Sorry to hear about your colleague's family member getting this diagnosis, Nima.
In clinic, there would be a few routes I would take with a client presenting with liver cancer. The extent to which an alternative treatment is successful is probably largely determined by how far the individual is willing to go and how dedicated they are to recovering.
Here are some possible avenues that may be worth exploring:
We know that cancer is characterised by defective cellular respiration, and that restoring proper respiration reverses the cancer. This can be by restoring one of the depleted intermediates, or by simply reversing the oxygen deficiency (hypoxia). A cell can no longer utilise glucose efficiently as a fuel, and so reverts back to a primitive state of metabolism called glycolysis that is not reliant on oxygen. This way it "wastes" sugar. Another interesting thing is that cancer cells can also synthesise amino acids and fat for both maintenance and fuel. There is generally an elevated level of free fatty acids in cancer patients. So, assuming this person is not willing to go full-blown ketogenic (which may not even be appropriate in this situation and could exacerbate the issue), then limiting the release of free fatty acids is an option.
[quote author=https://www.nature.com/nrc/journal/v16/n11/full/nrc.2016.89.html]
Work over the past two decades has clearly established altered lipid metabolism as an important metabolic phenotype of cancer cells. Blocking lipid provision in cancer cells should therefore have dramatic consequences for cancer cell bioenergetics, membrane biosynthesis and intracellular signalling processes. Moreover, altered lipid availability can also affect cancer cell migration, induction of angiogenesis, metabolic symbiosis, escape from immune surveillance and drug resistance in cancer. Availability of FAs in the blood and peripheral tissues depends on lifestyle and diet and is likely to be altered in patients who are obese or have metabolic syndrome179. Thus, effects of FAs on tumorigenic processes may provide mechanistic insight into the increased cancer risk associated with these conditions.[/quote]
Vitamin B3 (niacinamide) is a potent inhibitor of free fatty acid release, and also is a precursor to the vitally important NAD+. Fwiw, cancer cells generally lack NAD+ to oxidise substrate and produce ATP, and so an NAD+ deficiency is present amongst all types of cancer. Niacinamide has been shown to prevent and reverse many different conditions by restoring respiratory efficiency, but I could only find one which points to its potential benefits in the case of liver cancer:
The inverse relationship between NAD+ and cancer awakened the curiosity of the researchers: could an increase in NAD+ have beneficial effects on the disease? When the scientists supplemented the diet in genetically modified mice with nicotinamide riboside, a derivative of vitamin B3 that increases intracellular levels of NAD+, they did not observe tumour development. Surprisingly, when they gave this diet to mice that had already developed the disease, the size of the tumours was reduced and they eventually disappeared.
[quote author=http://www.cell.com/cancer-cell/fulltext/S1535-6108(14)00392-4]Molecular mechanisms responsible for hepatocellular carcinoma (HCC) remain largely unknown. Using genetically engineered mouse models, we show that hepatocyte-specific expression of unconventional prefoldin RPB5 interactor (URI) leads to a multistep process of HCC development, whereas its genetic reduction in hepatocytes protects against diethylnitrosamine (DEN)-induced HCC. URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription of enzymes implicated in L-tryptophan/kynurenine/nicotinamide adenine dinucleotide (NAD+) metabolism, thereby causing DNA damage at early stages of tumorigenesis.
Restoring NAD+ pools with nicotinamide riboside (NR) prevents DNA damage and tumor formation. Consistently, URI expression in human HCC is associated with poor survival and correlates negatively with L-tryptophan catabolism pathway. Our results suggest that boosting NAD+ can be prophylactic or therapeutic in HCC
...
Here we demonstrate that NAD+ deficit-induced genotoxic stress is critical to initiate liver tumorigenesis and unravel a critical link between nutrient metabolism and genome integrity. Because our findings are relevant in human HCC, we propose that nutritional supplementation of NR, a vitamin B3 derivative, or other NAD+ boosters can be used as preventive and curative therapies in oncogene-induced NAD+ depletion-mediated DNA damage and carcinogenesis, especially in patients with precancerous lesions.
[/quote]
I would opt for a variety of phytonutrients, most likely high-dose curcumin. Here is some information on curcumin and liver cancer:
[quote author=http://www.academia.edu/10931793/Curcumin_and_Liver_Cancer_A_Review]Several studies have investigated the pharmacological effects of curcumin and its analogs in DENA-induced HCC. Chuang et al have shown that
curcumin protected against DENA-induced hyperplasia and HCC in rodents. The authors of the aforementioned studies also investigated the underlying biochemical mechanisms of curcumin in DENA-treated rodents.
Curcumin strongly inhibited the DENA-induced increase in the expression of the oncogenic p21 and tumor suppressor p53 protein as well as the elevated levels of proliferating cell nuclear antigen as well as NF-KB. Thapliyal and coworkers [153] have also documented the
attenuation of DENA-induced hepatocarcinogenesis in rats by dietary curcumin. The suppressive effects of curcumin in the DENA-initiated and 2-acetylaminofluorene-promoted alteration of hepatic foci in rats was accompanied by the restoration of the normal levels of several hepatic metabolic enzymes [154]. Sreepriya and Bali [155, 156] utilized the well-characterized DENA-initiated and PB-promoted two-stage model to investigate the potential anti-hepatocarcino-genic properties of curcumin. In these studies, curcumin ad-ministration prevented hepatocellular carcinogenesis in rats.
