Colloidal Gold Suspension Sub Micrometer Sized Particles Gold Biology Essay


Colloidal gold13 is a suspension (or colloid) of sub-micrometre sized particles of gold in a fluid which is usually water. The color of the liquid is usually either an intense red color (for particles less than 100 nm), or a dirty yellowish color (for larger particles). Due to the unique optical, electronic and molecular-recognition properties of AuNPs, they are subjected to substantial research, with applications in a wide variety of areas, including electron microscopy, electronics, nanotechnology and materials science.

5.2. History:

Nanogold is nothing but trademarked variety of colloidal gold. In ancient times, the synthesis of colloidal gold was originally used for staining glass. Modern scientific evaluation of colloidal gold was begun by Michael Faraday in 1850s. A so-called Elixir of Life, a potion made from gold, was discussed in ancient times. Colloidal gold has been used since Ancient Roman times to color glass with intense shades of yellow, red, or mauve, depending on the concentration of gold. In 16th century, the alchemist Paracelsus claimed to have created a potion called Aurum Potabile (Latin: potable gold). In 17th century the glass-coloring process was refined by Andreus Cassius and Johann Kunckel. In 1842, John Herschel invented a photographic process called Chrysotype (from the Greek word for gold) that used colloidal gold to record images on paper. Paracelsus work have inspired Michael Faraday to prepare the first pure sample of colloidal gold, which he called 'activated gold', in 1857. He used phosphorus to reduce a solution of gold chloride.

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Faraday was the first to recognize that the color was due to the minute size of the gold particles. In 1898 Richard Adolf Zsigmondy prepared the first colloidal gold in diluted solution. Apart from Zsigmondy, Sevdberg who invented ultracentrifugation and Mie, who provided the theory for scattering and absorption by spherical particles, were also interested in the synthesis and properties of colloidal gold.


Generally, AuNPs are produced in a liquid ("liquid chemical methods") by reduction of chloroauric acid (H[AuCl4]), although more advanced and precise methods do exist. After dissolving H[AuCl4], the solution is rapidly stirred while a reducing agent is added. This causes Au3+ ions to be reduced to neutral gold atoms. As more and more of these gold atoms form, the solution becomes supersaturated, and gold gradually starts to precipitate in the form of sub-nanometer particles. The rest of the gold atoms that adheres to the existing particles and, if the solution is stirred vigorously enough, the particles will be fairly of uniform size.

To prevent the particles from aggregating, some sort of stabilizing agent that adheres to the nanoparticle surface is usually added. It is functionalized with various organic ligands to create organic-inorganic hybrids with advanced functionality. It can also be synthesized by laser ablation25.

5.3.1. Turkevich method

The method pioneered by J. Turkevich et al. in 1951 and refined by G. Frens in 1970s, is the simplest method. Generally, it is used to produce modestly monodisperse spherical AuNPs suspended in water of around 10-20 nm in diameter. It involves the reaction of small amounts of hot chloroauric acid with small amounts of sodium citrate solution. The colloidal gold will form because the citrate ions act as both a reducing agent, as well a capping agent.

Recently, the evolution of the spherical AuNPs in the Turkevich reaction has been elucidated. Interestingly, extensive networks of gold nanowires are formed as a transient intermediate which are responsible for the dark appearance of the reaction solution before it turns ruby-red.

To produce larger particles, less sodium citrate should be added (possibly down to 0.05%). The reduction in the amount of sodium citrate will reduce the amount of the citrate ions available for stabilizing the particles, and this will cause the small particles to aggregate into bigger ones (until the total surface area of all particles becomes small enough to be covered by the existing citrate ions).

5.3.2.Brust method

This method was discovered by Brust and Schiffrin in early 1990s, and can be used to produce gold nanoparticles in organic liquids that are normally immiscible with water (like toluene). It involves the reaction of a chlorauric acid solution with tetraoctylammonium bromide (TOAB) solution in toluene and sodium borohydride which acts as an anti-coagulant and a reducing agent, respectively.

