Milk Thistle (PDQ®): Complementary and alternative medicine - Health Professional Information [NCI]
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Purpose of This PDQ Summary
This PDQcancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the use of milk thistle as a treatment for cancer. The summary is reviewed regularly and updated as necessary by the PDQ Cancer Complementary and Alternative Medicine Editorial Board.
Information about the following is included in this summary:
- A brief history of milk thistle research.
- The results of clinical studies of milk thistle.
- Possible side effects of milk thistle use.
This summary is intended as a resource to inform and assist clinicians and other health professionals who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Some of the reference citations in the summary are accompanied by a level of evidence designation. These designations are intended to help the readers assess the strength of the evidence supporting the use of specific interventions or treatment strategies. The PDQ Cancer Complementary and Alternative Medicine Editorial Board uses a formal evidence ranking system in developing its level of evidence designations. These designations should not be used as a basis for reimbursement determinations.
This summary is also available in a patient version, which is written in less technical language.
This complementary and alternative medicine (CAM) information summary provides an overview of the use of milk thistle as a treatment and adjunct agent in cancer therapy.
The summary includes a brief history of milk thistle, a review of the laboratory studies and clinical trials, and a description of adverse effects associated with milk thistle use.
This summary contains the following key information:
- Milk thistle is a plant whose fruit and seeds have been used for more than 2,000 years as a treatment for liver and biliary disorders.
- The active substance in milk thistle, silymarin, is a mixture of flavonolignans, primarily consisting of four isomers: silybin, isosilybin, silychristin (also known as silichristin), and silydianin (also known as silidianin). In the biological literature, silybin is referred to as silibinin.
- Laboratory studies demonstrate that silymarin functions as a potent antioxidant, stabilizes cellularmembranes, stimulates detoxification pathways, stimulates regeneration of liver tissue, inhibits the growth of certain cancer cell lines, exerts direct cytotoxic activity toward certain cancer cell lines, and may increase the efficacy of certain chemotherapy agents.
- Human clinical trials have investigated milk thistle or silymarin primarily in individuals with hepatitis or cirrhosis. No clinical trials in individuals with cancer have been published.
- Few adverse side effects have been reported for milk thistle, but little information about interactions with anticancer medications or other drugs is available.
- Milk thistle is available in the United States as a dietary supplement.
Many of the medical and scientific terms used in the summary are hypertext linked (at first use in each section) to the NCI Dictionary, which is oriented toward nonexperts. When a linked term is clicked, a definition will appear in a separate window. All linked terms and their corresponding definitions will appear in a glossary in the printable version of the summary.
Reference citations in some PDQ CAM information summaries may include links to external Web sites that are operated by individuals or organizations for the purpose of marketing or advocating the use of specific treatments or products. These reference citations are included for informational purposes only. Their inclusion should not be viewed as an endorsement of the content of the Web sites, or of any treatment or product, by the PDQ Cancer CAM Editorial Board or the National Cancer Institute (NCI).
The botanical name for milk thistle is Silybum marianum (L.) Gaertn. Milk thistle is also referred to as holy thistle, Marian thistle, Mary thistle, Our Lady's thistle, St. Mary thistle, wild artichoke, Mariendistel (German), and Chardon-Marie (French). The plant is indigenous to Europe but can also be found in the United States and South America. Traditionally, the leaves have been used in salads, and the fruit of the flower has been roasted as a coffee substitute. The seeds of milk thistle are the medicinal parts of the plant. The primary active constituent of milk thistle is silymarin, which is composed of four isomers: silybin, isosilybin, silychristin, and silydianin. Most supplements are standardized according to their silybin content. In turn, silybin and isosilybin are both mixtures of two diastereomers, silybins A and B and isosilybins A and B, respectively. Special formulations of silybin have been developed to enhance the bioavailability of the herbal product; these forms are sold under the names Legalon, silipide, and Siliphos. Because of milk thistle's lipophilic nature, it is usually administered in capsule or tablet form rather than as an herbal tea. In Europe, silybin is administered intravenously as the only effective antidote for Amanita phalloides (Fr.) Link toxin. Humans exposed to this mushroom toxin develop serious liver failure that ultimately progresses to death.