The investigators also reported that curcumin normalized the elevated levels of several enzymes of liver function and bili-rubin, increased glutathione content, elevated antioxidant enzymes and attenuated lipid peroxidation. Curcumin has also been shown to suppress the formation of hepatic ade-nomas in mice treated with, 2,2-dihydroxy-di-n-propylnitro-samine (DHPN) [157].[/quote]
[quote author=http://hrjournal.net/article/view/1325]
Adjuvant curcumin along with the current modalities of treatment may help to overcome the side effects and also have synergistic action as an anti-cancer agent.
Curcumin has been reported to inhibit telomerase activity in human cancer cell lines.[74] Synergistic anti-cancer effects of curcumin has also been demonstrated in conjunction with chemotherapeutic drugs such as doxorubicin and paclitaxel by in vivo animal models, and with cisplatin, 5-FU, and adriamycin by in vitro studies.[75-79]
Synergistic effects of curcumin have also been demonstrated in combined treatment with anti-angiogenic agents such as leflunomide and perindopril in in vivo mice models.[80]
...
Thus, to conclude, curcumin has a lot of potential to act as an adjuvant remedy in liver cancer. As far as toxicity issue is concerned, herbal medicines are much safer, have less adverse effects and relatively cheaper than conventional medicines.
Curcumin as an adjunct would have a synergistic anti-cancer action and would also protect against the side effects of the current chemotherapeutic agents. Previous studies have also claimed its antitumor effects against various types of cancers due to its inhibitory effects on many types of pathways. In this article we have discussed various pharmacological activities of curcumin along with its various antitumor mechanisms.
As we have discussed, oxidative stress is a risk factor cancer.
Curcumin, being a strong antioxidant has been proved to scavenge reactive species and can control tumor cell proliferation. Although preclinical results are promising but its clinical use in the treatment of HCC and HB remains to be elucidated.
Curcumin has the ability to modify many signaling pathways demonstrating its anti-tumor potential. Also, we noticed that curcumin has been proved to possess strong anti-oxidant and anti-inflammatory properties. Curcumin also targets principal anti-antigenic molecules like VEGF and COX-2. All these properties of curcumin are essential for its use as a therapeutic anti-tumor agent. It provides a future perspective for the development of a novel adjuvant anticancer agent for humans.[/quote]
Another substance is methylene blue - mentioned on
this thread. If you read the thread, you will see that methylene blue is effective against cancer on multiple levels. Here are some tidbits that may relate specifically to liver function:
[quote author=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3087269/]Methylene blue, an inhibitor of nitric oxide synthase and guanylate cyclase has many uses in medicine. It has been found to improve the hypotension associated with various clinical states.1
It also improves hypoxia and hyper dynamic circulation in cirrhosis of liver and severe hepatopulmonary syndrome.2 It also results in transient and reproducible improvement in blood pressure and cardiac function in septic shock.3[/quote]
SIRT1 activation by methylene blue, a repurposed drug, leads to AMPK-mediated inhibition of steatosis and steatohepatitis.
"...In mice fed on a high-fat diet for 8 weeks, MB treatment inhibited excessive hepatic fat accumulation and steatohepatitis. The ability of MB to activate SIRT1 promotes mitochondrial biogenesis and oxygen consumption and activates AMPK, contributing to anti-lipogenesis in the liver. Our results provide new information on the potential use of MB for the treatment of steatosis and steatohepatitis."
https://www.ncbi.nlm.nih.gov/pubmed/24486702
Another possibility is Aspirin:
Abnormal lipid metabolism is a hallmark of tumorigenesis. Hence, the alterations of metabolism enhance the development of hepatocellular carcinoma (HCC). Aspirin is able to inhibit the growth of cancers through targeting nuclear factor κB (NF-κB). However, the role of aspirin in disrupting abnormal lipid metabolism in HCC remains poorly understood. In this study, we report that aspirin can suppress the abnormal lipid metabolism of HCC cells through inhibiting acyl-CoA synthetase long-chain family member 1 (ACSL1), a lipid metabolism-related enzyme. Interestingly, oil red O staining showed that aspirin suppressed lipogenesis in HepG2 cells and Huh7 cells in a dose-dependent manner. In addition, aspirin attenuated the levels of triglyceride and cholesterol in the cells, respectively. Strikingly, we identified that aspirin was able to down-regulate ACSL1 at the levels of mRNA and protein. Moreover, we validated that aspirin decreased the nuclear levels of NF-κB in HepG2 cells. Mechanically, PDTC, an inhibitor of NF-κB, could down-regulate ACSL1 at the levels of mRNA and protein in the cells. Functionally, PDTC reduced the levels of lipid droplets, triglyceride and cholesterol in HepG2 cells. Thus, we conclude that aspirin suppresses the abnormal lipid metabolism in HCC cells via disrupting an NFκB-ACSL1 signaling. Our finding provides new insights into the mechanism by which aspirin inhibits abnormal lipid metabolism of HCC. Therapeutically, aspirin is potentially available for HCC through controlling abnormal lipid metabolism.
Furthermore, you could recommend
Photobiomodulation. Also vitamin C and a couple of other things are discussed elsewhere on the forum. Hope this helps and best of luck!
