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If you are considering using alternative therapies, talk to your cancer doctor for advice and support. Doctors are generally supportive of people using any complementary therapies that may help them cope better with their illness.
But they usually advise against using alternative therapies. If you decide to use an alternative therapy, it is important to check it is safe. Always check the credentials of the therapist. Alternative therapies can be expensive, and some can cause serious side effects.
They can also make you feel unwell and be harmful to your health. There are many types of alternative therapy. In this information we explain the alternative therapies that are most well-known to people with cancer.
These include:. If you would like to talk to someone about alternative therapies, you can call the Macmillan Support Line on 00 They are available to speak to 7 days a week, 8am-8pm.
You can also chat online to a Cancer Information Nurse Specialist. Amygdalin is a compound found in bitter almonds, peach stones and apricot stones. When amygdalin is processed by the body, it changes to cyanide. Cyanide is a type of poison.
A man-made form of amygdalin is called Laetrile ®. Some suppliers call it vitamin B But it is not actually a vitamin. Many websites that sell Laetrile claim it can slow or stop the growth of cancer. They also claim it can poison cancer cells, without damaging normal cells and tissues.
But there is no medical evidence to support this. There has been a review of studies that were looking at the outcomes for people with cancer taking Laetrile. The review found no evidence to show that it can control or cure cancer. Laetrile can have serious side effects. Some people have had cyanide poisoning while taking it, and a few people have died as a result.
The sale of Laetrile has been banned by the European Commission and by the Food and Drugs Administration FDA in the USA. Unlike conventional medicines, the manufacture of Laetrile is not controlled. So if you buy Laetrile, there is no way of knowing what it contains or if it is contaminated with other substances.
It is important not to take Essiac during cancer treatment, or with any other medicines, without checking with your cancer doctor first. Some websites claim Essiac can slow down the growth of cancer, or even cure it.
But there is no medical evidence to show that taking Essiac helps treat cancer or improves your quality of life. Essiac affects an enzyme in the body that regulates hormones and vitamin D. It also affects how the body deals with toxins.
This means that taking Essiac with other cancer treatments could make them less effective or increase side effects. Many types of cannabis oil are sold online. CBD oil is also sold in some shops, such as health food shops. There is no reliable, medical evidence to show whether cannabis in any form can effectively and safely treat cancer in humans.
If you are thinking about using cannabis oil or CBD oil, there are some important things to consider:. Metabolic treatments vary from one therapist to another.
One of the most well-known therapies is called Gerson therapy. This may include:. These are said to flush toxins out of the body.
But there is no medical evidence to show that they help treat cancer. If you have any questions about alternative diets or are thinking of following one, get advice from your cancer doctor, specialist nurse or dietitian.
Metabolic therapists think cancer is caused by a build-up of toxic substances in the body. They claim they can treat it by removing toxins and strengthening the immune system. One study compared the effects of using a metabolic therapy with the effects of chemotherapy.
The metabolic therapy included enzymes, nutritional supplements, detoxification and organic foods. The study found that the patients who had the chemotherapy lived three times longer and had a better quality of life than those who had metabolic therapy.
Possible side effects of metabolic or Gerson therapy include nausea, vomiting, stomach cramps, a high temperature and headaches. The high levels of hormones and extracts used can sometimes make people feel unwell. The risks of using coffee enemas include infections and serious damage to the large bowel.
It is understandable that some people are attracted to diets that seem to offer hope. But there is no medical evidence to show that these diets can cure cancer, or help people with advanced cancer live longer.
Talk to your cancer doctor, specialist nurse or dietitian before cutting out any food group from your diet. Some diets claim to remove toxins from the body.
Many of these diets are vegetarian or vegan. They involve eating food that is raw, sugar-free and low in salt. Sometimes vegetable or fruit juices, and high doses of vitamins, minerals or enzymes are used.
Other diets are based on claims that some foods feed cancer, or affect the pH levels acidity of the body. If you choose to follow a diet that cuts out some food types, it is important to make sure you are not missing out on important nutrients. For example, if you follow a dairy-free diet it is important to replace the calcium that you would usually get from dairy products, with other calcium-rich foods.
Diets that are high in fibre and low in calories and protein, are not suitable if you have problems maintaining your weight because of cancer or its treatment.
If you are underweight, you need protein and calories from any source of food. This type of alternative therapy involves taking very large doses of vitamins as a way of preventing and treating cancer.
: Anti-cancer natural therapies| Complementary and Alternative Medicine | Journal of Ethnopharmacology reviewed that berberine potentially represses tumor progression and is expected to be safe, effective and affordable agent for cancer patients [ 9 ]. If speaking to someone face-to-face feels too intimidating, there are a variety of online resources and counseling services available. And that it might help with treatment side effects. Get Help Now. Curcumin can also exert immunomodulatory effects against cancer cells. |
| Alternative cancer diets | Cancer Research UK | CEP is widely used in Japan for the treatment of many acute and chronic diseases [ ]. Johnson, who is part of Yale COPPER Center for cancer research, had the medical training to recognize good sources of cancer research. GA Fig. These liposomes accumulate in the liver and prolong its retention time and exert better inhibitory effects than wogonin in human hepatocellular carcinoma HepG2 cells. Shikonin can enhance the pro-apoptotic effect of taxol in human breast cancer MBA-MD cells, and this combination improves mice survival and inhibits tumor growth in MDA-MB xenograft mice [ ]. This is because there is no way of checking whether the effect someone has described is because of the alternative therapy or something else. Some of the therapies listed below still need more research to prove that they can be helpful. |
| Alternative cancer diets | They claim they can treat it by removing toxins and strengthening the immune system. One study compared the effects of using a metabolic therapy with the effects of chemotherapy. The metabolic therapy included enzymes, nutritional supplements, detoxification and organic foods. The study found that the patients who had the chemotherapy lived three times longer and had a better quality of life than those who had metabolic therapy. Possible side effects of metabolic or Gerson therapy include nausea, vomiting, stomach cramps, a high temperature and headaches. The high levels of hormones and extracts used can sometimes make people feel unwell. The risks of using coffee enemas include infections and serious damage to the large bowel. It is understandable that some people are attracted to diets that seem to offer hope. But there is no medical evidence to show that these diets can cure cancer, or help people with advanced cancer live longer. Talk to your cancer doctor, specialist nurse or dietitian before cutting out any food group from your diet. Some diets claim to remove toxins from the body. Many of these diets are vegetarian or vegan. They involve eating food that is raw, sugar-free and low in salt. Sometimes vegetable or fruit juices, and high doses of vitamins, minerals or enzymes are used. Other diets are based on claims that some foods feed cancer, or affect the pH levels acidity of the body. If you choose to follow a diet that cuts out some food types, it is important to make sure you are not missing out on important nutrients. For example, if you follow a dairy-free diet it is important to replace the calcium that you would usually get from dairy products, with other calcium-rich foods. Diets that are high in fibre and low in calories and protein, are not suitable if you have problems maintaining your weight because of cancer or its treatment. If you are underweight, you need protein and calories from any source of food. This type of alternative therapy involves taking very large doses of vitamins as a way of preventing and treating cancer. However, there is no evidence that taking large doses of vitamins is helpful in treating cancer. Some vitamins can be harmful in high doses. It is important to tell your cancer doctor before having high doses of vitamin C during, or within a few weeks of, cancer treatment. High-dose vitamin C is one of the most common types of megavitamin therapy. High-dose vitamin C can make many cancer treatments less effective. This includes:. It may also affect how radiotherapy works. High-dose vitamin C may also interact with some complementary and alternative therapies. Below is a sample of the sources used