Several companies distribute milk thistle as a dietary supplement. In the United States, dietary supplements are regulated as foods, not drugs. Therefore, premarket evaluation and approval by the Food and Drug Administration (FDA) are not required unless specific disease prevention or treatment claims are made. Because dietary supplements are not formally reviewed for manufacturing consistency, ingredients may vary considerably from lot to lot; in addition, there is no guarantee that ingredients identified on product labels are present at all or are present in the specified amounts. It is important to note that the FDA has not approved the use of milk thistle as a treatment for cancer patients or patients with any other medical condition.
To conduct clinical drug research in the United States, researchers must file an Investigational New Drug (IND) application with the FDA. The IND application process is confidential, and IND information can be disclosed only by the applicants. To date, only one investigator has announced holding an IND to study milk thistle as an adjunct cancer treatment.
Despite milk thistle's long history of being used to treat liver and biliary complaints, it was not until 1968 that silymarin was isolated from the seeds of the plant, and it was proposed that silymarin might be the active ingredient. Silymarin was later determined to be a flavonolignan that is composed of four structurally similar compounds: silybin, isosilybin, silydianin, and silychristin. Researchers have investigated the role that silibinin may play in the treatment of hepatitis and cirrhosis. Most studies have investigated the isolated compound silymarin or its most active isomer silybin, rather than the herbal plant in its whole form.
Silymarin is most well known for its purported effects on the liver. In laboratory studies, silymarin has been found to stabilize cellmembranes, thus preventing toxic chemicals from entering the cell.[3,5,6,7] Laboratory studies have also demonstrated that silymarin stimulates synthesis and activity of enzymes responsible for detoxification pathways and exhibits potent antioxidant properties.[6,7,8,9,10,11,12,13,14,15,16,17] Specifically, silymarin has been shown to stimulate the glutathione S-transferase pathway and alter the intracellular concentration of glutathione (a potent antioxidant). Silymarin has also been shown to neutralize a wide range of free radicals.
Laboratory experiments conducted using cancer cell lines have suggested that silibinin enhances the efficacy of cisplatin and doxorubicin against ovarian and breast cancer cells. Silybin appears to have direct anticancer effects against prostate, breast, and ectocervical tumor cells. Silybin may also affect the cell cycle in cancer cells by slowing down cell growth, as demonstrated with prostate cancer cell lines. Laboratory studies using leukemia cell lines found that silybin did not stimulate growth of leukemia cells.
No human clinical trials on milk thistle or silymarin as a cancer treatment or as an adjunctive therapy in individuals with cancer have been published. Most clinical trials have investigated silymarin's effectiveness in the treatment of patients with hepatitis, cirrhosis, or biliary disorders.[22,23,24,25,26,27,28,29,30,31] These studies have employed a wide range of doses (120–560 mg/day) and have yielded conflicting results. Many of the well-designed, large-scale trials have reported a beneficial effect rather than no effect. The most commonly reported adverse effects are a mild laxative effect and gastrointestinal upset.
Milk thistle has been used for more than 2,000 years, primarily as a treatment for liver dysfunction. The oldest reported use of milk thistle was by Dioscorides, who recommended the herb as a treatment for serpent bites. Pliny the Elder (A.D. 23–79) reported that the juice of the plant mixed with honey is indicated for "carrying off bile."[1,2] In the Middle Ages, milk thistle was revered as an antidote for liver toxins.[1,2] The British herbalist Culpepper reported it to be effective for relieving obstructions of the liver.[1,2] In 1898, eclectic physicians Felter and Lloyd stated the herb was good for congestion of the liver, spleen, and kidney.[1,2] Native Americans use milk thistle to treat boils and other skin diseases. Homeopathic practitioners used preparations from the seeds to treat jaundice, gallstones, peritonitis, hemorrhage, bronchitis, and varicose veins. The German Commission E recommends milk thistle use for dyspeptic complaints, toxin-induced liver damage, hepaticcirrhosis, and as a supportive therapy for chronicinflammatory liver conditions.
Laboratory / Animal / Preclinical Studies
Research studies conducted in the laboratory have investigated the properties of silymarin or its isomer silybin using cell lines and animal models. Other substances in milk thistle have not been extensively studied.
Several research studies have investigated the effects of silymarin or silybin in a noncancer context. These studies have tested silymarin or silybin:
- In healthy animal liver and kidney cells.
- As a prophylaxis against toxic chemicals.