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Here, the AuNPs will be around 5-6 nm. NaBH4 is the reducing agent, and TOAB is both the phase transfer catalyst and the stabilizing agent. It is important to note that TOAB does not bind to the AuNPs particularly strongly, so the solution will aggregate gradually over the course of approximately two weeks. To prevent this, a stronger binding agent, like a thiol (in particular, alkanethiols), which will bind to gold covalently, producing a near-permanent solution. Alkanethiol protected AuNPs can be precipitated and then redissolved. Some of the phase transfer agent may remain bound to the purified nanoparticles, which may affect physical properties such as solubility. In order to remove as much of this agent as the nanoparticles must be further purified by soxhlet extraction.

5.3.4. Perrault Method

In 2009, Perrault and Chan in 2009, used hydroquinone to reduce HAuCl4 in an aqueous solution that contains gold nanoparticle seeds. This process is similar to that in photographic film development, in which silver grains within the film grow through addition of reduced silver onto their surface. Similarly, AuNPs can act in conjunction with hydroquinone to catalyze reduction of ionic gold onto their surface. The presence of a stabilizer such as citrate controls particle growth. Typically, the nanoparticle seeds are produced using the citrate method. The hydroquinone method complements that of Frens, as it extends the range of monodispersed spherical particle sizes that can be produced. Whereas the Frens method is ideal for particles of 12-20 nm, the hydroquinone method can produce particles of at least 30-250 nm.

5.3.5. Martin Method

This method, discovered by the Eah and coworkers in 2010, generated "naked" AuNPs in water by reducing HAuCl4 with NaBH4. Even without any other stabilizer like citrate, AuNPs are stably dispersed. The size distribution is nearly monodisperse and the diameter can be precisely and reproducibly tuned from 3.2 to 5.2 nm. The key is to stabilize HAuCl4 and NaBH4 in the aqueous stock solutions with HCl and NaOH for >3 months and >3 hours respectively. In addition, the ratio of NaBH4-NaOH ions to HAuCl4-HCl ions must be precisely controlled in the "sweet zone". "Naked" AuNPs are coated with a monolayer of 1-dodecanethiol and then phase-transferred to hexane simply by shaking a mixture of water, acetone, and hexane for 30 seconds. Since all the reaction byproducts remain in the water-acetone phase, no post-synthesis cleaning is needed for AuNPs in the hexane phase. The amount of 1-dodecanethiol is only 10% of gold atoms in number. All these synthesis procedures take just <10 minutes.

5.3.6. Sonolysis

Another experimental method for the generation of gold particles is by sonolysis. In one such process based on ultrasound, the reaction of an aqueous solution of HAuCl4 with glucose, the reducing agents are hydroxyl radicals and sugar pyrolysis radicals (forming at the interfacial region between the collapsing cavities and the bulk water) and the morphology obtained is that of nanoribbons with width 30--50 nm and length of several micrometers. These ribbons are very flexible and can bend with angles larger than 90°. When glucose is replaced by cyclodextrin (a glucose oligomer) only spherical gold particles are obtained suggesting that glucose is essential in directing the morphology towards a ribbon.

5.3.7. Electron Microscopy

a) Immunogold labelling

Colloidal gold and various derivatives have long been among the most widely-used contrast agents for biological electron microscopy. Colloidal gold particles can be attached to many traditional biological probes such as antibodies, lectins, superantigens, glycans, nucleic acids, and receptors. Particles of different sizes are easily distinguishable in electron micrographs, allowing simultaneous multiple-labeling experiments.

5.4. Health and medical applications

5.4.1.Colloidal gold can be used as a carrier for targeting the drug

Colloidal gold has been successfully used in therapy for rheumatoid arthritis in rats. In a related study, the implantation of gold beads near arthritic hip joints in dogs has been found to relieve pain.