in our complementary therapies information. If you would like more information about the sources we use, please contact us at cancerinformationteam macmillan. uk Cassilieth B. The Complete Guide to Complementary Therapies in Cancer Care: Essential Information for Patients Survivors and Health Professionals. Ernst E, et al. Oxford Handbook of Complementary Medicine. It has been reviewed by expert medical and health professionals and people living with cancer. It has been approved by Dr Saul Berkovitz. Our cancer information has been awarded the PIF TICK. We understand that people are worried about coronavirus COVID You may have questions about the different vaccines, or you may be worried about how the pandemic will affect your cancer treatment. We have detailed information about coronavirus and cancer treatment here. We know cancer throws a lot your way, and right now, the coronavirus pandemic is making it even tougher. If you're worried about something, and you need to talk to someone, whatever is on your mind, we're here to listen. To speak to our experts, you can:. Chat online anonymously to others who understand what you are going through. Our cancer information meets the PIF TICK quality mark. This means it is easy to use, up-to-date and based on the latest evidence. Learn more about how we produce our information. Alternative therapies. Many alternative therapies claim to treat or even cure cancer. But no alternative therapies have ever been proven to cure cancer or slow its growth. On this page. What are alternative therapies? Why do people consider alternative therapies? Why can alternative therapies sound convincing? Misleading advertising. Unreliable evidence. Individual stories. Getting a second opinion If your doctor tells you that further treatment will not help control the cancer, you may find it very hard to accept. Getting advice and support before using an alternative therapy If you are considering using alternative therapies, talk to your cancer doctor for advice and support. Think twice before declining conventional treatments. But if you do decline recommended treatment, make sure you understand the pros and cons of doing so, including the possibility of shorter survival. Robert H. Shmerling, MD , Senior Faculty Editor, Harvard Health Publishing; Editorial Advisory Board Member, Harvard Health Publishing. As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician. This Special Health Report is designed to guide you through the next stage of your cancer journey. Thanks for visiting. Don't miss your FREE gift. The Best Diets for Cognitive Fitness , is yours absolutely FREE when you sign up to receive Health Alerts from Harvard Medical School. Sign up to get tips for living a healthy lifestyle, with ways to fight inflammation and improve cognitive health , plus the latest advances in preventative medicine, diet and exercise , pain relief, blood pressure and cholesterol management, and more. Get helpful tips and guidance for everything from fighting inflammation to finding the best diets for weight loss from exercises to build a stronger core to advice on treating cataracts. PLUS, the latest news on medical advances and breakthroughs from Harvard Medical School experts. Sign up now and get a FREE copy of the Best Diets for Cognitive Fitness. Stay on top of latest health news from Harvard Medical School. Recent Blog Articles. Flowers, chocolates, organ donation — are you in? What is a tongue-tie? What parents need to know. Which migraine medications are most helpful? Some journal articles don't give enough detail on how the researchers did the studies. It is difficult to know how reliable the research is and which herbs may be helpful. But there are trials looking into this. Chinese researchers did a cohort study in A cohort is a group of people, so cohort studies look at groups of people. The researchers follow the group over a period of time. The researchers in this study looked at people with oesophageal food pipe cancer. And who might develop a second primary new cancer of the head and neck. The researchers followed the group over 10 years. One part of the group received Chinese Herbal Medicine CHM and the other part did not. The results showed that the group of people who took CHM had fewer cases of a second primary cancer of the head and neck. This was when the researchers compared them to the group that did not take CHM. The researchers suggested that CHM might prevent a second primary cancer of the head and neck in people with oesophageal cancer. The results looked promising. But the people in the study received different types of CHM. This might make the results of the study less accurate. There is evidence that some herbal remedies might prevent or relieve cancer symptoms. And that it might help with treatment side effects. But we need results from large clinical trials. This way we can know which herbs are safe to use alongside conventional cancer treatment. A Cochrane review of studies in looking at preventing a dry mouth in people having radiotherapy for head and neck cancer. They found that there was not enough evidence to say that Chinese Herbal Medicine CHM can prevent the feeling of dry mouth. This was in people who had radiotherapy with or without chemotherapy to the head and neck. Another Cochrane review of studies in found that there was not enough evidence to use CHM as a treatment for oesophageal cancer. But they said that it might help with quality of life. And that it might relieve some side effects caused by radiotherapy and chemotherapy. A third Cochrane review of studies in looked at moxibustion. Moxibustion involves the burning of herbs above the skin at acupuncture pressure points. The researchers found little evidence to say that it helped with side effects of radiotherapy and chemotherapy. Or that it helped with quality of life in people with cancer. But the researchers felt that the evidence was not clear enough to rule out some benefits or risks of this treatment. They suggested better quality studies. Another review in looked at whether acupuncture and moxibustion could help with cancer related fatigue tiredness. Some of the studies suggested that these types of Chinese medicine might help with fatigue. They say more research is needed with better quality studies. Chinese researchers did a review study in The researchers looked at studies that used different types of CHM. The studies looked at how to relieve perimenopausal symptoms in women who had surgery, chemoradiotherapy or hormone treatment for breast cancer. Perimenopausal means the transition time to full menopause. The researchers found that CHM might improve perimenopausal symptoms. But suggested better quality, precise and in-depth studies. Some laboratory tests have found certain plants or plant extracts have anti-cancer qualities. Manufacturers made these into cancer drugs such as Taxol from the Pacific yew tree. But, there is no scientific evidence from human trials that herbal medicine can treat or cure cancer. We need large trials to prove this. Researchers did a laboratory study in They looked at the use of Chang-wei-qing CWQ as a treatment to prevent a certain type of bowel cancer. The researchers found that CWQ showed an anti-cancer anti-tumour effect. But this was a laboratory study, and we need more research. Chinese researchers did a case study of patients with pancreatic cancer. All of the patients received Chinese Herbal Medicine CHM. It showed that people having herbal medicine might survive longer. We need more research. They looked at several studies on CHM. The researchers said that CHM showed positive results. This was as a therapy to use with other types of cancer treatment. They also said that CHM can help chemotherapy and radiotherapy to work better. They felt that CHM can help to control certain cancer genes. And that it can influence the way cancer cells work. But they recommended more research to understand exactly how CHM works. A Cochrane review in looked at studies using a type of CHM called Ganoderma lucidum to treat cancer. The researchers found that there was not enough evidence to use Ganoderma lucidum as a treatment for cancer. But they suggested that it might be used alongside conventional cancer treatment to boost immunity. The researchers also said that future research should be of better quality studies. Your first consultation with a herbalist will usually cost more than further appointments. Follow up appointments are generally shorter, so are likely to cost less. You will also have to pay for the herbs your herbalist prescribes. These costs may vary from place to place in the UK. Some herbal products in health food shops and pharmacies have to meet quality standards. They also need to provide information about their product. |
| Herbal Medicine and Cancer | The researchers looked at studies that used different types of CHM. Massage can be light and gentle, or it can be deep with more pressure. Medical Professionals. Advertising revenue supports our not-for-profit mission. One study compared the effects of using a metabolic therapy with the effects of chemotherapy. Follow Mayo Clinic. |
Anti-cancer natural therapies -
Clinical evidence and extensive studies showed that curcumin has various pharmacology effects, including anti-cancer, anti-inflammatory, and anti-oxidative activities [ 12 , 13 , 14 ].
Curcumin and its analogues are shown to be emerging as effective agents for the treatment of several malignant diseases such as cancer. Numerous studies have shown that curcumin and its preparations can inhibit tumors in almost all parts of the body, including head and neck, ovarian, skin and gastric cancers [ 15 , 16 , 17 , 18 , 19 , 20 ].
