Liver cancer nicely treated by high dose vitamin D for 16 weeks (early stage, in rats)
Vitamin D3 suppresses the early stages of chemically induced hepatocarcinogenesis in rats: a dose-response analysis
Nutrire 201843:12, https://doi.org/10.1186/s41110-018-0065-2. Published: 23 April 2018
Mariana B. Tablas, Renata L. Goto, Brunno F. R. Caetano, SΓ©rgio A. A. dos Santos and Luis F. Barbisan
* Overview Vitamin D Dose-Response has the following chart*
* 10,400 IU daily will get most humans to 80 ng in a few months (8 studies)π Download the PDF from Vitamin D Life
Average of 20,000 IU/kg of body weight of vitamin D daily (G5) for 16 weeks was enough

Increased Vitamin D ==> less liver cancer

Background
The aim of this study was to investigate dose-response effects of vitamin D3 (VD3) supplementation on the early stages of diethylnitrosamine (DEN) and carbon tetrachloride (CCl4)-induced hepatocarcinogenesis in rats.
Methods
The animals were randomly allocated into six experimental groups (10 rats each) treated as follows: group 1: no treatment; groups 2β6: single intraperitoneal injection of N-diethylnitrosamine; groups 2β6: intragastric CCl4; groups 3β6: intragastric VD3 at
10,000,
20,000,
40,000, and
60,000 IU/kg b.w., respectively.
Results
Serum 25-hydroxyvitamin D (25-OHD) levels in the VD3-supplemented groups were significantly higher than those in the control groups (G1 and G2, pβ<β0.001). Serum levels of phosphate were higher in the groups supplemented with VD3 at 10,000 and 60,000 IU/kg (G3 and G6, pβ<β0.005). VD3 higher doses reduced cell proliferation and the number of larger placental glutathione S-transferase (GST-P)-positive hepatocellular preneoplastic lesions. Neither the DEN/CCl4 regimen nor the VD3 supplementation altered vitamin D receptor (VDR) protein expression in the liver.
Conclusion
The results indicate that high-dose VD3 supplementation reduced the development of DEN/CCl4-induced preneoplastic lesions in the liver.