An in vitro experiment has shown that the combination of microwave radiation and colloidal gold can destroy the beta-amyloid fibrils and plaque which are associated with Alzheimer's disease. The possibilities for numerous similar radiative applications are also currently under exploration29.

5.4.2.Drug carrier

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AuNPs are being investigated as carriers for drugs such as Paclitaxel. The administration of hydrophobic drugs require molecular encapsulation and it is found that nanosized particles are particularly efficient in evading the reticuloendothelial system.

5.4.3.Tumor detection

In cancer research, colloidal gold can be used to target tumors and hence detection using SERS (Surface Enhanced Raman Spectroscopy) in vivo can be performed. These AuNPs are surrounded with Raman reporters which provide light emission that is over 200 times brighter than quantum dots. It was found that the Raman reporters were stabilized when the nanoparticles were encapsulated with a thiol-modified polyethylene glycol coat. This allows for compatibility and circulation in vivo. To specifically target tumor cells, the pegylated gold particles are conjugated with an antibody (or an antibody fragment such as scFv), against e.g. Epidermal growth factor receptor, which is sometimes overexpressed in cells of certain cancer types. Using SERS, these pegylated AuNPs can then detect the location of the tumor.

5.4.4. Photothermal agents30

Gold nanorods are being investigated as photothermal agents for in-vivo applications. Gold nanorods are rod shaped AuNPs whose aspect ratios tune the surface plasmon resonance (SPR) band from the visible to near infrared wavelength. The total extinction of light at the SPR is made up of both absorption and scattering. For the smaller axial diameter nanorods (~10 nm), absorption dominates, whereas for the larger axial diameter nanorods (>35 nm), scattering can dominate. Consequently, for in-vivo applications, small diameter gold nanorods are being used as photothermal converters of near infrared light due to their high absorption cross sections. Since near infrared light transmits readily through human skin and tissue, these nanorods can be used as ablation components for cancer, and other targets. When coated with polymers, gold nanorods have been known to circulate in-vivo for greater than 15 hours half life.

5.5.Polymer profile:

5.5.1. Pullulan31

Pullulan is a water-soluble, neutral polysaccharide formed extracellularly by certain strains of the polymorphic fungus Aureobasidium pullulans. It is now widely accepted that pullulan is a linear polymer with maltotriosyl repeating units joined by α-(1→6) linkages. The maltotriosyl units consist of α-(1→4) linked d-glucose. Consequently, the molecular structure of pullulan is intermediate between amylose and dextran because it contains both types of glycosidic bonds in one polymer.

5.5.2. Quality Parameters:




white or yellowish-white powder

Water solubility (25ËšC)

easy soluble

Specific optical activity [α]D20 (1% in water)

min. +160Ëš

Polypeptides %

max. 0, 5

pH (sol. 1 %)

5 - 7

Mineral residue-ash (sulphated), %

max. 3

Moisture (loss on drying), %

max. 6

Content of glucose polymer,


min. 80

Apparent viscosity (rotary

viscometer, 1300 s-1), of a 2

% solution, mPa·s


Molecular weight (mean),

viscosimetric and HPLC, kDa


5.5.3.Structural Features

Structure of pullulan

The polysaccharide possesses hydroxyl groups at position 2, 3 and 4 of different reactivity. The repeating unit linked by α-(1→6) bond shows a greater motional freedom than the units connected by α(1→4),which may influence the functionalization pattern obtained by chemical modification in particular homogeneously in dilute solution. As an edible, bland and tasteless polymer, the chief commercial use of pullulan is in the manufacture of edible films that are used in various breath freshener or oral hygiene products such as Listerine Cool Mint PocketPaks. As a food additive, it is known by the E number E1204.  Addition of pullulan is more natural, involving no toxic chemicals, much less environment polluting in its production process32.

