Abstract
Introduction: Previous studies have alluded to the beneficial effects of vitamin D, particularly with regard to cancer. Vitamin D has been suggested to decrease negative effects of cancer treatments, hinder growth of tumor cells and reduce overall inflammation. Therefore, making sure patients have sufficient vitamin D is highly recommended. Breast cancer is something heavily researched. It is of interest to see if the development of cancerous cells is hindered by appropriate supplementation of Vitamin D. Design: A retrospective study to bring attention to hereditary cancer along with potential causes of the development of cancer cells associated with insufficient Vitamin D levels. Methods: Our preliminary study searched to determine if there was a correlation between BRCA1 and BRCA2 mutation carriers and vitamin D deficiency/insufficiency. Data was obtained from a community based oncology clinic and compared to data from a study from the same clinic in 2006. We tested 36 patients with BRCA1 and BRCA2 deleterious mutations, whereby 75% (27/36) of the patients had a Vitamin D level less than 30 ng/mL. Results: There was a correlation between vitamin D insufficiency with BRCA1 and BRCA2 deletions within this group of patients (n=2 deficient, n=25 insufficient, n=9 normal levels). The 9 patients with normal levels in this study averaged 38.9 ng/mL, which is significantly lower than the average literature level of 52 ng/mL (P < 0.05). Of the 20 patients with normal vitamin D levels (30-74 ng/mL), all had deletions within exonic regions. The majority of the locations of the deletions were premature truncations, where there were no intronic deletions found. Conclusions: We have shown a correlation of Vitamin D insufficiency and BRCA deleterious mutations. Out of the 36 patients studied with deleterious BRCA mutations, 27 of them has had insufficient vitamin D. Based on our findings, providers in our community need to be more vigilant in assessment and treatment of Vitamin D as this may impact the incidence of cancer in high risk patients. Recommendations: The possibility of reducing inflammation through normalizing vitamin D levels should be enough reason for primary care providers to screen everyone. There is the potential to prevent cellular damage that consequently could affect cell checkpoints, leading to the development of cancerous cells in high risk populations. Future work could include study of germline vs. somatic cells and the effect of vitamin D on the genetic integrity of the cells.
