Cancer Risk: Worse than by bad luck?

YOUNGWOOD, Pa. - Jan. 8, 2015 - PRLog -- .

Introduction
Recently, Science [1] reported genomic changes occur in an organ simply by chance during DNA replication rather than as traditionally thought by carcinogens. Hence, a strong correlation is predicted between the lifetime number of divisions among stem cells and the lifetime risk of cancer arising in an organ. Stem cells were selected because they can self-renew during the lifetime development and maintenance of the tissue architecture. The study showed that although melanocytes and basal epidermal cells of the skin are both exposed to the same dose of UV from solar radiation, melanomas are much less common than basal cell carcinomas because the larger number of basal epidermal cells undergo a higher number of divisions than melanocytes.

However, not all agreed. The contrarian argument [2] may be made that cancer need not be proportional to the number of replications that the DNA undergoes, but by carcinogens that damage the DNA independent of replications.

In this PR, DNA damage is limited to UV radiation. However, solar or other external source of UV radiation are ruled out because for the same dose of UV, melanomas are much less common than nearby basal cell carcinoma, a fact that is explained in [1] by the greater chance of DNA mutations because of the larger number of stem cell divisions in basal cells.

But chance is not necessary as there is a causal explanation:

Melanosomes that form in the melanocytes contain melanin granule NPs that emit UV radiation causing DNA damage that leads to mostly basal cell carcinomas with  few melanomas. NPs stands for nanoparticles.

Indeed, it widely known the antimicrobial action of NPs is caused by damaging the DNA of bacteria, but by the same reason NPs also damage human DNA, that if not repaired, may lead to cancer. Less known [3] is NPs produce QED induced EM radiation at UV levels that in body fluids damages the DNA. QED stands for quantum electrodynamics and EM for electromagnetic. Moreover, the NPs may be man-made or biological.  Indeed, the human body naturally [4] creates NPs that may damage the DNA, e.g., epithelial tissue is organized by a submicron thick < 100 nm basement membrane, the breakdown of which produces NPs associated [5] with the spread of tumors.

QED Induced EM Radiation
The cancer risk of UV radiation from melanin granule NPs is depicted in the thumbnail. Melanocyte cells located in the basal layer of the dermis have dendrite structures that penetrate into the lower epidermis. Melanosones having sizes of about 1 micron formed within the melanocytes pass through the outer tips of the dendritesinto the dermis. Removed from melanocytes, the melanosomes are collections of < 100 nm melanin granule NPs.

By the theory of QED induced EM radiation, the melanin NPs absorbing heat from the thermal surroundings cannot increase in temperature [3] because of quantum mechanics. Provided the refractive index of the NP is greater than that of the cellular surroundings, the heat is conserved by QED inducing the melanin NPs to emit UV radiation, a condition that is satisfied [6] for 30 nm melanin NPs having an index of 1.7 while that of the surroundings is 1.35. In this way, the emission of UV radiation from the melanin NPs damages the DNA in both melanocytes and basal cells. But because of the small number of melanocytes in the basal layer, most DNA damage caused by the UV radiation from the melanin NPs occurs in the basal cells with little, if any DNA damage in the melanocytes. By QED radiation, the risk of basal cell carcinoma therefore far exceeds that of melanoma consistent with observations [1].

Conclusions
Cancer is caused by DNA damage that may occur during DNA replication. It therefore is reasonable that the more rounds of replication the DNA undergoes, the greater the chance of cancer. But this is questionable as DNA damage may also occur by carcinogens without DNA replication, and therefore the number of cancers occurring by chance or bad luck may be relatively unimportant to those caused by carcinogens.

QED induced UV radiation from < 100 nm melanin NPs provides a reasonable explanation for the higher risk of basal cell carcinoma than melanoma, but other comparative cancer risks remain to be assessed. For example, whether melanin NPs explain why cancers of the small intestinal epithelium are three times less common than brain tumors, even though intestinal epithelial cells are exposed to much higher levels of environmental carcinogens than cells in the brain protected by the blood-brain barrier.

Cancer risk may not be a matter of chance or bad luck. Rather, cancer may be caused solely by DNA damage from QED induced UV radiation in NPs. Setting aside DNA damage by chemicals, the hypothesis may be made that UV radiation from melanin NPs in melanocytes is the sole cause of cancers because of the DNA damage in surrounding tissue. But the NPs need not be limited to melanin - all biological and man-made NPs damage the DNA, e.g., the nicotine NPs that enter lung tissue by smoking. A literature review of cancer risk based on the presence of < 100 nm NPs in all cancers is required to begin the assessment of this hypothesis.

References
[1] C. Tomasetti & B. Vogelstein, “Variation in cancer risk among tissues can be explained by the number of stem cell divisions,” Science, 347, 78-81, 2015.
[2] The Guardian. See http://www.theguardian.com/science/grrlscientist/2015/jan/02/bad-luck-bad-journalism-and-cancer-rates
[3] T. Prevenslik, See diverse QED applications at http://www.nanoqed.org  -  2009 - 2015.
[4] T. Prevenslik, “Cancer by Nanoparticles,” NanoSafe 2010, November 18-20, Minatec, Grenoble, 2010.
[5] T. Prevenslik, "Cancer by Epithelial Disorganization," See  http://prlog.org/10793056
[6] D. S. Gareau, et al., “Noninvasive Imaging of Melanoma with Reflectance Mode Confocal Scanning Laser Microscopy in a Murine Model,” J. Invest. Derma, 127, 2186-2190, 2007.