Turmeric may help prevent and treat liver cancer.

Natural Turmeric Help to Prevent and Treat Liver Cancer

Research suggests that turmeric and its compounds could help prevent liver cancer. This is good news, since rates of hepatocellular carcinoma (also known as hepatoma) are increasing. Hepatocellular carcinoma is aggressive and is the most common type of cancer that first develops in the liver. Symptoms may include upper abdominal pain, swollen abdomen, and/or jaundice. (vi.1664240326)

The curcumin compounds in turmeric may also help treat cholangiocarcinoma. This highly aggressive, often fatal tumor grows in cells that line the bile ducts, which are part of the liver's biliary system(vi.137)

Risk Factors for Liver Cancer

Inflammation and chronic injury (technically called cirrhosis) which lead to fibrotic scarring cause most cases of liver cancer. (vi.64)

Risk factors that can lead to liver fibrosis include:

For cholangiocarcinoma, risk factors include: (vi.4137)

Treating Liver Cancer is Difficult

Surgery is considered the best treatment, especially if the cancer is caught early. Unfortunately, tumors in the liver and cholangiocarcinoma are rarely discovered at that point. In fact, only about 10% of patients with cholangiocarcinoma, and 10-30% of those with hepatocellular carcinoma, even have a surgical treatment option. This is because the cancer is usually caught after it has spread throughout the liver or bile ducts and beyond. (vi.64137326)

Even in those where surgery is an option, both types of cancer frequently recurs and the prognosis is usually poor. About 20% of patients with liver cancer show some response to chemotherapy, but it does not improve survival rates. (vi.64137326)

How Turmeric Works Against Liver Cancer

The nutrients and polyphenols in turmeric can help keep the liver healthy and functioning well. This is particularly important because cancer in the liver is most often caused by scarring or chronic injury related to infection, toxins, or disease. (vi.64)

In addition, turmeric and its compounds also show antitumor effects specifically against liver cancer cells. Some of turmeric compounds work similarly to FDA-approved chemotherapy drugs(vi.678184137275327330-331)

Figure VI.24 - How Turmeric's Compounds Stop Liver Cancer Cells

Figure VI.24: How Turmeric's Compounds Stop Liver Cancer Cells

Table VI.38: Turmeric and Turmeric Compound Antitumor and Chemopreventive Effects
Turmeric Compound What It Does

Ar-turmerone (vi.330)

Kinase proteins that generate free radicals and trigger apoptotic cell death in liver cancer cells. (vi.330)

Tumor suppressors and other proteins that promote or carry out cancer cell death. (vi.330)

Growth of liver cancer cells(vi.330)

Caffeic acid (vi.74)

MMP-9, enzymes that promote invasiveness. (vi.78275)

Calebin-A (vi.306)

Growth of liver cancer cells and triggered cancer cell death better than curcumin. (vi.332)

Curcumin (vi.74)

Apoptotic cell death in liver cancer cell lines by stimulating production of caspase enzymes and death receptors(vi.137)

Beneficial transcription factors that produce natural antioxidants and/or block growth of tumor cells, including liver cancer. (vi.137)

Detoxification enzymes that help prevent DNA damage and liver tumors. (vi.240)

Entry of all major types of hepatitis C into liver cells. (vi.333)

Oncogenes, transcription and epigenetic factors, and cytokines that promote liver cancer cell growth. (vi.240275)

Enzyme activity of growth factor receptors that promote cancer growth. (vi.275)

Inflammatory enzymes and growth factors that promote new blood vessel growth that feed cancer cells. (vi.67)

MMP-9, enzymes expressed in highly invasive liver cancer cells. (vi.275)

Survival proteins that help cancer cells resist natural cell death mechanisms. (vi.137)

Angiogenesis (the development of new blood vessels that allow tumors to grow and are necessary for them to spread). (vi.16)

Metastasis of liver tumors in animal studies. (vi.240)

Oral administration of curcumin in animal studies also significantly inhibited the toxic, liver-cancer causing effects of toxins. It reduced both the incidence of hepatocarcinoma (by 62%) and the number of tumors (by 81%). (vi.16)

Eugenol (vi.74)

Antioxidant compound that helps prevent liver cancer caused by toxins(vi.78)

Farnesol (vi.110)

DNA damage from carcinogens. (vi.111)

Development of liver cancer by blocking metabolism of toxins(vi.111)

Number and size of precancerous lesions. (vi.111)

Growth of liver cancer cells by arresting them in the G phase of the cell cycle. This stops the cancer cells before they get to the S phase where they replicate. (vi.111)

Ferulic acid (vi.138)

Growth of liver cancer cells. (vi.334)

Apoptosis in liver cancer cells. (vi.334)

Geraniol (vi.112)

Cancer cell death in patients with liver cancer. (vi.78)

