanin, the following sequence takes place. 1. A signal is sent to the “mother” melanocyte cell, telling it to detach from the basement membrane, withdraw from the 36 keratinocytes in its epidermal melanin unit (EMU) and divide in order to form a new “daughter” melanocyte cell. 2. A signal is sent to the mother melanocyte cell, telling it to stop dividing. 3. A signal is sent to both the mother and daughter melanocyte cells, telling them to reattach themselves to the basement membrane, connect with 34 to 36 keratinocytes (in order to form two new EMUs) and to begin producing the melanin necessary to protect the nucleus of the keratinocytes from UVR damage. For reasons not presently understood, the signal telling the mother melanocyte cell to quit dividing sometimes gets scrambled, and the melanocyte continues dividing. When any cell loses the ability to quit dividing, it becomes a cancer. When the rapidly dividing (and out-of-control) cell is a melanocyte, the cancer formed is CMM. As you can see, the only link between UVR and CMM is a coincidental correlation—not a causal correlation. The failure of the public to understand this important distinction has made it possible for the dermatology community, the sunscreen industry and the various melanoma-related organizations to use F.E.A.R. (False Emanations Appearing Real) to promote their personal and professional interests. Just consider the following “inconvenient facts” that these groups choose to ignore even though they know, or reasonably ought to know, that the facts prove UVR is not the cause of CMM. There is no molecular signature. Several recent studies have confirmed the fact that there is a distinct and repeatable molecular signature showing that UVR overexposure can damage the DNA of keratinocytes which, in turn, can lead to basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). However, these same studies also confirm that there is no molecular signature showing that UVR damages the DNA of melanocytes. Sunscreens do not prevent CMM. If UVR was truly the cause of CMM, it would logically follow that sunscreen use over the past three decades should have prevented the increase in the incidence of CMM. But, study after study has shown that the use of sunscreen does not prevent the development of any form of skin cancer, including CMM. Authors’ Note: So, how did the dermatology community, the sunscreen industry and the various melanoma-related organizations react to this information? First, they blamed the messenger and attacked the authors of the studies. When this approach failed due to the sheer number of studies available, they next claimed that it was the failure of the public to apply enough sunscreen to prevent CMM. Whenthis approach also failed, the groups switched to their latest defense—saying that the longer UVA wavelengths are responsible for causing CMM and sunscreen did not previously contain UVA filters. If you study the timing, you will find that the decision to blame UVA coincides with the introduction of products containing UVA filters. Lucky coincidence? We don’t think so. And, of course, these groups have failed to acknowledge the several authors that have published scientific papers showing that UVA wavelengths do not cause CMM. CMM occurs most often on parts of the body not exposed to UVR. Researchers found that UVR exposure to one arm caused the number of melanocytes to increase in that arm (as expected) and also in the other arm, which was shielded from exposure (not expected). Further experiments showed that UVR exposure to one part of the body results in an increase in the number of melanocytes in the skin of the entire body. This explains how a melanocyte dividing in a part of the body not exposed to sunlight can be affected by a scrambled signal and become a CMM. This also explains why intense, intermittent UVR overexposure is more likely to result in a CMM—the person has more melanocytes dividing at the same time in an attempt to supply the necessary melanin. There is no world-wide epidemic of CMM. In an article titled, “Melanoma Epidemic: A Midsummer Night’s Dream?,” the authors concluded that the large increase in reported incidence of CMM is likely due to diagnostic drift, which classifies benign lesions as stage 1 melanoma. In other words, the so-called CMM epidemic is the result of the rapid increase in the number of dermatologists who are now removing a large number of lesions that were previously classified as benign and calling them a CMM.
|