Curcumin is shown to exhibit many anti-cancer effects through the inhibition of cell proliferation, promotion of cell apoptosis, prevention of tumor angiogenesis and metastasis, and the induction of autophagy [ 21 , 22 , 23 , 24 , 25 ]. Curcumin inhibits cell growth, induces cell cycle arrest and apoptosis in esophageal squamous cell carcinoma EC1, EC, KYSE, TE13 cells through STAT3 activation [ 12 ].
It also induces oxidative stress, which disrupts the mitochondrial membrane potential and causes the release of cytochrome c, thus inducing apoptosis [ 26 ].
Besides, curcumin is shown to induce autophagy [ 8 , 21 , 27 , 28 , 29 , 30 ]. Moreover, curcumin can ameliorate Warburg effect in human non-small cell lung cancer NSCLC H, breast cancer MCF-7, cervical cancer HeLa and prostate cancer PC-3 cells through pyruvate kinase M2 down-regulation, a key regulator of Warburg effect [ 18 ].
In addition, tumor metastasis has always been a frustrating problem for anti-cancer therapy, and curcumin also exhibits anti-metastasis effects [ 31 , 32 , 33 , 34 , 35 ]. By pulmonary administration of curcumin in mice, it overcomes the problem of its low bioavailability, and inhibits lung metastasis of melanoma [ 35 ].
The main target molecules and signaling involved in the pharmacological processes include reactive oxygen species ROS , matrix metalloproteinases MMPs , nuclear factor kappa-light-chain-enhancer of activated B cells NF-κB , signal transducer and activator of transcription and cell cycle-related proteins [ 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 ].
In addition, mammalian target of rapamycin mTOR plays a vital role in curcumin-induced autophagy and apoptosis [ 30 , 48 , 49 , 50 ]. Curcumin can also exert immunomodulatory effects against cancer cells. Theracurmin, a highly bioavailable form of curcumin, decreases pro-inflammatory cytokine secretion from activated T cells, and enhances T cell-induced cytotoxicity in human esophageal adenocarcinoma OE33 and OE19 cells, so it increases the sensitivity of the cells to T cell-induced cytotoxicity [ 51 ].
The natural killing NK cells can directly kill cancer cells, and curcumin can enhance the cytotoxicity effect of NK cells when NK cells are co-cultured with human breast cancer MDA-MB cells, which is highly associated with signal transducer and activator of transcription 4 STAT4 and signal transducer and activator of transcription 5 STAT5 activation [ 52 ].
Besides, myeloid-derived suppressor cells MDSCs are immune-suppressive cells which are found in most cancer patients. Curcumin decreases interleukin IL -6 levels in the tumor tissues and serum of Lewis lung carcinoma LLC -bearing mice to impair the growth of MDSCs, so targeting MDSCs is important for the treatment of lung cancer [ 13 ].
In order to overcome the solubility issues of curcumin and facilitate its intracellular delivery, a curcumin-loaded nanoparticle, curcumin-PLGA-NP, is synthesized. It has a tenfold increase in water solubility compared to curcumin, and shows threefold increased anti-cancer activities in human breast cancer MDA-MB and NSCLC A cells [ 56 ].
Another curcumin-capped nanoparticle exhibits promising anti-oxidative and selective anti-cancer activities in human colorectal cancer HT and SW cells [ 57 ].
Moreover, a curcumin analog, WZ35, has high chemical stability, and higher efficacy in anti-cancer effects compared to curcumin in human gastric cancer SGC cells and SGC xenograft mice [ 20 ].
Another analog, B63, induces cell death and reduces tumor growth through ROS and caspase-independent paraptosis in human gastric cancer SGC, BGC and SNU cells, 5-fluorouracil-resistant gastric cancer cells, and SGC xenograft mice [ 58 ].
Curcumin can be used with other chemotherapeutic agents to achieve synergistic effects, reduce adverse effects and enhance sensitivity. Tamoxifen and curcumin are packed into a diblocknanopolymer, and this nanopolymer reduces the toxicity of tamoxifen in normal cells and exhibits better anti-proliferative and pro-apoptotic effects in human breast cancer tamoxifen-sensitive and -resistant MCF-7 cells [ 59 ].
Triptolide has strong liver and kidney toxicities, and when combined with curcumin, they exert synergistic anti-cancer effects in ovarian cancer, as well as reduce the side effects of triptolide [ 60 ]. In addition, adriamycin, sildenafil, 5-fluorouracil, irinotecan, doxorubicin, paclitaxel, sorafenib, Kruppel-like factor 4, emodin, docosahexaene acid and apigenin are shown to exhibit synergistic effects with curcumin [ 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 ].
Similarly, copper supplementation significantly enhances the anti-tumor effects of curcumin in several oral cancer cells [ 72 ], while epigallocatechingallic acid ester EGCG increases the ability of curcumin to inhibit cell growth and induce apoptosis in human uterine leiomyosarcoma SKN cells [ 73 ].
Clinical trials can confirm or reveal the effects, adverse reactions and pharmacokinetics of the drugs. As the bioavailability of curcumin is very poor, many curcumin preparations are synthesized and tested in clinical trials [ 74 , 75 , 76 ].
A phase I study was conducted to investigate the safety and pharmacokinetics of theracurmin in pancreatic and biliary tract cancer patients who failed with standard chemotherapy [ 76 ]. They administered theracurmin every day with standard gemcitabine-based chemotherapy.
No new adverse effects and no increase in the incidence of adverse effects were observed among these patients. This study has provided additional evidence for a high response rate and better tolerability with the use of curcumin during cancer therapy [ 77 ].
EGCG, also known as epigallocatechingallate Fig. Epidemiological studies have indicated that consumption of green tea has potential impact of reducing the risk of many chronic diseases, such as cardiovascular diseases and cancer [ 78 , 79 ].
EGCG possesses various biological effects including anti-obesity and anti-hyperuricemia, anti-oxidative, anti-viral, anti-bacterial, anti-infective, anti-angiogenic, anti-inflammatory and anti-cancer activities [ 80 , 81 , 82 , 83 , 84 ].
It is reported to present anti-cancer effects in variety of cancer cells, including lung, colorectal, prostate, stomach, liver, cervical, breast, leukemia, gastric, bladder cancers [ 85 , 86 , 87 , 88 , 89 , 90 ].
Among its anti-cancer activities, EGCG exhibits multiple pharmacological actions, including the suppression of cell growth, proliferation, metastasis and angiogenesis, induction of apoptosis, and enhancement of anti-cancer immunity [ 85 , 86 , 91 , 92 , 93 , 94 ].
EGCG can inhibit cell proliferation through multiple ways in many types of cancer cells. It inhibits cell proliferation in human bladder cancer SW, breast cancer MDA-MB and NSCLC A cells, and inhibits tumor growth in gastric cancer SGC xenograft mice [ 89 , 94 , 95 ].
It also induces apoptosis in human oral cancer KB, head and neck cancer FaDu, NSCLC A, and breast cancer MCF-7 cells [ 96 , 97 ]. Besides, EGCG induces autophagy, and inhibition of autophagy can enhance EGCG-induced cell death in human mesothelimoa ACC-meso, Y-meso, EHMES, EHMES-1 and MSTOH, and primary effusion lymphoma BCBL-1 and BC-1 cells [ 98 , 99 ].