- In stimulating detoxification pathways (enzyme concentrations and activity).
- For antioxidant properties.
Silymarin or silybin has also been investigated in cancer models. The effects of silymarin and/or silybin have been investigated in prostate (DU 145, LNCaP, PC-3),[1,2,3,4,5]breast (MDA-MB 468, MCF-7),[6,7,8]hepatic (HepG2),[9,10] epidermoid (A431),colon (Caco-2),ovarian (OVCA 433, A2780),histiocytic lymphoma (U-937), and leukemia (HL-60) [14,15]cells. In animal tumor models, tongue cancer, skin cancer,[17,18,19,20,21,22]bladder cancer, and adenocarcinoma of the colon [24,25] and small intestine have been investigated. These studies have tested the ability of silymarin or silibinin to:
- Mitigate the toxicity associated with chemotherapy agents.
- Enhance the efficacy of chemotherapy agents.
- Inhibit the growth of cancer cell lines and inhibit tumor initiation or tumor promotion.
Although many of these studies have produced encouraging results, none of the findings have been replicated in human clinical trials.
Laboratory data suggest that silymarin and silybin protect the liver from damage induced by toxic chemicals. Animal studies have found that liver cells treated with silybin and then exposed to toxins do not incur cell damage or death at the same rate as liver cells that are not treated with silybin. This finding suggests that silybin can prevent toxins from entering the cell or effectively exports toxins out of the cell before damage ensues.[10,26,27,28,29,30] Alternatively, this may be related to the effect of silymarin on detoxification systems. In vitro data have shown silybin to stimulate and/or inhibit phase I detoxification pathways in silybin-treated human liver cells. However, this effect was found to be dose-dependent, and these levels are not physiologically attainable with the current manufacturer dose recommendations.[31,32]
Silymarin has been shown to stimulate phase II detoxification pathways in mice. Administration of silymarin (100 or 200 mg/kg body weight/day) to SENCAR mice for 3 days significantly increased glutathione S-transferase activity in the liver (P < .01–.001), lung (P < .05–.01), stomach (P < .05), small bowel (P < .01), and skin (P < .01). This effect appeared to be dose-dependent. Administration of silymarin to rats challenged with a toxin (50 mg/kg body weight) resulted in higher levels of glutathione in liver cells, decreased levels of oxidative stress (measured by malondialdehyde concentrations), and less elevated liver function tests (measured by levels of aspartate aminotransferase [AST] and alanine aminotransferase [ALT]). Silymarin and silybin have also been found to accelerate cell regeneration in the liver through stimulation of precursors to DNA synthesis and enhancement of production of the cellular enzymes required for synthesis of DNA.[34,35,36,37,38,39] Laboratory studies have also shown silymarin and silybin to be potent antioxidants.[27,28,40,41,42,43,44,45,46,47] Silymarin has been shown to mitigate oxidative stress in cells treated with pro-oxidant compounds.
A number of laboratory studies have investigated the effect of silymarin or silybin on the efficacy and toxicity of chemotherapy agents or have measured their direct cytotoxic activity. In an investigation of the effect of a variety of flavonoids on the formation of DNA damage, silymarin did not induce DNA damage in colon (Caco-2) cells, hepatoma (HepG2) cells, and human lymphocytes. At higher concentrations of silymarin (400–1,000 µmol/L) DNA damage was induced in an epithelial cell line (HeLa cells). At higher concentrations (1,000 µmol/L) DNA damage was observed in human lymphocytes. Cell growth was inhibited as the flavonoid concentration was increased in human lymphocytes and HeLa cells. Only at very high concentrations was cell viability affected by silymarin in HepG2 cells. Although this study demonstrated that the flavonolignans of Silybum marianum (L.) are capable of inhibiting cellular proliferation and inducing DNA strand breaks, the results were obtained at very high concentrations that may be difficult to achieve in humans. This study also showed that silymarin does not stimulate cell growth in the HeLa, Burkitt lymphoma, and human hepatoma cell lines.