Pullulan Structure33:

Pullulan is natural water-soluble polysaccharide, produced from starch by fermentation. Available as a white powder it is odorless, flavorless, and highly stable. Pullulan is an extremely versatile ingredient providing a technology platform for product innovation. It is an excellent film-former, producing a film which is heat sealable with good oxygen barrier properties and which can also be printed. Pullulan film is sometimes referred to as 'edible packaging'. Importantly colors, flavors and functional ingredients can be entrapped in the film matrix and effectively stabilized. Pullulan can be formed into capsules for use with pharmaceutical and nutraceutical products. Its non-animal origin means there are no BSE concerns and it is also suitable for all consumers groups.

5.5.4. Uses of Pullulan:

Pullulan can be used as either an innovative or decorative film or used in granule form for31:




Pan coating




Sauces and dressings


Innovative soft candy








A number of potential applications have been reported for pullulan as a result of its good film-forming properties; pullulan can form thin film which is transparent, oil resistant and impermeable to oxygen. Pullulan may be used as a coating and packaging material, as a sizing agent for paper, in plywood manufacturing, and in dielectric condensors, as a starch replacer in low-calorie food formulations, in cosmetic emulsions, and in other industrial and medicinal applications. Other potential applications include use as an adhesive binder, thickener and encapsulating agent. In conclusion, this polysaccharide is of economic importance with increased applications to the food, pharmaceutical and chemical industries34.

5.6. Drug Profiles:



Fluorouracil (5-FU)13 (brand names Adrucil, Carac, Efudex and Fluoroplex). Fluorouracil is a drug that is a pyrimidine analog which is used in the treatment of cancer. It works through noncompetitive inhibition of thymidylate synthase. Due to its noncompetitive nature and effects on thymidine synthesis, 5-FU is frequently referred to as the "suicide inactivator". It belongs to the family of drugs called antimetabolites. It is typically administered with leucovorin.

Pharmacologic class: Antimetabolite

Therapeutic class: Antineoplastic

Drug Mechanism of Action35:

As a pyrimidine analogue, it is transformed inside the cell into different cytotoxic metabolites which are then incorporated into DNA and RNA, finally inducing cell cycle arrest and apoptosis by inhibiting the cell's ability to synthesize DNA. It is an S-phase specific drug and only active during certain cell cycles. In addition to being incorporated in DNA and RNA, the drug has been shown to inhibit the activity of the exosome complex, an exoribonuclease complex of which the activity is essential for cell survival. Capecitabine is a prodrug that is converted into 5-FU in the tissues. It can be administered orally.

Adverse effects:

Include myelosuppression, mucositis, dermatitis, diarrhea and cardiac toxicity.

5-FU injection and topical even in small doses cause both acute CNS damage and progressively worsening delayed degeneration of the CNS in mice. This latter effect is caused by 5-FU-induced damage to the oligodendrocytes that produce the insulating myelin sheaths.

When using a pyrimidine-based drug, users must be aware that some people have a genetic inability to metabolize them. Current theory points to nearly 8% of the population having what is termed DPD deficiency.

5.5.7. Pharmacokinetics36

Half life: 10-20 minutes

Bioavailability: 28 to 100%

Protein Binding: 8 to 12%

Metabolism: Intracellular and hepatic (CYP-mediated)

Melting Point: 282ËšC to 283ËšC (-198F)

Excretion: Renal


•Hypersensitivity to drug or its components

• Bone marrow depression

• Dihydropyrimidine dehydrogenase enzyme deficiency (with topical route)

• Poor nutritional status

• Serious infection

• Pregnancy or breastfeeding


 Consult facility's cancer protocols to ensure correct dosage, administration technique, and cycle length.

• Antiemetic should be given before fluorouracil, as ordered, to reduce GI upset.

• The drug may be given without dilution by direct I.V. injection over 1 to 3 minutes.

• For I.V. infusion, it is diluted with dextrose 5% in water, sterile water, or normal saline solution in plastic bag (not glass bottle). Infusion may be given over a period of 24 hours or more.

• Infusion site frequently checked to detect extravasations.

• Nonmetal applicator or appropriate gloves must be used to apply topical form.

• Application of topical form to mucous membranes or irritated skin must be avoided.

