Rebecca Willis 4/1/09

Vitamin D and Cancer

Introduction:
Vitamin D, or 1,25(OH)2D3, while initially labeled as a vitamin, is in fact a steroid "synthesized in the
body as a result of ultraviolet radiation (UVR) exposure."(2) While vitamin D can be found in the diet, its
contribution is almost negligible. (2) The article "Vitamin D" stated that vitamin D is "essential for normal
skeletal development and maintenance of calcium homeostasis."(2) It is also needful for proper muscle
function.(2) In addition, as asserted in Francis P. Boscoe's article, many studies have shown that vitamin D "has
benefits against a variety of cancer types,"(1) even skin cancer.(2) In the article, "In Vivo," Dixon conceded
that UVR exposure may result in skin carcinogenesis, however his studies have shown that vitamin D "reduced
the level of UVR-induced cell death in human skin cells" and reduces damage in surviving cells by a raid
response pathway. (3) Its presence in irradiated skin decreased cyclobutane pyrimidine dimers (CPD) and
immunosuppression, which contributes to skin cancer development, and vitamin D decreased cell death of
sunburned cells.(3)

Objectives:
To prove that vitamin D was "inversely correlated with cancer mortality and survival" in many
internal cancer sites and to prove it has potential for therapeutic use in the prevention of skin cancer. (1,2,3)
Further, the objective was to prove that "where you live determines your sun exposure."(1)

Materials and Methods:

Boscoe and Schymura used "cancer incidence and mortality data... from 3,108 counties" in the
United States totaling nearly 7 million cases and deaths. (1) The data was acquired from the North American
Association of Central Cancer Registries. White non-Hispanics were the group in study while the black
population was used as the comparison group because they are much less able to absorb vitamin D from the
sun. Age groups were divided up by tens and ranged from 35 to 85+. The data was further analyzed on the
basis of gender. The study was even more thorough by collecting solar UV-B exposure data taken of
different areas of the United States by NASA's Total Ozone Mapping Spectrometer (TOMS). (1) Dixon
irradiated 69 human neonatal foreskins (in vitro) which were pretreated with vitamin D analogs, and albino,
hairless mice (in vivo) which were given several different treatments immediately following irradiation. (3)
The treatments included: vehicle, 1,25(OH)2D3, and low calcemic, rapid-acting analog JN. Skin samples
from the mice and the human samples were analyzed for sunburn, CPD, and immunosuppression. (3)

Results:
Boscoe and Schymura found that sun exposure was inversely related to cancer sites: "bladder,
colon, Hodgkin Lymphoma, myeloma, other biliary, prostate, rectum, stomach, uterus, and vulva, male
esophagus, female gallbladder" and less so in "female breast, kidney, leukemia, non-Hodgkin lymphoma,
pancreas, small intestine, female esophagus and thyroid, and male gallbladder."(1) The particular county in
the US had considerable effect on UV-B rays in relation to cancer incidences or lack thereof. Dixon's
results were "based on quadruplicates of each treatment from experiments performed at least twice with
similar results."(3) Dixon found that those samples treated with 1,25(OH)2D3 or JN had "reduced cell
loss...to 15.4%" after irradiation that those treated with vehicle which had 37% cell loss. Sunburned cells
were reduced significantly when treated with 1,25(OH)2D3 or JN. Finally, "1,25(OH)2D3 and JN
significantly reduced levels of UVR-induced immunosuppression in mice."(3) All were decreased by at
least 50% with the application of 1,25(OH)2D3 or JN.(3) Thus, vitamin D had inhibitory effects on skin
and several internal cancers.

Summery and Discussion:

Boscoe and Schymura's study discussed the effect of sun exposure as it relates to vitamin D
synthesis and cancer prevention. They found that in most cancer sites studied, sun exposure was negatively
correlated with incidences of cancer. In Dixon's study, the consistent decrease in carcinogenic effectors
proved the photoprotective effect of 1,25(OH)2D3, by the rapid pathway.(3) That conclusion was drawn
because JN had similar photoprotective effects as 1,25(OH)2D3 while conformationally limited to the rapid
pathway. Finally, because repair of CPD damage reduces skin cell apoptosis and prevents UVR-induced
mutation and immunosuppression and because vitamin D provided said photoprotective effect, it was
concluded that vitamin D is protective against skin cancer by at least 50%.
Rebecca Willis 4/1/09

References

Boscoe, Francis P., & Maria J. Schymura. (2006, November 10). Solar Ultraviolet-B
exposure and cancer incidence and mortality in the United States. BMC Cancer.
10:264-314. Retrieved March 18, 2009, from
http://www.biomedicalcentral.com/1471- 2407/6/264.

Dixon, Katie M., Rebecca S. Mason. (2008 June 10). Vitamin D. The International
Journal of Biochemistry and Cell Biology, doi:10.1016.

Dixon, K.M., S.S. Doe, A.W. Norman, J.E. Bishop, G.M. Halliday, V.E Reeve, R.S.
Mason. (2007). In Vivo Relevance for Photoprotection by the Vitamin D Rapid
Response Pathway. Journal of Steroid Biochemistry & Molecular Biology. 103,
451-456.