An interesting study published recently, in January of 2018, in npj Precision Oncology, makes a strong case for adding IV Vitamin C in the treatment of liver cancer (hepatocellular carcinoma).

Liver cancer of the actual liver cells needs to be distinguished from metastasis of other cancers (colon, breast, etc.) localized in the liver.

Liver cancer is one of the deadliest cancers known, leading to a terminal state in about less than 2 years.

In this study, involving over 600 patients who had previously undergone a partial liver resection due to hepatocellular cancer, Vitamin C given in intravenous form was shown to kill cancerous liver cells and prolong the survival time of the treated patients.

Intravenous administration of Vitamin C has a high degree of safety as long as several basic precautions are followed.

In our clinic we advise several blood tests before the IV is given, such as a G6PD test and others. infusions usually take about two hours plus depending on the amount of Vitamin C given. Further details need to be tailored to the individual situation.

Following is an excerpt of the abstract of the article:

Vitamin C (L-ascorbic acid, ascorbate, VC) is a potential chemotherapeutic agent for cancer patients. However, the anti-tumor effects
of pharmacologic VC on hepatocellular carcinoma (HCC) and liver cancer stem cells (CSCs) remain to be fully elucidated. Panels of
human HCC cell lines as well as HCC patient-derived xenograft (PDX) models were employed to investigate the anti-tumor effects of
pharmacologic VC. The use of VC and the risk of HCC recurrence were examined retrospectively in 613 HCC patients who received
curative liver resection as their initial treatment. In vitro and in vivo experiments further demonstrated that clinically achievable
concentrations of VC induced cell death in liver cancer cells and the response to VC was correlated with sodium-dependent vitamin
C transporter 2 (SVCT-2) expressions. Mechanistically, VC uptake via SVCT-2 increased intracellular ROS, and subsequently caused
DNA damage and ATP depletion, leading to cell cycle arrest and apoptosis. Most importantly, SVCT-2 was highly expressed in liver
CSCs, which promoted their self-renewal and rendered them more sensitive to VC. In HCC cell lines xenograft models, as well as in
PDX models, VC dramatically impaired tumor growth and eradicated liver CSCs. Finally, retrospective cohort study showed that
intravenous VC use was linked to improved disease-free survival (DFS) in HCC patients (adjusted HR = 0.622, 95% CI 0.487 to 0.795,
p o 0.001). Our data highlight that pharmacologic VC can effectively kill liver cancer cells and preferentially eradicate liver CSCs,
which provide further evidence supporting VC as a novel therapeutic strategy for HCC treatment.
Reference: npj Precision Oncology (2018) 2:1 ; doi:10.1038/s41698-017-0044-8