In contrast, it induces cell death via apoptosis and autophagy in oral squamous cell carcinoma SCC-4 cells [ 84 ], so autophagy plays a dual role in EGCG-induced cell death. It can also suppress metastasis in human melanoma SK-MEL-5, SK-MEL, A and G, NSCLC CL, A and H cells, and lung metastasis mice [ 85 , 93 , ].
In addition, EGCG suppresses tumor angiogenesis in human NSCLC A cells and A xenograft mice [ ]. EGCG mediates apoptosis which involves pro- and anti-apoptotic proteins in various cancer cells.
It up-regulates pro-apoptotic proteins such as Bclassociated X protein Bax , and down-regulates anti-apoptotic proteins including B-cell lymphoma 2 Bcl-2 , B-cell lymphoma-extra large Bcl-xL and survivin [ 97 , , , ]. ER stress also plays an important role in EGCG-induced cell death.
EGCG inhibits endoplasmic reticulum ER stress-induced protein kinase R-like endoplasmic reticulum kinase PERK and eukaryotic translation-initiation factor 2α eIF2α phosphorylation [ ]. Besides, poly ADP-ribose polymerase PARP 16 is shown to activate ER stress markers, PERK and inositol-requiring enzyme 1α IRE1α [ ].
ER stress-induced apoptosis, PERK and eIF2α phosphorylation by EGCG are suppressed in PARPdeficient hepatocellular carcinoma QGY cells, so EGCG mediates apoptosis through ER stress, which is dependent on PARP16 [ ]. In addition to anti-cancer effects, EGCG shows a significant inhibitory effect on interferon-γ IFN-γ -induced indoleamine 2,3-dioxygenase IDO expression, an enzyme that guides cancer to regulate immune response, in human colorectal cancer SW cells [ ], so this suggests that EGCG might be useful for chemoprevention and colorectal cancer treatment, and could be a potential agent for anti-tumor immunotherapy.
EGCG is also found to be a potential immune checkpoint inhibitor, which down-regulates IFN-γ-induced B7 homolog 1 B7-H1 levels, an immunoglobulin-like immune suppressive molecule, in human NSCLC A cells [ ].
Although EGCG has numerous biological activities through different pathways, its efficacy demonstrated in in vivo studies is not always consistent with the results of in vitro studies.
This can be due to its low oil solubility, metabolic instability and poor bioavailability [ ]. Therefore, EGCG analogs and EGCG-loaded nanoparticles by modifying EGCG are developed, and they have been reported to enhance anti-cancer effects [ , , ].
Besides, EGCG-DHA docosahexaenoic ester, a lipophilic derivative of EGCG, shows improved anti-oxidative effects compared to EGCG, and suppresses colon carcinogenesis in mice [ , ].
These EGCG nanoparticles can improve the targeting ability and efficacy of EGCG, which greatly promote the clinical application and development of EGCG analogs.
EGCG antagonizes toxicity induced by anti-cancer chemotherapeutic agents, and sensitizes chemo-resistant cancer cells. It also exerts synergistic effects with anti-cancer agents in various cancer cells, such as cisplatin, oxaliplatin, temozolomide, resveratrol, doxorubicin, vardenafil, curcumin, erlotinib [ , , , , , , , ].
EGCG can enhance the sensitivity of cisplatin through copper transporter 1 CTR1 up-regulation, which results in the accumulation of cellular cisplatin and cisplatin—DNA adducts in human ovarian cancer SKOV3 and OVCAR3 cells, and the combination of EGCG and cisplatin suppresses tumor growth in OVCAR3 xenograft mice [ ].
The combined low concentration of EGCG and curcumin remarkably inhibits cell and tumor growth in human NSCLC A and NCI-H cells, and A xenograft mice through cell cycle arrest [ ].
To evaluate the tolerance, safety, pharmacokinetics and efficacy of EGCG in humans, clinical trials have been or are currently being conducted for cancer treatment. During a phase I clinical trial for the treatment of radiation dermatitis, patients with breast cancer received adjuvant radiotherapy and EGCG solution.
It was found that the maximum dose μM of EGCG was well tolerated and the maximum tolerated dose was undetermined [ ].
It was concluded that EGCG was effective for treating radiation dermatitis. Moreover, a phase II clinical trial was conducted to investigate the benefits of EGCG as a treatment for acute radiation-induced esophagitis ARIE for patients with stage III lung cancer. The oral administration of EGCG was shown to be effective and phase III clinical trial to study the potential effects of EGCG to ARIE treatment was anticipated [ ].
Berberine Fig. Berberine has diverse pharmacological effects and is normally used for the treatment of gastroenteritis [ , ]. It exhibits significant anti-cancer effects in a wide spectrum of cancers including ovarian, breast, esophageal, and thyroid cancers, leukemia, multiple myeloma, nasopharyngeal carcinoma, and neuroblastoma, through inducing cell cycle arrest and apoptosis, inhibiting metastasis and angiogenesis [ , , , , , , , , ].
Berberine can induce cell cycle arrest in various cancer cells [ , , ]. However, berberine induces G1 phase arrest in human estrogen receptor positive breast cancer MCF-7 cells but not in estrogen receptor negative MDA-MB cells [ ].
Besides, it inhibits cell proliferation by inducing apoptosis in human colorectal cancer HCT-8 cells [ ]. In pnull leukemia EU-4 cells, berberine induces pindependent and X-linked inhibitor of apoptosis protein XIAP -mediated apoptosis, which is associated with mouse double minute 2 homolog MDM2 and proteasomal degradation [ ].
Mitochondrial-mediated apoptosis with Bcllike protein 11 Bim up-regulation and Forkhead box O FoxO nuclear retention is vital in berberine-induced apoptosis [ ].
In contrast, berberine induces protective autophagy in human malignant pleural mesothelioma NCI-H cells, and inhibition of autophagy promotes berberine-induced apoptosis [ ]. Therefore, autophagy plays a dual role in berberine-induced apoptosis.
Furthermore, berberine also inhibits tumor migration and invasion [ , ]. It up-regulates plasminogen activator inhibitor-1 PAI-1 , a tumor suppressor that down-regulates urokinase-type plasminogen activator uPA and antagonizes uPA receptor to suppress metastasis in human hepatocellular carcinoma Bel and SMMC cells [ ].
Berberine interacts with diverse molecular targets as it binds to nucleic acids via specific deoxyribonucleic acid DNA sequences [ ].
Berberine also induces mitochondrial-mediated apoptosis through the loss of mitochondrial membrane potential, cytochrome c release, caspase and PARP activation, up-regulation of pro-apoptotic Bcl-2 family proteins, and down-regulation of anti-apoptotic Bcl-2 family proteins [ , , , ].
It can also activate apoptosis-inducing factor to induce ROS-mediated cell death in pancreatic, breast, and colon cancers [ , , ]. Immunotherapy has made great progress to cancer treatment over the past few years. Toll-like receptors TLRs can activate innate immune responses for host defense [ ].
Berberine inhibits proto-oncogene tyrosine kinase Src activation and TLR4-mediated chemotaxis in lipopolysaccharide LPS -induced macrophages [ ]. Besides, IDO1 inhibitors are promising candidates for cancer immunotherapy [ ]. Berberine and its derivatives are shown to exhibit anti-cancer activity through cell killing by NK cells via IDO1 [ ].
IL-8 is associated with metastasis, and berberine decreases IL-8 levels to inhibit cell growth and invasion in triple-negative breast cancer cells [ ]. Berberine has low oral bioavailability as well as poor intestinal absorption [ ]. As it has pronounced anti-microbial activity against gut microbiota, high dosage can translates into adverse events [ ].