• Occlusive dressings over topical form must be avoided.

• Pyridoxine may be given with fluorouracil to reduce risk of palmar-plantar erythrodysesthesia (hand-foot syndrome).

5.5.8. Dosing information37:

 Advanced colorectal cancer

Adults: 370 mg/m2 I.V. for 5 days, preceded by leucovorin 200 mg/m2 daily for 5 days; may be repeated for 4 to 5 weeks. No single daily dose should exceed 800 mg.

 Haepatic and Breast Cancers:

Adults: Initially, 12 mg/kg/day I.V. for 4 days, followed by 1 day of rest; then 6 mg/kg I.V. every other day for four to five doses. Or 7 to 12 mg/kg/day I.V. for 4 days, followed by 3-day rest, then 7 to 10 mg/kg I.V. q 3 to 4 days for three doses. For maintenance, 7 to 12 mg/kg I.V. q 7 to 10 days, or 300 to 500 mg/m2/day I.V. for 4 to 5 days, repeated monthly. No single daily dosage should exceed 800 mg.

Poor-risk patients: 3 to 6 mg/kg/day I.V. for 3 days, then 3 mg/kg/day I.V. on days 5, 7, and 9 (not to exceed 400 mg/dose).

 Actinic (solar) keratoses

Adults: 1% solution or cream applied once or twice daily to lesions on head, neck, or chest; 2% to 5% solution or cream may be needed for other areas.

Superficial basal cell carcinoma

Adults: 5% solution or cream applied b.i.d. for 3 to 6 weeks (up to 12 weeks)

Adverse reactions:

CNS: confusion, disorientation, euphoria, ataxia, headache, weakness, malaise, acute cerebellar syndrome or dysfunction.

CV: angina, myocardial ischemia, thrombophlebitis.

EENT: vision changes, photophobia, lacrimation, lacrimal duct stenosis, nystagmus, epistaxis

GI: nausea, vomiting, diarrhea, stomatitis, anorexia, GI ulcer, GI bleeding

Hematologic: anemia, leukopenia, thrombocytopenia

Skin: alopecia, maculopapular rash, melanosis of nails, nail loss, palmar-plantar erythrodysesthesia, photosensitivity, local inflammation reaction (with cream), dermatitis

Other: fever, anaphylaxis


Used cautiously in:

• renal or hepatic impairment, infections, edema, ascites

• obese patients


Drug-drug. Bone marrow depressants (including other antineoplastics): additive bone marrow depression.

Irinotecan: dehydration, neutropenia, sepsis

Leucovorin calcium: increased risk of fluorouracil toxicity

Live-virus vaccines: decreased antibody response to vaccine, increased risk of adverse reactions

5.6. Disease profile:

5.6.1. Liver cancer36:

Liver cancer (hepatocellular carcinoma) is a cancer arising from the liver. It is also known as primary liver cancer or hepatoma. The liver is made up of different cell types (for example, bile ducts, blood vessels, and fat-storing cells). However, liver cells (hepatocytes) make up 80% of the liver tissue. Thus, the majority of primary liver cancers (over 90--95%) arises from liver cells and is called hepatocellular cancer or carcinoma.

Also physicians are often referring to cancer that has spread to the liver, having originated in other organs (such as the colon, stomach, pancreas, breast, and lung). More specifically, this type of liver cancer is called metastatic liver disease (cancer) or secondary liver cancer. This is a much more common problem around the world than primary liver cancer and frequently leads to confusion, because the term liver cancer actually can refer to either metastatic liver cancer or hepatocellular cancer.

Liver cancer is the third most common cancer in the world. A deadly cancer, liver cancer will kill almost all patients who have it within a year. In 2000, it was estimated that there were about 564,000 new cases of liver cancer worldwide, and a similar number of patients died as a result of this disease. About three-quarters of the cases of liver cancer are found in Southeast Asia (China, Hong Kong, Taiwan, Korea, and Japan). Liver cancer is also very common in sub-Saharan Africa (Mozambique and South Africa).

