Molecular Mechanism of Cancer Susceptibility Associated with Fok1 Single Nucleotide Polymorphism of VDR in Relation to Breast Cancer
Asian Pac J Cancer Prev. 2019 Jan 25;20(1):199-206.
Raza S1, Dhasmana A, Bhatt MLB, Lohani M, Arif JM.
Note: Breast Cancer appears to be able to mutate the VDR so as to prevent being having to defend itself against Vitamin D
So, many times BC ==> deactivate VDR, instead of Deactivated VDR ==> Breast Cancer
Vitamin D Receptor category has the following
Vitamin D tests cannot detect Vitamin D Receptor (VDR) problems
A poor VDR restricts Vitamin D from getting in the cells
It appears that 30% of the population have a poor VDR (40% of the Obese )
A poor VDR increases the risk of 55 health problems click here for details
The risk of 44 diseases at least double with poor Vitamin D Receptor as of Oct 2019
VDR at-home test $29 - results not easily understood in 2016
There are hints that you may have inherited a poor VDR
Compensate for poor VDR by increasing one or more:
| Increasing | Increases |
| 1) Vitamin D supplement Sun, Ultraviolet -B | Vitamin D in the blood and thus in the cells |
| 2) Magnesium | Vitamin D in the blood AND in the cells |
| 3) Omega-3 | Vitamin D in the cells |
| 4) Resveratrol | Vitamin D Receptor |
| 5) Intense exercise | Vitamin D Receptor |
| 6) Get prescription for VDR activator paricalcitol, maxacalcitol? | Vitamin D Receptor |
| 7) Quercetin (flavonoid) | Vitamin D Receptor |
| 8) Zinc is in the VDR | Vitamin D Receptor |
| 9) Boron | Vitamin D Receptor ?, etc |
| 10) Essential oils e.g. ginger, curcumin | Vitamin D Receptor |
| 11) Progesterone | Vitamin D Receptor |
| 12) Infrequent high concentration Vitamin D Increases the concentration gradient | Vitamin D in the cells |
| 13) Sulfroaphone and perhaps sulfur | Vitamin D Receptor |
Note: If you are not feeling enough benefit from Vitamin D, you might try increasing VDR activation. You might feel the benefit within days of adding one or more of the above
Far healthier and stronger at age 72 due to supplements Includes 6 supplements which help the VDR
Items in both Vitamin D Life categories Breast Cancer and Vitamin D Receptor are listed here:
- Breast cancer associated with Vitamin D Receptor (14th study) – Oct 2019
- After breast cancer treatment 4,000 IU of Vitamin D was not enough to help if have poor Vitamin D receptor – June 2019
- Breast Cancer death 1.8 X more likely if poor Vitamin D Receptor – April 2019
- Breast Cancer and Vitamin D review – March 2018
- Women with Breast Cancer were 16.9 times more likely to have a poor Vitamin D Receptor – Jan 2019
- Cancer treatment by Vitamin D sometimes is restricted by genes – Oct 2018
- Two chemicals increase the Vitamin D receptor and decrease the growth of breast cancer cells in the lab - March 2018
- Breast Cancer reduces receptor expression and thus block Vitamin D to the cells– July 2017
- Vitamin D receptor as a target for breast cancer therapy (abstract only) – Feb 2017
- Breast Cancer was 4.6 times more likely if have a poor Vitamin D Receptor – Dec 2016
- Increased Breast Cancer metastasis if low vitamin D or poor VDR – Feb 2016
- Increased risk of some female cancers if low vitamin D (due to genes) – meta-analysis June 2015
- Vitamin D receptor in breasts and breast cancer vary with race – March 2013
- Breast Cancer incidence change by 40 percent with vitamin D receptor genes – Oct 2012
- Genes breast cancer and vitamin D receptor - Sept 2010
Download the PDF from Vitamin D Life
Breast cancer is the leading cause of death among women worldwide. It is a multi-factorial disease caused by genetic and environmental factors. Vitamin D has been hypothesized to lower the risk of breast cancer via the nuclear vitamin D receptor (VDR). Genetic variants of these vitamin D metabolizing genes may alter the bioavailability of vitamin D, and hence modulate the risk of breast cancer.
MATERIALS AND METHODS:
The distribution of Fok1 VDR gene (rs2228570) polymorphism and its association with breast cancer was analysed in a case–control study based on 125 breast cancer patients and 125 healthy females from North Indian population, using PCR-RFLP. An In silico exploration of the probable mechanism of increased risk of breast cancer was performed to investigate the role of single nucleotide polymorphisms (SNPs) in cancer susceptibility.
RESULTS:
The Fok1 ff genotype was significantly associated with an increased risk of breast cancer (p=0.001; χ2=13.09; OR = 16.909; %95 CI=2.20 - 130.11). In silico analysis indicated that SNPs may lead to a loss in affinity of VDR to calcitriol, and may also cause the impairment of normal interaction of liganded VDR with its heterodimeric partner, the retinoid X receptor (RXR), at protein level, thereby affecting target gene transcription.
CONCLUSION:
Breast cancer risk and pathogenesis in females can be influenced by SNPs. SNPs in VDR may cause alterations in the major molecular actions of VDR, namely ligand binding, heterodimerization and transactivation. VDRE binding and co-activator recruitment by VDR appear to be functionally inseparable events that affect vitamin D-elicited gene transcription. This indicates that breast cancer risk and pathogenesis in females may be influenced by SNPs.
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