To digress a minute let me talk about the P53 gene and P53 protein this gene produces as both are important in cancer suppression and progression. The P53 gene is called the cancer suppressor gene. P53 is known for both slowing the cell replication cycle and destroying cells. 

By slowing the cell replication cycle this allows repairs to damaged cell’s DNA to occur. Repair or if necessary, destruction of cells infected with viruses, bacteria or so irreparably damaged they cannot be repaired-cancerous ones. 1,2,3

The p53 gene is also crucial to the production of pro-opiomelanocortin (POMC}. It is produced for example by the cleaving of a substance called pre-pro-opiomelanocortin. This cleaving in the pituitary produces POMC. POMC is called a neuropeptide. 

POMC is acted on in the pituitary gland located in the central nervous system (CNS) for endocrine function (acting throughout the body). It however can also occur elsewhere in the body. Including the peripheral nervous system (PNS) to produce POMC and several other neuropeptides a paracrine function. 

A paracrine function (localized to the area) to produce POMC and the neuropeptides produced from it to act only on cells close by. For example, an infection of the prostrate. As only that area needs these neuropeptides effect. These neuropeptides act receptors to activate many cellular functions.

POMC can for example be modified into two shorter neuropeptides-melanocyte stimulating hormone (MSH) and adrenocorticotropin (ACTH). MSH stimulates the production of melanin, which gives skin its dark color and for those with lighter colored skin a tan following ultraviolet light exposure. 

MSH also causes the increased production of melanin that protects the cell’s nucleus from deleterious effects of ultraviolet light. The melanin accumulates in the cells in between where the UV-B enters the cell and the cell’s nucleus. As it absorbs like 98% of ultraviolet light it protects the cell’s DNA. 

That is, it acts to absorb the UV-B but also the UV-A before it contacts the cell nucleus. As both can damage to the cell’s DNA. Damaged DNA can lead to cancer. Vitamin D3 formed in skin attaches to the vitamin D binding protein (DBP). 

Vitamin D consumed orally is attached to DBP after it is converted in calcifediol-25 hydroxy vitamin D3 in the liver. DBP is important in immune function as it is what is called vitamin d binding protein- macrophage activating factor (DBP-MAF). DBP-MAF may be effective against cancer.4  

Those of you who are into cancer genetics are aware of how important mutations in the P53 gene are to developing cancer. For example, mutational inactivation of the p53 gene is noted in nearly half of human tumors. 5


There is a lot of evidence associating chronic inflammation with cancer. In fact, at least 15% of cancers are started by infections. 10 As cells fighting infections release free radicals that form substances like peroxynitrate that can damage our DNA. 11

Also during infection new cells are being created to replace damaged ones. Thus, these new cells are more sensitive to DNA damage from substances like peroxynitrate. Resulting in P53 mutations. These p53 mutations are similar in number in both cancer and autoimmune diseases. 12 

Curiously one of the cancers associated with infections is colon cancer. 13 Vitamin D3 benefits for cancer are perhaps most strongly associated with reducing risk of, you guessed it colon cancer. 14  See, macrophages release macrophage migration inhibitory factor (MIF) to help fight infections. 

Well MIF shuts off P53. 15 Thus, chronic infections can both damage our p53 gene and shut this gene off. In the short term we can tolerate this but long term it appears to increase our risk of cancer. If infections go on too long it can cause cellular damage which with the P53 gene shut off is not repaired. 

It shuts off the P53 gene thus blunting our ability to repair damaged cells by slowing the cell cycle or kill the cells that are so damaged that they cannot be repaired. Thus leading to cancers forming and progressing. 

  1. Drayman N, Ben-nun-Shaul O, Oppenheim A, et al. (July 2016). p53 elevation in human cells halt SV40 infection by inhibiting T-ag expression.
  2. Kastenhuber ER, Lowe SW. (September 17, 2017). Putting p53 in context. Cell. 170: 1062-78.
  3. Siegel C, Prusty BK, Rudel T, et al. (November 6, 2014) Tumor suppressor p53 alters host cell metabolism to limit chlamydia trachomatis infection. 9(3):918-29.
  4. Yamamoto N, Suyama H, Yamamoto N (July 2008). Immunotherapy for prostate cancer with Gc protein derived macrophage activating factor, GcMaF” Translational Oncology. 1 (2):65-72.
  5. Hamzehloie T, Mojarrad M, Shekouhi S. (Mar 2012). The role of tumor protein 53 mutations in common human cancers and targeting the murine double minute 2-P53 interaction for cancer therapy. Iran J Med Sci. 37(1):3-8
  6. W Mohan SV, Chang AL. (2014) Advanced basal cell carcinoma: epidemiology and therapeutic innovations. Curr Dermatol Rep. 3(1): 40-45.
  7. Macathur M, Hold GL, El-Omar EM. (2004). Inflammation and cancer II. Role of chronic inflammation and cytokine gene polymorphisms in the pathogenesis of gastrointestinal malignancy. J Physio. 286(4): G515-G520.
  8. Coussens LM, Webb Z. (December 19-26, 2002). Inflammation and cancer. Nature. 420(6917):860-867.
  9. Balkwill F, Mantovani A. (February 17, 2001). Inflammation and cancer: back to Virchow? The Lancet. 357(9255):539-545.
  10. Kuper H, Adami HO, Trichopoulos D. (2000). Infections as a major cause of human cancer. J Intern Med. 248:171-183.
  11. Maeda H, Akaike T. (1998). Nitric oxide and oxygen radicals in infection, inflammation and cancer. 63:854-865.
  12. Yamanishi Y, Boyle DL, Firestein, et al. (July 23, 2002). Regional analysis of p53 mutations in rheumatoid arthritis synovium. 99(15):10025-10030.
  13. Kostic AD, Chun E, Meyerson M, Garrett WS. (September 2013). Microbes and inflammation in colorectal cancer. Cancer Immunol Res. 1(3):150-7.
  14. McCullough ML, Zolstick ES, Smith-Warner SA, et al. (Feb 2019). Circulating vitamin D and colorectal cancer risk: An international pooling project of 17 cohorts. J Nat Cancer Inst. 111(2):158-169.
  15. Hudson JD, Shoaibi MA, Beach DH, et al. (1999). A proinflammatory cytokine inhibits p53 tumor suppressor activity. J Exp Med. 190:1375-1382.

*The information posted above is for educational purposes only. Always check with your doctor before initiating any changes in your medical treatment. If you do not, then The Two-Minute Health Fact, Dr. Judson Somerville, nor The Optimal Dose is responsible!


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