This limits the clinical use of berberine, and different approaches have been applied to improve the bioavailability of berberine. d -α-Tocopheryl polyethylene glycol succinate enhances the intestinal absorption of berberine by inhibiting P-gp activity in rats [ ].
A self-microemulsifying drug delivery system is developed to improve the bioavailability of berberine, the bioavailability is increased by 2. Ber8, a 9-alkylated derivative of berberine, has better cytotoxicity and cellular uptake than berberine, and further inhibits cell proliferation and induces cell cycle arrest in different cell lines, including SiHa, HL, and A cells [ ].
The combination of berberine and chemo- or radio-therapies provides synergistic anti-cancer effects [ , ]. Taxol combined with berberine significantly slows down cell growth in human epidermal growth factor receptor 2 HER2 -overexpressed breast cancer cells [ ], while the combined administration of berberine and caffeine enhances cell death through apoptosis and necroptosis in human ovarian cancer OVCAR3 cells [ ].
The combination therapy of berberine and niraparib, a PARP inhibitor, markedly enhances apoptosis and inhibits tumor growth in ovarian cancer A xenograft mice [ ]. Therefore, combination of berberine with other therapies is a promising treatment for the alternative cancer therapy.
Previous pre-clinical research and animal studies have demonstrated the anti-tumor action of berberine hydrochloride. The people with a history of colorectal cancer might be at higher risk for adenomas, thus they are particularly suitable for the study of the chemopreventive effects of berberine hydrochloride in adenomas.
A randomized, double-blind, placebo-controlled trial was designed to determine whether the daily intake of mg of berberine hydrochloride could decrease the occurrence of new colorectal adenomas in patients with a history of colorectal cancer, and it is currently ongoing.
Another phase II clinical trial of berberine and gefitinib is also ongoing in patients with advanced NSCLC and activating EGFR mutations. Artemisinin Fig.
Since the Nobel Prize in Physiology or Medicine conferred to Chinese scientist, Youyou Tu, artemisinin drew attention to worldwide [ ]. Beside from their well-established anti-malarial effects, artemisinin and its derivatives ARTs , including dihydroartemisinin DHA , artesunate, artemether and arteether, are also found to exhibit potent anti-cancer activities in many studies [ , , , , , ].
DHA and artesunate are the most studied ART derivatives for cancer treatment, and artesunate will be discussed in a separate section. The anti-cancer effects of ARTs are demonstrated in a broad spectrum of cancer cells including lung, liver, pancreatic, colorectal, esophageal, breast, ovarian, cervical, head and neck, and prostate cancers [ , , , , , , , , ].
The anti-cancer activities of ARTs include induction of apoptosis and cell cycle arrest, inhibition of cell proliferation and growth, metastasis and angiogenesis [ , , , , ].
ART inhibits cell proliferation, migration and invasion, and induces apoptosis in human breast cancer MCF-7 cells [ , ], while DHA suppresses cell growth through cell cycle arrest and apoptosis in human hepatocellular carcinoma HepG2 cells and HepG2 xenograft mice [ ].
Similarly, ART induces apoptosis in murine mastocytome P cells and hamster kidney adenocarcinoma BSR cells, and inhibits tumor growth in P xenograft mice [ ]. Moreover, autophagy plays a vital role in ART-mediated anti-cancer activities [ , , , , , ].
DHA can induce autophagy-dependent cell death in human cervical cancer HeLa cells, cholangiocarcinoma KKU, KKU and KKU, and tongue squamous cell carcinoma Cal cells [ , , ], while ART induces autophagy-mediated cell cycle arrest in human ovarian cancer SKOV3 cells [ ].
DHA is also shown to induce autophagy by suppressing NF-κB activation in several cancer cells including RPMI , NB4, HCT, and HeLa cells [ ]. Furthermore, ART and DHA can also inhibit metastasis in various cancer cells such as non-small-cell lung carcinoma NSCLC , ovarian and lung cancer cells [ , , ].
Apart from apoptosis and metastasis, the inhibition of angiogenesis is also a crucial approach in cancer treatment.
ART inhibits angiogenesis through mitogen-activated protein kinase MAPK activation in osteosarcoma [ ], whilst DHA exerts strong anti-angiogenic effect by repressing extracellular signal—regulated kinase ERK and NF-κB pathways in human umbilical vein endothelial cells HUVECs and pancreatic cancer, respectively [ , ].
In the past decades, studies have been focused on studying the anti-cancer mechanisms of ARTs, but there are contentions. ARTs inhibit cancer cell proliferation mainly by the induction of apoptosis through mitochondrial-dependent pathways [ , , ].
ART mediates the release of cytochrome c and caspase-9 cleavage, leading to increased apoptosis in human breast cancer MCF-7 cells [ ]. DHA induces apoptosis through Bcl-2 down-regulation in human cervical cancer HeLa and Caski cells [ ], and via Bim-dependent intrinsic pathway in human hepatocellular carcinoma HepG2 and Huh7 cells [ ].
Interestingly, ART is demonstrated to be an inhibitor of anti-cancer target, histone deacetylases HDAC [ ]. In addition, another mechanism of killing tumor cells by ARTs is iron-dependent cell death called ferroptosis, a new form of cell death, so ferroptosis becomes an attractive strategy for cancer treatment [ , ].
DHA can enhance the anti-tumor cytolytic activity of γδ T cells against human pancreatic cancer SW, BxPC-3 and Panc-1 cells [ ], and ART also potentiates the cytotoxicity of NK cells to mediate anti-tumor activity [ ]. Similarly, ART inhibits tumor growth through T cell activation and T reg suppression in breast cancer 4T1 xenograft mice [ ].
Therefore, this provides a novel strategy for treating pancreatic cancer with immunotherapy. ART has poor water solubility and bioavailability. In order to solve this issue, ART is encapsulated into micelles by nanoprecipitation to form ART-loaded micelles [ ].
The ART-loaded micelles enhance the drug exposure time and accumulation in breast cancer 4T1 xenograft mice, and shows specific toxicity in human and murine breast cancer MCF-7 and 4T1 cells.
A mitochondrial-targeting analog of ART is also synthesized to specifically target mitochondria for enhancing the inhibition of cell proliferation in various cancer cells including HCT, MDA-MB, HeLa and SKBR3 cells [ ].
Moreover, dimmers of ART are also synthesized by polyamine linkers, and they further inhibit cell proliferation in human breast cancer MCF-7 cells and angiogenesis in HUVECs [ ].
Many studies show the synergistic effects of ARTs with other compounds or therapeutic approaches. The combined treatment of ART and resveratrol markedly inhibits cell proliferation and migration, and enhances apoptosis and ROS production in human cervical cancer HeLa and hepatocellular carcinoma HepG2 cells [ ].
Similarly, the use of combined DHA and gemcitabine exhibits strong synergistic effects on the loss of mitochondrial membrane potential and induction of apoptosis in human NSCLC A cells [ ].
DHA also reinforces the anti-cancer activity of chemotherapeutic agent, cisplatin, in cisplatin-resistant ovarian cancer cells [ ]. Studies also demonstrate the enhancement of sensitivity by DHA in photodynamic therapy in esophageal cancer [ , ].
Therefore, this suggests that ARTs could be potential anti-cancer agents. The salivary DHA concentration was proportionally correlated with the plasma DHA concentration, so saliva is a good use for monitoring DHA levels in the body.
An artemisinin analog, Artenimol-R, was shown to improve clinical symptoms and tolerability in patients with advanced cervical cancer [ ]. Ginsenosides Fig. Chen, Panax ginseng and Cinnamomum cassia Presl. Ginsenosides mainly exert anti-cancer effects in colorectal, breast, liver and lung cancers, through inhibiting cell proliferation and migration, angiogenesis, and reversing drug resistance [ 7 , , , , , , , , ].