5.6.2. Causes of liver cancer38:

Hepatitis B infection:

Hepatitis B virus (HBV) infection can be caught from contaminated blood products or used needles or sexual contact but is frequent among Asian children from contamination at birth or even biting among children at play.

Hepatitis C infection:

Hepatitis C virus (HCV) infection is more difficult to get than hepatitis B. It usually requires direct contact with infected blood, either from contaminated blood products or needles. HCV is also associated with the development of liver cancer. In fact, in Japan, hepatitis C virus is present in up to 75% of cases of liver cancer.


Cirrhosis caused by chronic alcohol consumption is the most common association of liver cancer in the developed world.


Aflatoxin B1 is the most potent liver cancer-forming chemical known. It is a product of a mold called Aspergillus flavus, which is found in food that has been stored in a hot and humid environment. This mold is found in such foods as peanuts, rice, soybeans, corn, and wheat. Aflatoxin B1 has been implicated in the development of liver cancer in Southern China and sub-Saharan Africa. It is thought to cause cancer by producing changes (mutations) in the p53 gene. These mutations work by interfering with the gene's important tumor suppressing (inhibiting) functions.

Drugs, medications, and chemicals

There are no medications that cause liver cancer, but female hormones (estrogens) and protein-building (anabolic) steroids are associated with the development of hepatic adenomas. These are benign liver tumors that may have the potential to become malignant (cancerous). Thus, in some individuals, hepatic adenoma can evolve into cancer.

Certain chemicals are associated with other types of cancers found in the liver. For example, thorotrast, a previously used contrast agent for diagnostic imaging studies, caused a cancer of the blood vessels in the liver called hepatic angiosarcoma. Also, vinyl chloride, a compound used in the plastics industry, can cause hepatic angiosarcomas that appear many years after the exposure.


Liver cancer will develop in up to 30% of patients with hereditary hemochromatosis (a disorder in which there is too much iron stored in the body, including in the liver). Patients at the greatest risk are those who develop cirrhosis with their hemochromatosis.

Diabetes and obesity

Fatty liver disease like this causes damage to the individual liver cells and may lead to cirrhosis in some people, thereby increasing the risk of liver cancer.


Individuals with most types of cirrhosis of the liver are at an increased risk of developing liver cancer.

Liver cancer symptoms and signs

Abdominal pain, unexplained weight loss decreased appetite, jaundice, ascites, or encephalopathy (altered mental state of ascites)


Liver blood tests:

Blood tests: elevated liver tests (bilirubin or transaminase), reduced albumin, elevated AFP, elevated blood urea nitrogen (BUN), or low serum sodium.

There is no reliable or accurate screening blood test for liver cancer. The most widely used biochemical blood test is alpha-fetoprotein (AFP), which is a protein normally made by the immature liver cells in the fetus.

2. Imaging studies play an important role in the diagnosis of liver cancer. A good study can provide information as to the size of the tumor, the number of tumors, and whether the tumor has involved major blood vessels locally or spread outside the liver.

3. Ultrasound, CT, and MRI scans.

Liver biopsy or aspiration

Diagnosis of liver cancer is always based on microscopic (histological) confirmation.

This technique is called fine needle aspiration. When a larger needle is used to obtain a core of tissue, the technique is called a biopsy.


The only proven cure for liver cancer is liver transplantation for a solitary, small (<3cm) tumor. Small tumor can be surgically removed (partial hepatic resection) without the need for a liver transplantation.

However, most patients with liver cancer also have cirrhosis of the liver and would not tolerate liver resection surgery.

Systemic (entire body) chemotherapy:

The most commonly used systemic chemotherapeutic agents are doxorubicin (Adriamycin) and 5-fluorouracil (5 FU). These drugs are quite toxic. Recent studies suggest that combinations of drugs such as gemcitabine, cisplatin, or oxaliplatin can shrink the tumors in some people.


