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Melanoma cancer growth slowed by increased Vitamin D Receptor (yet again) – Oct 2019

Vitamin D-VDR signaling inhibits Wnt/beta-catenin-mediated melanoma progression and promotes anti-tumor immunity

Cancer Research DOI: 10.1158/0008-5472.CAN-18-3927

VitaminDWiki

The risk of 44 diseases at least double with poor Vitamin D Receptor as of Oct 2019
Vitamin D Receptor Activation can be increased by any of:
Resveratrol, Omega-3, Magnesium, Zinc, non-daily Vitamin D dosing, etc
   Note: The founder of VitaminDWiki uses 10 of the 12 known VDR activators


I suspect that increased Vitamin D and Increased Vitamin D Receptor will PREVENT as well as TREAT many Cancers - Founder of VitaminDWiki Oct 2019


Vitamin D Receptor and Cancers

Items in both categories Vitamin D Receptor and Cancer - Breast:

Items in both categories Vitamin D Receptor and Cancer - Colon:

Items in both categories Vitamin D Receptor and Cancer

Items in both categories Vitamin D Receptor and Cancer - other:

Items in both categories Vitamin D Receptor and Cancer - Skin:

Items in both categories Vitamin D Receptor and Cancer - Prostate:


Vitamin D makes melanoma cells less aggressive Medical News report on this study

Sathya Muralidhar, Anastasia Filia, Jérémie Nsengimana, Joanna Poźniak, Sally J. O'Shea, Joey M Diaz, Mark Harland, Juliette A. Randerson-Moor, Jörg Reichrath, Jonathan P Laye, Louise van der Weyden, David J. Adams, D.T. Bishop and Julia Newton-Bishop

1α,25-dihydroxyvitamin D3 signals via the Vitamin D Receptor (VDR). Higher serum vitamin D is associated with thinner primary melanoma and better outcome, although a causal mechanism has not been established. As melanoma patients commonly avoid sun exposure, and consequent vitamin D deficiency might worsen outcomes, we interrogated 703 primary melanoma transcriptomes to understand the role of vitamin D-VDR signalling and replicated the findings in TCGA metastases.
VDR expression was independently protective for melanoma death in both primary and metastatic disease.
High tumor VDR expression was associated with upregulation of pathways mediating anti-tumor immunity and correspondingly with higher imputed immune cell scores and histologically detected tumor infiltrating lymphocytes (TILs).
High VDR expressing tumors had downregulation of proliferative pathways, notably Wnt/beta-catenin signaling.
Deleterious low VDR levels resulted from promoter methylation and gene deletion in metastases. Vitamin D deficiency (< 25 nmol/l ~ 10 ng/ml) shortened survival in primary melanoma in a VDR-dependent manner.
In vitro functional validation studies showed that elevated vitamin D-VDR signaling inhibited Wnt/beta-catenin signaling genes. Murine melanoma cells overexpressing VDR produced fewer pulmonary metastases than controls in tail vein metastasis assays.
In summary, vitamin D-VDR signaling contributes to controlling pro-proliferative /immunosuppresive Wnt/beta-catenin signaling in melanoma and this is associated with less metastatic disease and stronger host immune responses.
This is evidence of the causal relationship between vitamin D-VDR signaling and melanoma survival which should be explored as a therapeutic target in primary resistance to checkpoint blockade.

Created by admin. Last Modification: Saturday November 9, 2019 16:03:26 GMT-0000 by admin. (Version 10)
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