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Research Events Jiler Conference Research Podcasts. Cancer Prevention Research Conference Boston, June , It can also bind directly to heterogeneous nuclear ribonucleoprotein A1 to induce immunogenic cell death in human breast cancer MDA-MB cells [ ].

Shikonin is also reported to be used as an immunotherapy modifier in cell-based cancer vaccine systems, suggesting its potential application in cancer immunotherapy [ ]. Derivatives are developed to enhance the anti-cancer and tumor targeting effects of shikonin. The naphthazarin ring of shikonin is modified to produce DMAKO, which can specifically target cancer cells instead of normal cells [ ].

DMAKO can also suppress cell survival in human colorectal cancer HCT cells, and inhibits tumor growth in colorectal cancer CT xenograft mice [ ]. Besides, it inhibits cell proliferation and migration, and induces cell cycle arrest and apoptosis in murine melanoma B16F0 cells [ ].

Another novel shikonin derivative, cyclopropylacetylshikonin, exhibits strong anti-tumor and pro-apoptotic effects in human melanoma WM and MUG-MEL2 cells [ ]. In addition, drug delivery system is also developed to promote the intracellular delivery of shikonin.

The shikonin-loaded nanogel enhances RIP1- and RIP3-dependent necroptosis in human osteosarcoma B cells [ ]. There is an increased accumulation of shikonin-loaded nanogel in the tumor tissue, and this nanogel can further inhibit tumor growth and metastasis in B xenograft mice.

Furthermore, the modified shikonin-loaded liposomes have higher cytotoxicity, and inhibit cell proliferation, metastasis in human breast cancer MDA-MB cells [ ]. The combination therapy is widely used to provide synergistic effects of anti-cancer activities.

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 [ ].

Besides, shikonin can also potentiate the anti-cancer effects of gemcitabine through NF-kB suppression and by regulating RIP1 and RIP3 expressions in human pancreatic cancer [ , ]. Shikonin is also reported to promote the efficacy of adriamycin in lung cancer and osteosarcoma [ , ], and enhance sensitization to cisplatin in colorectal cancer [ ].

Apart from the synergistic effect of shikonin, the combination of shikonin and paclitaxel reverses MDR in human ovarian cancer A cells [ 10 ].

The single or combined therapies with shikonin show promising anti-cancer effects in vitro and in vivo, so pre-clinical data has confirmed its therapeutic use in cancer treatment, as a result, clinical trials will be carried out to further to confirm its safety and efficacy in humans.

GA Fig. hanburyi and G. Morella [ ]. It has multiple biological activities such as anti-oxidative, anti-inflammatory, and anti-cancer activities [ , ]. Plenty of evidence shows that GA inhibits cell proliferation, invasion, survival, metastasis and chemo-resistance, and induces angiogenesis in many types of cancers such as gastric and prostate cancers, leukemia, multiple myeloma, osteosarcoma, and renal carcinoma through multiple signaling mechanisms [ , , , , , , ].

Many studies have reported the anti-cancer effects of GA in human breast cancer [ , , , ]. GA at low concentrations 0. GA also induces apoptosis via ROS production in human bladder T24 and UMUC3 cells [ ].

At earlier time points, GA induces ROS-mediated autophagy, which produces a strong cell survival response. However, at later time points, caspases are activated which degrade autophagic proteins and cell survival proteins, and this eventually induces apoptosis.

Similarly, GA-induced autophagy via ROS provides a cytoprotective effect to human pancreatic cancer Panc-1 and BxPC-3 cells [ ], and ROS scavenger, N-acetylcysteine, can reverse GA-induced autophagy in human NSCLC NCI-H cells [ ].

Moreover, GA inhibits cell invasion and migration through reversion-inducing-cysteine-rich protein with kazal motifs RECK up-regulation in human NSCLC A cells and A xenograft mice [ ], and prevents TNF-α-induced invasion in human prostate cancer PC-3 cells [ ]. It also inhibits angiogenesis in HUVECs, and prevents tumor growth through the inhibition of tumor angiogenesis [ ].

ROS-related pathways play a vital role in GA-induced cell death [ , , , , , , , ]. GA induces apoptosis mainly through ROS accumulation in human pancreatic cancer Panc-1 and BxPC-3, NSCLC NCI-H, castration-resistant prostate cancer PCAP-1, melanoma A, breast cancer MCF-7 cells [ , , , , ].

It also induces oxidative stress-dependent caspase activation to mediate apoptosis in human bladder cancer T24 and UMUC3 cells [ ]. Moreover, GA increases the expressions of ER stress markers such as GRP78, CHOP, activating transcription factor 6 ATF-6 and caspase, and co-treatment with chemical chaperone, 4-PBA, significantly reduces these expressions and apoptosis in human NSCLC A cells, so it is suggested that GA induces ER stress to mediate apoptosis [ ].

Previous studies have shown some immunomodulatory activities of GA [ , ]. The activation of TLRs is important to initiate immune responses, and TLR4 forms a complex with myeloid differentiation factor 2 MD2 to recognize its ligand, like LPS.

Similarly, it also reduces pro-inflammatory cytokine production including TNF-α, IL-1β and IL-6 by suppressing p38 pathway in murine macrophage RAW GA has low solubility, instability and poor pharmacokinetic properties [ ]. In order to increase its water solubility, GA is conjugated with a cell-penetrating peptide, trans-activator of transcription, to form GA-TAT [ ].