Silymarin has also been investigated as a possible adjunctive agent in mitigating some of the toxicity associated with chemotherapy agents. Silybin and silychristin exerted a protective effect on monkey kidney cells exposed to vincristine and especially cisplatin chemotherapy. Silybin (200 mg/kg body weight) administration with cisplatin in rats resulted in statistically significant reductions in measures of kidney toxicity. Significant decreases in weight loss, faster recovery of urinaryosmolality measures, and depressions in the increase in activity of urinary alanine aminopeptidase ([AAP], a marker of kidney toxicity) were observed. Silybin had no effect on magnesium excretion or glomerular function. Silybin (2 g/kg body weight) administration in rats receiving cisplatin prevented reductions in creatinine clearance, increases in ureaplasma levels, and large increases in urinary AAP. No effect on magnesium excretion was observed. Silybin did not interfere with the antineoplastic effects of cisplatin or ifosfamide in germ cell tumors. In experiments with ovarian and breast cancer cell lines, silybin potentiated the effect of cisplatin and doxorubicin. IdB 1,016, a form of silybin bound to a phospholipid complex, was found to enhance the activity of cisplatin against A2780 ovarian cancer cells but had no effect on its own. Silybin increased the chemosensitivity of DU 145 prostate cancer cells resistant to chemotherapy.
Studies have also investigated the effect of silymarin on tumor initiation and promotion. Silymarin appears to have a chemopreventive effect through perturbations in the cell cycle, altering cell signaling that induces cellular proliferation, affecting angiogenesis, or through its anti-inflammatory properties.[1,6,12,18,53] These findings have been supported in human prostate, breast, ectocervical, ovarian, hepatic, leukemia, and epidermoid cell lines.[4,6,8,9,14,54] An investigation of the effect of silymarin on ultraviolet B radiation-induced nonmelanoma skin cancer in mice found that silymarin treatment significantly reduced tumor incidence (P < .003), tumor multiplicity (P < .0001), and tumor volume (P < .0001). These findings suggest that silymarin plays a prominent role in the reduction of cancer cells and in preventing the formation of cancer cells. A number of studies have investigated the mechanism through, which silymarin may affect tumor promotion in mouse skin tumor models. Studies have found that silymarin reduces transcription of markers of tumor promotion and activity, inhibits transcription of tumor promoters, stimulates antioxidant activities,[18,22] interferes with cell signaling, inhibits inflammatory actions,[18,21] and modulates cell-cycle regulation.
In prostate cancer cell lines, silybin has been shown to inhibit growth factors and stimulate cell growth,[1,2,3,5] promote cell cycle arrest,[1,4] and inhibit antiapoptotic activity. In rats with azoxymethane-induced colon cancer, dietary silymarin resulted in a reduction in the incidence and multiplicity of adenocarcinoma of the colon in a dose-dependent manner.[24,25] Dietary silymarin had no effect on small intestinal adenocarcinoma, but exerted a preventive effect in mice with N-butyl-N-(4-hydroxybutyl) nitrosamine–induced bladder cancer  and in F344 rats with 4-nitroquinoline 1-oxide–induced cancer of the tongue. Dietary silybin administered to nude mice with prostate carcinoma increased production of insulin-like growth factor-binding protein-3 in the plasma of mice and significantly inhibited tumor volume (P < .05).
Human / Clinical Studies
There are no published clinical trials of milk thistle or silymarin in patients with cancer. Two published case reports describe the use of milk thistle as either a treatment or an adjunctive therapy in individuals with cancer. One case report describes the use of milk thistle in a 34-year-old woman with promyelocytic leukemia. The investigators administered 800 mg of silymarin during the patient's maintenance therapy, which consisted of treatment with methotrexate and 6-mercaptopurine. During the 4 months of treatment with silymarin, the patient who previously required intermittent breaks in therapy due to abnormal liverenzyme levels had normal liver enzyme levels with no further interruption of therapy. A second case report describes a 52-year-old man with hepatocellular carcinoma. The patient began taking 450 mg of silymarin per day, and spontaneous regression of the tumor was reported in the absence of initiation of anticancer therapy. These findings have not been reproduced in a clinical trial.
Most clinical trials of milk thistle have been conducted in patients with either hepatitis or cirrhosis. Other studies have investigated milk thistle in patients with hyperlipidemia, diabetes, and Amanita phalloides mushroom poisoning. Eight randomized trials [3,4,5,6,7,8,9,10] have been reported in patients with hepatitis or cirrhosis, and one randomized trial has reported the use of silymarin as a prophylaxis to iatrogenic hepatictoxicity.Endpoints for these trials have included serum levels of bilirubin and/or the liver enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT), as higher levels are an indicator of liver inflammation, damage, or disease. The lowering of these serum levels is a sign of an improving condition. In patients with hepatitis A and B, one clinical trial found silymarin (140 mg daily for 3–4 weeks) resulting in lower levels of AST, ALT, and bilirubin by day 5, compared with a placebo group. In another randomized, placebo-controlled study of patients with viral hepatitis B, silymarin (210 mg daily) had no effect on course of disease or enzyme levels.