Ginsenoside Rg3, ginsenoside Rh2, and compound K are the primary bioactive compounds among ginsenosides for cancer prevention.
Ginsenoside Rg3 inhibits cell viability and induces cell apoptosis in human ovarian cancer HO cells [ ], hepatocellular carcinoma Hep, HepG2 and SMMC, breast cancer MCF-7, MDA-MB, MDA-MB and BT, and NSCLC A, H23 and Lewis lung carcinoma cells [ , , , , , , ].
It induces cell cycle arrest at G1 phase in human melanoma A, and multiple myeloma U, RPMI and SKO cells [ , ], and inhibits cell migration in human colorectal cancer LoVo, SW and HCT cells [ ]. Ginsenoside Rg3 can also modulate the tumor environment through inhibiting angiogenesis and enhancing anti-tumor immune responses [ ].
Moreover, ginsenoside Rh2 exhibits anti-tumor activity in human NSCLC H cells and H xenograft mice, through the induction of ROS-mediated ER-stress-dependent apoptosis [ ].
It also suppresses cell proliferation and migration, and induces cell cycle arrest in human hepatocellular carcinoma HepG2 and Hep3B cells, and inhibits tumor growth in HepG2 xenograft mice [ ].
Compound K, an intestinal bacterial metabolite of ginsenosides, also induces cell cycle arrest and apoptosis in human colorectal cancer HCT cells, and suppresses tumor growth in HCT xenograft mice [ ]. It also efficiently inhibits cell proliferation and induces apoptosis through mitochondrial-related pathways in human hepatocellular carcinoma MHCCH cells [ ].
Furthermore, 20 S -ginsenoside Rg3 induces autophagy to mediate cell migration and invasion in human ovarian cancer SKOV3 cells [ ]. In contrast, it sensitizes NSCLC cells to icotinib and hepatocellular carcinoma cells to doxorubicin through the inhibition of autophagy [ , ].
Besides, ginsenoside Rh2 inhibits cell growth partially through the coordination of autophagy and β-cateninin signaling in human heptocellular carcinoma HepG2 and Huh7 cells [ ]. Therefore, autophagy plays a dual role in cancer via different signaling routes.
Moreover, 20 S -ginsenoside Rh2 is shown to bind to recombinant and intracellular annexin A2 directly, and this inhibits the interaction between annexin A2 and NF-κB p50 subunit, which decreases NF-κB activation [ ]. NF-κB is important in cell survival, and 20 S -ginsenoside Rh2 can inhibit cell survival through NF-κB pathway.
Furthermore, p53 also plays a vital role in ginsenoside-induced anti-cancer activities [ , , ]. For the promotion of immunity, ginsenoside Rg3 can enhance lymphocyte proliferation and T helper type 1 cell Th1 -related cytokine secretion including IL-2 and IFN-γ in hepatacellular carcinoma Hbearing mice, and inhibit tumor growth partly through the induction this cellular immunity [ ].
Ginsenoside Rg3 can also down-regulate the levels of B7-H1 and B7 homolog 3 B7-H3 , immunoglobulin-like immune suppressive molecules, to modulate tumor microenvironment and enhance anti-tumor immunity, and these molecules are negatively associated with overall survival in colorectal cancer patients [ ].
In addition, ginsenoside Rh2 can also enhance anti-tumor immunity in melanoma mice by promoting T cell infiltration in the tumor and cytotoxicity in spleen lymphocytes [ ].
The combination of ginsenosides with other chemotherapeutic agents provides significant advantages for cancer treatment. Ginsenoside Rg3 alone demonstrates modest anti-angiogenic effects, and displays additive anti-angiogenic effects in B6 glioblastoma rats when combined with temozolomide [ ].
When it is combined with paclitaxel, it enhances cytotoxicity and apoptosis through NF-κB inhibition in human triple-negative breast cancer MDA-MB, MDA-MB and BT cells [ ]. Ginsenosides have a long history of use as traditional medicine to treat many diseases in China.
Relatively few clinical studies have been performed in humans eventhough ginseng products are widely recognized to have therapeutic effects when used alone or in combination with other chemotherapeutic agents. Therefore, clinical studies are needed to confirm the safety of such uses.
A phase II clinical trial is conducting to assess the safety and efficacy of ginsenoside Rg3 in combination with first-line chemotherapy in advanced gastric cancer.
Patients with advanced NSCLC and epidermal growth factor receptor-tyrosine kinase inhibitor EGFR-TKI mutation were recruited in a study that investigated the safety and efficacy of the combined therapy, ginsenoside Rg3 and EGFR-TKI.
It was shown that this therapy increased progression-free survival, overall survival and objective response rate compared to EGFR-TKI alone [ ]. In another study, the safety and efficacy of combined ginsenoside Rg3 and transcatheter arterial chemoembolization TACE were studied in patients with advanced hepatocellular carcinoma.
The results showed that this therapy ameliorated TACE-induced adverse effects and prolonged the overall survival compared to the use of TACE alone [ ]. As an ursane-type pentacyclic triterpenic acid, UA Fig.
cranberry , Arctostaphylos uva - ursi L. Spreng bearberry , Rhododendron hymenanthes Makino , Eriobotrya japonica, Rosemarinus officinalis, Calluna vulgaris, Eugenia jambolana and Ocimum sanctum, as well as in the wax-like protective coatings of fruits such as pears, apples and prunes [ ].
UA has numerous biochemical and pharmacological effects including anti-inflammatory, anti-oxidative, anti-proliferative, anti-atherosclerotic, anti-leukemic, anti-viral, and anti-diabetic effects [ , , , , , , ]. It also exerts anti-cancer activities in ovarian, breast, gastric, prostate, lung, liver, bladder, pancreatic, and colorectal cancers [ , , , , , , , , ].
UA can be used as a potential therapeutic agent for the treatment of various cancers [ , , , , , , , , ]. It induces apoptosis through both extrinsic death receptor and mitochondrial death pathways in human breast cancer MDA-MB cells [ ], and inhibits cell proliferation and induces pro-apoptosis in human breast cancer MCF-7 cells by FoxM1 inhibition [ ].
UA also inhibits cell and tumor growth through suppressing NF-κB and STAT3 pathways in human prostate cancer DU and LNCaP cells, and DU xenograft mice [ ], and induces apoptosis in human prostate cancer PC-3 cells [ ]. Similarly, UA induces apoptosis and inhibits cell proliferation in human colorectal cancer HCT, HCT, HT and Caco-2 cells [ , ].
UA is also shown to induce autophagy to mediate cell death in murine cervical cancer TC-1 cells [ ], and promote cytotoxic autophagy and apoptosis in human breast cancer MCF-7, MD-MB and SKBR3 cells [ ]. It also inhibits cell growth by inducing autophagy and apoptosis in human breast cancer cells T47D, MCF-7 and MD-MB cells [ ].
In contrast, UA induces autophagy, but the inhibition of autophagy enhances UA-induced apoptosis in human oral cancer Ca and SCC, and prostate cancer PC-3 cells [ , ]. Therefore, autophagy plays a dual role in UA-induced apoptosis via different signaling pathways.
In addition, UA inhibits tumor angiogenesis through mitochondrial-dependent pathway in Ehrlich ascites carcinoma xenograft mice [ ]. UA is demonstrated to have apoptosis-promoting and anti-proliferative capacities via modulating the expressions of mitochondrial-related proteins such as Bax, Bcl-2, cytochrome c and caspase-9 [ , ].