Treating liver cancer has been the understanding of the genetic makeup of these tumors, as well as the cancer cells' reliance upon blood vessels and molecules produced in the body that can help them grow. Drugs like sorafenib, bevacizumab are designed to block several components of the angiogenesis pathway, as well as other growth signals for individual cancer cells.

Hepatic arterial infusion of chemotherapy

The normal liver gets its blood supply from two sources: the portal vein (about 70%) and the hepatic artery (30%). However, liver cancer gets its blood exclusively from the hepatic artery. Making use of this fact, investigators have delivered chemotherapy agents selectively through the hepatic artery directly to the tumor. The theoretical advantage is that higher concentrations of the agents can be delivered to the tumors without subjecting the patients to the systemic toxicity of the agents.

In reality, however, much of the chemotherapeutic agents does end up in the rest of the body. Therefore, selective intra-arterial chemotherapy can cause the usual systemic (body-wide) side effects. In addition, this treatment can result in some regional side effects, such as inflammation of the gallbladder (cholecystitis), intestinal and stomach ulcers, and inflammation of the pancreas (pancreatitis). Liver cancer patients with advanced cirrhosis may develop liver failure after this treatment. but the benefit of intra-arterial chemotherapy is that fewer than 50% of patients will experience a reduction in tumor size.

Chemoembolization (trans-arterial chemoembolization or TACE)

This technique takes advantage of the fact that liver cancer is a very vascular (contains many blood vessels) tumor and gets its blood supply exclusively from the branches of the hepatic artery. This procedure is similar to intra-arterial infusion of chemotherapy. But in TACE, there is the additional step of blocking (embolizing) the small blood vessels with different types of compounds, such as gel foam or even small metal coils.


Radioembolization (also known as SIRT, or selective internal radiotherapy) involves attaching a radioactive molecule (called Yttrium) to tiny glass beads. These are then injected directly into the blood vessels feeding the cancers (as in TACE). The radiation particles can then kill tumor cells within a distance of 2.5 mm from them, so that any part of the cancer fed by tiny blood vessels will be exposed to the radiation.

Ablation techniques

Ablation refers to any method that physically destroys a tumor, and is generally only applicable to situations in which there is only one, two, or sometimes three individual cancers in a liver. When there are more than that, it is not possible to reach every one on its own, so a different method such as systemic chemotherapy or TACE must be used.

Radiofrequency ablation (RFA) therapy

In the U.S., RFA therapy has become the ablation (tissue destruction) therapy of choice among surgeons. The surgeon can perform this procedure laparoscopically (through small holes in the abdomen) or during open exploration of the abdomen.

Percutaneous ethanol (alcohol) injection

In this technique, which has been generally replaced by RFA, pure alcohol is injected into the tumor through a very thin needle with the help of ultrasound or CT visual guidance. Alcohol induces tumor destruction by drawing water out of tumor cells (dehydrating them) and thereby altering (denaturing) the structure of cellular proteins.


Instead of using heat, cryoablation sues a probe filled with liquid nitrogen to freeze the tumor and kill it that way.

Stereotactic radiosurgery

Stereotactic radiosurgery (SRS) is a new technique directing radiation (high-powered X-ray beams) directly to the tumor.

Proton beam therapy

This technique is able to deliver high doses of radiation to a defined local area. Proton beam therapy is used in the treatment of other solid tumors as well.


Surgical options are limited to individuals whose tumors are less than 5 cm and confined to the liver, with no invasion of the blood vessels.

Liver resection

The goal of liver resection is to completely remove the tumor and the appropriate surrounding liver tissue without leaving any tumor behind. This option is limited to patients with one or two small (3 cm or less) tumors and excellent liver function, ideally without associated cirrhosis.

Liver transplantation

Liver transplantation has become an accepted treatment for patients with end-stage (advanced) liver disease of various types (for example, chronic hepatitis B and C, alcoholic cirrhosis, primary biliary cirrhosis, and sclerosing cholangitis)13.