Development of liver cancer. (vi.85)

Growth of liver cancer. (vi.111)

Limonene (vi.74)

Natural antioxidant protection. (vi.134)

Carcinomas caused by chemical toxins(vi.124)

Myricetin (vi.79)

Growth of liver carcinoma cells. (vi.194)

Death of liver cancer cells. (vi.194)

Protocatechuic acid (vi.146)

Tumor suppressors and kinase enzymes that suppress liver cancer cell growth. (vi.334)

Quercetin (vi.79)

Nrf-2, a transcription factor protein that activates natural antioxidants. (vi.84)

Damage to liver cells from free radicals(vi.84)

Tumor suppressor proteins(vi.81)

Tumor cell growth. (vi.131)

MDR1, a gene that promotes resistance to chemotherapy treatment. (vi.131)

Death of liver cancer cells. (vi.194)

Tumor-killing effects of 5-fluorouracil, paclitaxel, TRAIL, and carboplatin and liver cancer cell lines. (vi.334)

Resveratrol (vi.83)

Tumor suppressor activity. (vi.84)

Apoptosis in liver cancer cells. (vi.84)

Invasiveness of hepatoma cells promoted by free radicals(vi.331)

Inflammatory enzymes that promote cancer growth. (vi.67331)

Cell cycle proteins that promote tumor cell proliferation. (vi.331)

Enhances effectiveness (by 25%) of chemotherapy treatment (5-FU) at reducing tumor size. (vi.331)

Turmeric or Curcumin

  • In lab studies, turmeric inhibited 80% of DNA mutations caused by aflatoxin B-1 (a fungal metabolite found in many grains and spices). Higher concentrations of curcumin showed even better results. (vi.26328)
  • In animals exposed to aflatoxin B-1, adding either turmeric or curcumin to the diet blocked precancerous lesions from forming. In ducklings given 5 µg/day of aflatoxin B-1, turmeric and curcumin both reversed the carcinogenic liver damage caused by the toxin. (vi.26328)

Turmeric Leaf Oil

Aflatoxins from Aspergillus flavus, a fungus known to cause liver cancer. Main components are ρ-cymene, and terpinolene(vi.335)

Dried, Powdered Turmeric Rhizome

DNA mutations (which could lead to cancer) caused by aflatoxins(vi.336-337)

Embolized Curcuma Aromatic Oil

Clinical Trial

In 32 patients with primary liver cancer, administration of turmeric oil by arterial infusion along with Chinese herbal medicine supplements resulted in: (vi.338)

  • 13 patients with partial remission (compared to 10 in the chemo-treated control group)
  • 1 patient with complete remission (none in the control group)

Although these results were not statistically significant, patients treated with the herbal therapies had better median survival times and greater 1-year survival rate. (vi.338)

Fermented Turmeric Supplements

In a clinical study, fermented turmeric supplements normalized liver enzymes. Experts suggest this could help prevent liver disease. (vi.339)

Concerns with Using Quercetin and Curcumin Together

The effect of quercetin and curcumin in combination (as separate supplements) should be taken into consideration when treating liver cancers. Administered together, quercetin actually causes more free-curcumin to pass through the liver. It does so by binding to albumin in the plasma and membranes in the liver. Albumin is also a substance present in tumor cells, but binding to albumin prevents curcumin from crossing the cancer cell membrane and entering the malignant cell. (vi.340)

Human papilloma virus.
Cancers that begin elsewhere in the body often metastasize, or spread, to the liver. (vi.64)
Primary sclerosing cholangitis. (vi.137)
Such as axitinib, bevacizumab, dasatinib, pazopanib, sorafenib tosylate, sunitinib malate, and temsirolimus. (vi.275)
JNK and ERK. (vi.330)
P53 and Bax. (vi.330)
Caspases -3, -8, and -9. (vi.330)
HepG2, Huh-7, and Hep3B liver carcinoma cell lines. (vi.330)
HepG2 hepatoma cell line. (vi.332)
DR4 and DR5. (vi.137)
Such as Nrf-2 and peroxisome proliferator-activated receptor gamma (PPAR-γ). (vi.137)
Specifically, c-Met and c-Myc. (275)
Including HAT, AP-1, ARNT, HIF-1, STAT-3, and NF-κB. (vi.137)
Such as IL-6. (vi.240)
For example, tyrosine kinase activity. (vi.275)
Platelet-derived growth factor receptors (PDGFRs). (vi.275)
COX-2 and VEGF. (vi.67)
Bcl-xL, Bcl-2, survivin, and cIAP-2. (vi.137)
P38. (vi.334)
JNK. (vi.334)
Specifically, p21, p27, and p53. (vi.81)
Specifically, p21 and p53. (vi.84)
COX-2. (vi.331)
Such as cyclin B proteins. (vi.331)

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