In patients with chronic liver disease, a randomized, placebo-controlled study found normalization of serum AST, ALT, and bilirubin levels after 1 month of treatment with silymarin (140 mg 3 times a day) in comparison to treatment with a placebo. In one of the largest observational studies involving 2,637 patients with chronic liver disease, 8-week treatment with 560 mg/day of silymarin resulted in reductions of serum AST, ALT, and gamma-glutamyltranspeptidase ([GGT], a marker of bile duct disease) and a decrease in the frequency of palpablehepatomegaly.
Another published report describes the use of silybin as the only effective antidote in patients with liver damage from Amanita phalloides (Fr.) Link poisoning. Patients were administered doses of 35 to 55 mg/kg body weight, with no reports of adverse events. A recent retrospective review of the treatment for Amanita phalloides poisoning suggests that silymarin continues to be a promising drug in the treatment of this rare mushroom poisoning. The beneficial effect of silymarin on liver histology suggests it has a role in the prevention of hepatitis and/or hepatocellular carcinoma; however, no clinical trials in humans have investigated the use of silymarin for prevention.
Clinical Studies Investigating Silymarin in the Treatment or Prevention of Liver Disease
|Reference Citation||Type of Study||Type of Disease||No. of Patients: Enrolled; Treated; Controla||Strongest Benefit Reported|
|||Double-blind, placebo-controlled, randomized clinical trial||Acute and subacute liver disease||106b; 47; 50||Decreased LFTs; improved histology|
|||Double-blind, placebo-controlled, randomized clinical trial||Cirrhosis||170; 87; 83||Increased survival|
|||Phase II randomized open trial||Viral or alcoholic hepatitis||60c; 60; 0||Reduction in ALT and gamma-glutamyl transpeptidase|
|||Controlled, randomized trial||Viral hepatitis B||52d; 20-silymarin, 20-misoprostol; 12||No significant findings|
|||Double-blind, placebo-controlled, randomized clinical trial||Alcohol-induced cirrhosis||200e; 58; 67||No significant findings|
|||Double-blind, placebo-controlled, randomized clinical trial||Alcohol-induced cirrhosis||60f; 24; 25||Significant increases in erythrocyteglutathione and decreased platelet MDA values; no significant differences in liver function tests|
|||Nonrandomizedpilot study||Primary biliary cirrhosis||27; 27; 0||No significant findings|
|||Controlled, randomized trial||Diabetic patients with cirrhosis||60; 30; 30||Decrease in lipid peroxidation and insulin resistance|
|||Double-blind, placebo-controlled, randomized clinical trial||Patients treated with silymarin as a prophylaxis to psychotropic drug-induced hepatic damage||60; 15-psychotropic drug+silymarin; 15-silymarin alone; 15-psychotropic drug+placebo; 15-placebo alone||Silymarin effective at reducing hepatotoxicity associated with psychotropic drug use|
Human studies of silymarin have shown minimal adverse effects in multiple large, blinded, placebo-controlled, randomized studies. Silymarin is well tolerated, with only rare reports of a mild laxative effect. Mild allergic reactions have been seen at high doses (>1,500 mg/day), although the details of these allergic reactions were not reported. A recent case report from Australia described a reaction to a milk thistle extract that included intermittent episodes of sweating, abdominal cramping, nausea, vomiting, diarrhea, and weakness. All symptoms resolved when the silymarin was discontinued. The authors suggested that the capsules were contaminated; the type of contamination was unknown.
According to the German Commission E, there are no reported side effects with milk thistle within the recommended doses. Rare cases of milk thistle having a laxative effect have been reported. Human studies have reported stomach upset, heartburn, and transient headaches; however, none of these symptoms were attributed to supplementation with milk thistle, and supplementation was not discontinued. One human dosing study reported nausea, heartburn, and dyspepsia in patients treated with 160 mg/day, dyspepsia in patients treated with 240 mg/day, and postprandial nausea and meteorism in patients treated with 360 mg/day. None of these side effects were dose related.