It can also induce oxidative stress and disruption of mitochondrial membrane permeability to mediate apoptosis in human osteosarcoma MG63 and cervical cancer HeLa cells [ , ].
In addition, p53 pathway also contributes to the anti-cancer effects of UA. UA induces apoptosis and cell arrest through pmediated p53 activation in human colorectal cancer SW and breast cancer MCF-7 cells [ , ], and this p53 activation is through inhibiting negative regulators of p53, MDM2 and T-LAK cell-originated protein kinase TOPK [ ].
Studies have reported the cancer immunomodulatory activities of UA [ , ]. UA down-regulates NF-κB to inhibit cell growth and suppress inflammatory cytokine levels including TNF-α, IL-6, IL-1β, IL and IFN-γ in human breast cancer T47D, MCF-7 and MDA-MB cells [ ].
It also modulates the tumor environment by modulating cytokine production such as TNF-α and IL in ascites Ehrlich tumor [ ]. UA is insoluble in water, with poor pharmacokinetic properties including poor oral bioavailability, low dissolution and weak membrane permeability [ ].
Some new drug delivery technologies have been developed to overcome these problems including the uses of liposomes [ , , , , ], solid dispersions [ ], niossomal gels [ ], and nanoliposomes [ ]. Liposome is the most commonly used drug delivery system. A chitosan-coated UA liposome is synthesized with tumor targeting and drug controlled release properties, and has fewer side effects [ ].
It enhances the inhibition of cell proliferation and tumor growth in human cervical cancer HeLa cells and U14 xenograft mice. Besides, a pH-sensitive pro-drug delivery system is also synthesized, and this pro-drug enhances cellular uptake and bioavailability of UA [ ].
It further inhibits cell proliferation, cell cycle arrest and induces apoptosis in human hepatocellular carcinoma HepG2 cells.
UA can also be used in combination with other drugs. The combined treatment of zoledronic acid and UA enhances the induction of apoptosis and inhibition of cell proliferation through oxidative stress and autophagy in human osteosarcoma U2OS and MG63 cells [ ], whilst the combination of UA and curcumin inhibits tumor growth compared to UA alone in skin cancer mice [ ].
A human clinical study was conducted to investigate the toxicity and pharmacokinetics of UA-liposomes UAL including dose-limiting toxicity and maximum tolerated dose in healthy adult volunteers and patients with advanced solid tumors [ ].
Silibinin Fig. Gaertn, is commonly exploited for the treatment hepatic diseases in China, Germany and Japan. Previous studies have reported that silibinin exerts remarkable effects in numerous cancers such as renal, hepatocellular and pancreatic carcinoma, bladder, breast, colorectal, ovarian, lung, salivary gland, prostate and gastric cancers, through the induction of apoptosis, inhibition of tumor growth, metastasis and angiogenesis [ , , , , , , , , , , ].
Silibinin suppresses epidermal growth factor-induced cell adhesion, migration and oncogenic transformation through blocking STAT3 phosphorylation in triple negative breast cancer cells [ ].
It strongly suppresses cell proliferation and induces apoptosis in human pancreatic cancer AsPC-1, BxPC-3 and Panc-1 cells, and induces cell cycle arrest at G1 phase in AsPC-1 cells [ ]. It can also induce apoptosis via non-steroidal anti-inflammatory drug-activated gene-1 NAG-1 up-regulation in human colorectal cancer HT cells [ ], and induces mitochondrial dysfunction to mediate apoptosis in human breast cancer MCF-7 and MDA-MB cells [ ].
Moreover, silibinin induces autophagic cell death via ROS-dependent mitochondrial dysfunction in human breast cancer MCF-7 cells [ ]. In contrast, it induces autophagy to exert protective effect against apoptosis in human epidermoid carcinoma A, glioblastoma A and SR, and breast cancer MCF-7 cells [ , , ], and autophagy inhibition enhances silibinin-induced apoptosis in human prostate cancer PC-3 cells [ ].
Silibinin also induces autophagy to inhibit metastasis in human renal carcinoma ACHN and O cells, and salivary gland adenoid cystic carcinoma cells [ ]. Therefore, autophagy plays a dual role in silibinin-induced anti-cancer effects. In addition, silibinin inhibits angiogenesis in human prostate cancer PCa, LNCaP and 22Rv1 cells [ ].
Silibinin exhibits anti-cancer activities mainly due to the cell cycle arrest [ , , , , ]. It induces G1 phase arrest in human pancreatic cancer SW and AsPC-1, and breast cancer MCF-7 and MCFA cells [ , , ], whilst it causes G2 phase arrest in human cervical cancer HeLa, and gastric cancer MGC and SGC cells [ , ].
It also decreases the expressions of CDKs such as CDK1, CDK2, CDK4 and CDK6 that are involved in G1 and G2 progression [ , ].
In addition, silibinin induces apoptosis and inhibits proliferation through the suppression of NF-κB activation [ , , , ]. On the other hand, silibinin is shown to induce apoptosis through the promotion of mitochondrial dysfunction, including increased cytochrome c and Bcl-2 levels, the loss of mitochondrial membrane potential, and decreased adenosine triphosphate ATP levels [ , , , ].
Silibinin has immunomodulatory effects in cancer and immunity. The MDSCs are associated with immunosuppression in cancer, and silibinin increases the survival rate in breast cancer 4T1 xenograft mice, and reduces the population of MDSCs in their blood and tumor [ ].
There was also a reduction in macrophage infiltration and neutrophil population in silibinin-treated prostate cancer TRAMPC1 xenograft mice [ ].
These studies suggest a role of immunity in its anti-tumor effects. Silibinin has poor water solubility and bioavailability, so it limits its efficacy in anti-cancer activities [ ]. Advanced technologies such as nanoprecipitation technique are used to solve this issue [ , , , , ].
Silbinin is encapsulated in Eudragit ® E nanoparticles in the presence of polyvinyl alcohol, and these nanoparticles enhance apoptosis and cytotoxicity in human oral cancer KB cells [ ].
The silibinin-loaded magnetic nanoparticles further inhibit cell proliferation in human NSCLC A cells [ ], while silibinin-loaded chitosan nanoparticles enhances cytotoxicity compared to silibinin alone in human prostate cancer DU cells [ ]. The combination of silibinin and other drugs are used in cancer treatment to enhance the efficacy of anti-cancer effects [ , , , ].
The combination of curcumin and silibinin enhances the inhibition of cell growth and reduction in telomerase gene expression compared to silibinin alone in human breast cancer T47D cells [ ]. The mixture of luteolin and silibinin also shows synergistic effects on the attenuation of cell migration and invasion, and induction of apoptosis in human glioblastoma LN18 and SNB19 cells [ ].
Silibinin and paclitaxel combination enhances apoptosis and up-regulates tumour suppressor genes, p53 and p21, in human ovarian cancer SKOV3 cells [ ]. Silibinin has been widely used as anti-cancer drug in vitro and in vivo, and its combination with other therapies is a promising treatment for cancer, so clinical trials are needed to confirm its safety and efficacy in humans, and to develop as an anti-cancer drug.
Emodin Fig. It exhibits remarkable biological effects such as anti-inflammation, anti-oxidant, prevention of intrahepatic fat accumulation and DNA damage [ , , , , , , ]. Many studies have shown that emodin can attenuate numerous cancers including nasopharyngeal, gall bladder, lung, liver, colorectal, oral, ovarian, bladder, prostate, breast, stomach and pancreatic cancers, through the inhibition of cell proliferation and growth, metastasis, angiogenesis, and induction of apoptosis [ , , , , , , , , , , , , ].
