At the time I did that I had not put my understanding of cancer all together yet. Well, cancer cells or at least many I have found so far significantly increase for one the production of the 24-hydroxylase enzyme produced by the CYP24A1 gene.
This enzyme converts the 1,25 dihydroxy vitamin D3, the active form of vitamin D3 into 24,25 dihydroxy vitamin D3. 1 Thus, if not completely inactivating it severely reducing its function as the 1.25 dihydroxy vitamin D3 is the most active form.
For example, the blood storage form 25 hydroxy vitamin D3 has biological activity much less than the 1,25 dihydroxy form.2 In my experience I have seen optimal dosing to reach optimal blood levels of the 1,25 form of vitamin D3 cure people with skin and ovarian cancer.
All anecdotal results but I would love to see studies done at these doses and blood levels of vitamin D3. I believe optimal blood levels of vitamin D3 might be a cure or at least arrest many other forms of cancer. The following types of cancer do to increase the production of 24-hydroxylase thus inactivating the active form of vitamin D3 allowing the cancer to proliferated:
- Melanoma 3
- Colon 4
- Thyroid 5
- Breast cancer 6
- Pancreatic cancer 7
- Lung cancer 8
- Prostate cancer 9
- Esophageal cancer 10
- Ovarian cancer 11
- Endometrial cancer 12
- Skin cancer 13
There will surely be more cancers found that have a similar way of stimulating the CYP24A1 gene that increases the production of 24-hydroxylase enzyme that inactivates 1, 25 dihydroxy vitamin D3-the active form of vitamin D3. Thus inactivating the cells intracellular immune response to abnormal cells-in this case cancer- and preventing apoptosis (cell death) cancer cells.
Those who have one, all or a combination of the following- vitamin D3 deficient, have a genetic defect in the vitamin D receptor, the intracellular machinery that activates vitamin D3, or the proteins that attach to the active form of vitamin D are more susceptible to these and possibly others.
- https://ghr.nlm.nih.gov/gene/CYP24A1#:~:text=The%2024%2Dhydroxylase%20enzyme%20brea ks,is%20stored%20in%20the%20body. (I separated this string of characters to have it format correctly, to look it up you will have to remove that space)
- Blunt JW, DeLuca HF and Schnoes HK. 25-Hydroxycholecalciferol. A biologically active metabolite of vitamin D3. Biochemistry 1968, 7, 10, 3317–3322. https://doi.org/10.1021/bi00850a001
- Campbell MJ, Trump DL. Vitamin D Receptor Signaling and Cancer.Endocrinol Meta. 46
- (2017) 1009-1038. https://doi.org/10.1016/ELSEVIER_CM_POLICY
- Hu N, Zhong H. CYP24Ai depletion facilitates the antitumor effect of vitamin D3on thyroid cancer cells. Experimental and Therapeutic Medicine. July 27, 2018. 2821-2830.
- Cai, H., Jiao, Y., Li, Y. et al. Low CYP24A1 mRNA expression and its role in prognosis of breast cancer. Sci Rep 9, 13714 (2019). https://doi.org/10.1038/s41598-019-50214-z
- Hummela D, Aggarwala A, Borkab K, Horváthc C, et al. The vitamin D system is deregulated in pancreatic diseases. The Journal of Steroid Biochemistry and Molecular Biology; October 2014. 144 (Part B):402-409.
- Anderson MG, Nakane M, Ruan X, Kroeger PE, Wu-Wong JR. Expression of VDR and CYP24A1 mRNA in human tumors. Cancer Chemother Pharmacol. 2006;57(2):234-240.
- Luo W, Karpf AR, Deeb KK, Trump D L, et al. Epigenetic Regulation of Vitamin D 24-Hydroxylase/CYP24A1 in Human Prostate Cancer. Cancer Research. July 2010. 70 (14): 5953-5962.
- Mimori K, Tanaka y, Yoshinaga K, Mori M, et al. Clinical significance of the overexpression of the candidate oncogene CYP24 in esophageal cancer. February 2004. 15 (2):236-241. Archive DOI:https://doi.org/10.1093/annonc/mdh056.
- Ibid (10)
- Bokhari AA, Lee LR, Raboteau D, et al. Progesterone potentiates the growth inhibitory effects of calcitriol in endometrial cancer via suppression of CYP24A1. Oncotarget. 2016;7(47):77576-77590. doi:10.18632/oncotarget.12725.
- Kaukinen, A., Siiskonen, H., Pelkonen, J. et al. Immunoreactivity to CYP24A1, but not vitamin D receptor, is increased in mast cells of keratinocyte skin cancers. Eur J Dermatol 27, 590–598 (2017). https://doi.org/10.1684/ejd.2017.3132