Silymarin has been well tolerated in high doses. Silymarin has been used in pregnant women with intrahepaticcholestasis at doses of 560 mg/day for 16 days, with no toxicity to the patient or the fetus. The published data on silymarin use in children focuses on intravenous doses of 20 to 50 mg/kg body weight for mushroom poisoning. Silymarin has also proved nontoxic in rats and mice when administered in doses as high as 5,000 mg/kg body weight. Rats and dogs have received silymarin at doses of 50 to 2,500 mg/kg body weight for a 12-month period. Investigations, including postmortem analyses, showed no evidence of toxicity.
It is not known whether milk thistle may reduce, enhance, or have no effect on the effectiveness of chemotherapy. Silymarin decreases the activity of the cytochrome P450 enzyme system, which is involved in the clearance of certain chemotherapy drugs. However, the dose at which inhibition is observed is high and not achieved with oral intake of silymarin. Milk thistle may also interact adversely with chemotherapy drugs that exert their cytotoxic effects through generation of free radicals. Silymarin and its metabolite inhibit P-glycoprotein-mediated cellular efflux, leading to potentiation of doxorubicin cytotoxicity. No trials have been performed to support or negate these theoretical considerations. No effects on indinavir and alcohol pharmacokinetics has been observed. Enhancement of antiarrhythmic effects of amiodarone in rats has been observed.
Overall Level of Evidence for Milk Thistle
To assist readers in evaluating the results of human studies of complementary and alternative medicine (CAM) treatments for cancer, the strength of the evidence (i.e., the levels of evidence) associated with each type of treatment is provided whenever possible. To qualify for a level of evidence analysis, a study must:
- Be published in a peer-reviewed scientific journal.
- Report on therapeutic outcome or outcomes, such as tumorresponse, improvement in survival, or measured improvement in quality of life.
- Describe clinical findings in sufficient detail for a meaningful evaluation to be made.
Separate levels of evidence scores are assigned to qualifying human studies on the basis of statistical strength of the study design and scientific strength of the treatment outcomes (i.e., endpoints) measured. The resulting two scores are then combined to produce an overall score. A level of evidence score cannot be assigned to milk thistle because there has been insufficient clinical research to date. For an explanation of the scores and additional information about levels of evidence analysis of CAM treatments for cancer, refer to Levels of Evidence for Human Studies of Cancer Complementary and Alternative Medicine.
Given the limited amount of human data, the use of milk thistle/silymarin as a treatment for cancer patients cannot be recommended outside the context of well-designed clinical trials.
Changes to This Summary (03 / 20 / 2008)
The PDQcancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Editorial changes were made to this summary.
ADDITIONAL INFORMATION ABOUT CAM THERAPIES
- The National Center for Complementary and Alternative Medicine (NCCAM).
- The National Cancer Institute Office of Cancer Complementary and Alternative Medicine (OCCAM).
- CAM on PubMed, a special subset of the PubMed scientific literature database created through a partnership between NCCAM and the National Library of Medicine.
- PDQ® - NCI's Comprehensive Cancer Database
Full description of the NCI PDQ database.
OTHER PDQ SUMMARIES
- PDQ® Cancer Information Summaries: Adult Treatment
Treatment options for adult cancers.
- PDQ® Cancer Information Summaries: Pediatric Treatment
Treatment options for childhood cancers.
- PDQ® Cancer Information Summaries: Supportive and Palliative Care
Side effects of cancer treatment, management of cancer-related complications and pain, and psychosocial concerns.
- PDQ® Cancer Information Summaries: Screening/Detection (Testing for Cancer)
Tests or procedures that detect specific types of cancer.
- PDQ® Cancer Information Summaries: Prevention
Risk factors and methods to increase chances of preventing specific types of cancer.
- PDQ® Cancer Information Summaries: Genetics
Genetics of specific cancers and inherited cancer syndromes, and ethical, legal, and social concerns.
- PDQ® Cancer Information Summaries: Complementary and Alternative Medicine
Information about complementary and alternative forms of treatment for patients with cancer.
This information is intended mainly for use by doctors and other health care professionals. If you have questions about this topic, you can ask your doctor, or call the Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
Date Last Modified: 2008-03-20