Emodin suppresses ATP-induced cell proliferation and migration through inhibiting NF-κB activation in human NSCLC A cells [ ], and induces apoptosis through cell cycle arrest and ROS production in human hepatocellular carcinoma HepaRG cells [ ].
It also induces autophagy to mediate apoptosis through ROS production in human colorectal cancer HCT cells [ ]. In the words of the Gerson Institute :. The Gerson Therapy targets the most significant metabolic requirements in your body. Believe it or not, this therapy allows you to reap the nutritional benefits of consuming 15—20 pounds of organically grown fruits and vegetables each day!
The moment a patient is put on the full therapy, the combined effect of the food, the juices and the medication causes the immune system to attack and kill tumor tissue, besides working to flush out accumulated toxins from the body tissues. This great clearing-out procedure carries the risk of overburdening and poisoning the liver — the all-important organ of detoxification, which, in a cancer patient, is bound to be already damaged and debilitated.
Over the years, I have been given a lot of different advice as well, so when I heard about Dr. Numerous, independent clinical cancer studies published in major medical journals world-wide confirm Dr. Over 40 years ago, Dr. Budwig presented clear and convincing evidence, which has been confirmed by hundreds of other related scientific research papers since, that the essential fatty acids were at the core of the answer to the cancer problem.
Willner, MD, Ph. In , Dr. During her research, she discovered that many of the conventional processed fats and hydrogenated oils were destroying the membranes of our cells, and this caused diseased cells and toxicity.
Developing a specific diet — in this case, the Budwig diet protocol — to counteract this cancer-causing process, Dr. Budwig claimed to have had over a 90 percent success rate with her protocol over a year period! Budwig found that consuming a mixture of cottage cheese, flaxseeds and flaxseed oil had the best results.
When cottage cheese which is rich in sulfur protein and saturated fats and flax which is high in electron-rich unsaturated fatty acids are combined this way, your body is able to absorb these vital nutrients easier and quicker.
Because of the changes in agriculture, I suggest this updated 21 st century version of the Budwig protocol:. Mix all the ingredients together in bowl or blender, and consume once daily.
Related: Artemisinin for Malaria, Viral Infections and Cancer Prevention. Beard focused on high dose porcine-based pancreatic enzyme therapy and eating a holistic diet to create an internal environment in which the body can more thoroughly heal itself. Gonzalez, MD, started to evaluate the concept at Cornell University Medical College in that people started to seriously consider this natural approach.
Basing his protocol off of Dr. He discovered that a vegetarian diet suppresses sympathetic function, whereas the opposite is true with a meat-rich diet. So after dividing patients into different categories based of their metabolic differences and genetic and physical make-up, here are the recommendations:.
In addition, these physicians recommend taking five grams of proteolytic enzymes three times daily on an empty stomach between meals to reduce inflammation. According to Dr. Josef Beuth, the research behind this natural cancer treatment is pretty airtight :. These studies demonstrated that systemic enzyme therapy significantly decreased tumor-induced and therapy-induced side effects and complaints such as nausea, gastrointestinal complaints, fatigue, weight loss, and restlessness and obviously stabilized the quality of life.
Chelation therapy uses chemicals or natural compounds to remove toxic metals from the body. When it is employed in the medical system, however, it is most commonly used to remove calcium deposits from arteries.
These pro-oxidant effects may also induce endogenous antioxidant systems in normal tissues that offer protection against carcinogenic insult! Along with vitamin C chelation, consuming more vitamin C-rich foods may also prevent and fight cancer.
Budwig recommends frankincense essential oil , especially when it comes to fighting brain tumors. Specifically, Indian frankincense Boswellia serrata has been shown clinically to be a potentially effective treatment for:.
Rub frankincense essential oil on your neck three times daily. Also, drink three drops in eight ounces of water three times daily. Be sure to discuss the potential benefits and risks of complementary therapies, as well as any interactions with other medications you may be taking.
If you have trouble communicating with your healthcare team, consider seeking a cancer navigator who can provide support and answer any of your questions.
However, remember that even natural treatments can have adverse effects and may not be suitable for everyone. Some will put you at high risk for serious side effects and complications. Kelly Johnson-Arbor, MD , medical toxicologist, co-medical director, and interim executive director at National Capital Poison Center says the FDA has an online and app-based tool to help patients understand whether a medication is approved:.
Johnson-Arbor explained. She also emphasized that natural remedies for cancer should be approached with caution. Johnson-Arbor added. Your healthcare team should also be your go-to source for information on FDA-approved cancer treatments and any potential side effects. A healthy mind is as essential as a healthy body during cancer treatment.
Feeling anxious or overwhelmed is normal, but focusing on what brings you joy and hope can help. Take time for yourself — find activities that bring you peace, such as those in the following list.
Acupuncture is an ancient Chinese practice involving thin needles insertion into specific body areas. Studies suggest that acupuncture may reduce pain and anxiety.
Massage is another natural therapy that may be beneficial in managing cancer-related pain and side effects associated with treatment.
Massage can help reduce stress and anxiety, increase energy levels, improve circulation, and even reduce nausea associated with chemotherapy treatments. Some cancer clinics now offer massage therapy as a complementary medicine.
Talk to your doctor about this option if you want to try massage therapy during treatment. Using essential oils may promote relaxation and reduce stress; may also help with other symptoms associated with cancer, such as nausea and fatigue.
Researchers have found meditation can reduce stress and anxiety and improve quality of life. Yoga may help reduce stress, improve quality of life, and aid in relaxation; it may also help with pain management and fatigue associated with cancer treatments.
Hypnotherapy uses guided meditation to help you relax and gain more control over your thoughts, feelings, and behaviors; it may be effective for pain and emotional stress. Music can be used to reduce stress and anxiety, as well as provide a sense of comfort and relaxation.
Writing aids in processing emotions in a healthy way. Talk therapy is also an excellent option for mental health support.
Chinese Medicine volume therapoesArticle number: Anti-cancsr Cite Ani-cancer article. Metrics nxtural. Numerous natural products Anti-cancer natural therapies from Chinese herbal medicine exhibit Managing hyperglycemia Anti-cancer natural therapies, including anti-proliferative, pro-apoptotic, Anti-cancer natural therapies, anti-angiogenic effects, as well as regulate autophagy, reverse multidrug resistance, balance immunity, and enhance chemotherapy in vitro fherapies in Therapoes. To provide Anti-cancer natural therapies insights naatural the critical Multivitamin supplements ahead, we systemically reviewed the most recent Anti-cancer natural therapies therxpies since on the key compounds with anti-cancer effects derived from Chinese herbal medicine curcumin, epigallocatechin gallate, berberine, artemisinin, ginsenoside Rg3, ursolic acid, silibinin, emodin, triptolide, cucurbitacin B, tanshinone I, oridonin, shikonin, gambogic acid, artesunate, wogonin, β-elemene, and cepharanthine in scientific databases PubMed, Web of Science, Medline, Scopus, and Clinical Trials. In addition, the present review has extended to describe other promising compounds including dihydroartemisinin, ginsenoside Rh2, compound K, cucurbitacins D, E, I, tanshinone IIA and cryptotanshinone in view of their potentials in cancer therapy. Up to now, the evidence about the immunomodulatory effects and clinical trials of natural anti-cancer compounds from Chinese herbal medicine is very limited, and further research is needed to monitor their immunoregulatory effects and explore their mechanisms of action as modulators of immune checkpoints. Cancer is a leading public health problem worldwide with an estimated
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