This GA-TAT enhances apoptosis through ROS accumulation in human bladder cancer EJ cells. Another study uses a co-polymer to encapsulate GA to form GA micelles [ ]. These GA micelles have better cellular uptake which can further enhance apoptosis in human breast cancer MCF-7 cells and the anti-tumor effects in MCF-7 xenograft mice.

Moreover, GA is encapsulated into the core of the nanoparticles to enhance the stability of GA and its circulation time [ ]. These nanoparticles have tumor targeting properties, and enhance the anti-tumor activities of GA without inducing higher toxicity.

The combination of GA and other chemotherapy agents has been widely used to improve the therapeutic effects against various cancers such as osteosarcoma, pancreatic and lung cancers [ , , , ]. Moreover, GA and retinoic acid chlorochalcone are loaded into glycol chitosan nanoparticles to form RGNP [ ].

The RGNP exhibits synergistic effects to inhibit cell proliferation and induces apoptosis in osteosarcoma. The combination of GA with doxorubicin synergistically reduces cell viability in human ovarian cancer platinum-resistance SKOV3 cells, and this combination also suppresses tumor growth in SKOV3 xenograft mice [ ].

The safety and efficacy of GA at different dosages in patients with advanced malignant tumors have been compared in a phase IIa clinical trial [ ]. The patients with GA administration on days 1—5 in a 2-week cycle showed a greater disease control rate and only Grades I and II adverse reactions.

To further investigate the safety and efficacy of GA, a phase IIb clinical trial involving a larger sample size of patients would be needed. Artesunate Fig. As an analog of ART, artesunate exerts better water solubility and higher oral bioavailability, due to its special structure with an additional hemisuccinate group that makes it a better candidate for cancer treatment [ ].

The anti-cancer effects of artesunate have been demonstrated in bladder, breast, cervical, colorectal, esophageal, gastric, ovarian and prostate cancer, renal carcinoma, leukemia, melanoma and multiple myeloma [ , , , , , , , , , , , ]. Its anti-cancer effects include induction of cell cycle arrest and apoptosis, inhibition of cell proliferation and growth, metastasis and angiogenesis [ , , ].

Artesunate can induce apoptosis in various cancers including human breast cancer MCF-7, MDA-MB and SKBR3 cells, gastric cancer SGC and HGC, colorectal cancer HCT, and esophageal cancer Eca and Ec cells [ , , , , , ]. Artesunate is also shown to induce autophagy to exert cytoprotective effects in human colorectal cancer HCT cells, and the inhibition of autophagy enhances artesunate-mediated apoptosis [ ].

Similarly, artesunate-induced mitophagy provides a protective effects against cell death in human cervical cancer HeLa cells [ ]. Moreover, it inhibits cell invasion and migration in human prostate cancer DU and LNCaP, cervical cancer Caski and HeLa cells, and uveal melanoma cells [ , , ], and suppresses tumor angiogenesis in HUVECs and renal carcinoma O xenograft mice [ , ].

In most cases, the inhibition effects of artesunate against cancer cells are resulted from apoptosis. Artesunate induces apoptosis through cyclooxygenase-2 COX-2 down-regulation in human bladder cancer T24 and RT4, and gastric cancer HGC cells [ , ].

Mitochondrial pathways also play an important role in artesunate-mediated anti-cancer effects [ , , ]. Artesunate inhibits tumor growth through ROS- and p38 MAPK-mediated apoptosis in human rhabdomyosarcoma TE cells [ ].

It also exerts anti-tumor activities through the loss of mitochondrial membrane potential, Bcl-2 down-regulation, Bax up-regulation, and caspase-3 activation in human gastric cancer SGC and HGC, esophageal cancer Eca and Ec cells, and breast cancer MCF-7 xenograft mice [ , , ].

In addition, gene expression analysis identifies that ER stress is the most relevant pathway for the anti-tumor activity of artesunate in B-cell lymphoma [ ]. Interestingly, artesunate selectively inhibits cell growth through iron-dependent and ROS-mediated ferroptosis in human head and neck cancer HN9 cells [ ].

Immunomodulation also plays a vital role in artesunate-mediated anti-cancer effects [ , , , ]. It also exerts anti-tumor effects through suppressing NK killing activity and lymphocyte proliferation, which results in decreased TGF-β1 and IL levels in colorectal cancer Colon and RKO cells [ ].

Besides, artesunate also exerts immunosuppression through forkhead box P3 Foxp3 down-regulation in T cells and decreases prostaglandin E 2 PGE 2 production in human cervical cancer Caski and HeLa cells [ ].

Moreover, it enhances γδ T cell-mediated anti-cancer effect through augmenting γδ T cell cytotoxicity and decreasing TGF-β1 levels to reverse immune escape in human hepatocellular carcinoma HepG2 cells [ ]. The treatment of artesunate with other therapies shows promising anti-cancer effects in several studies [ , , , , ].

Artesunate and cisplatin synergistically induce DNA double-strand breaks and inhibit clonogenic formation to mediate cytotoxic effects in human ovarian cancer A and HO cells [ ]. The combined treatment of artesunate and erlotinib enhances the inhibition of cell growth in human glioblastoma multiforme U87MG cells [ ].

Clinical studies are carried out to investigate the safety and efficacy of artesunate in patients with colorectal and breast cancers, and advanced solid tumor malignancies [ , , , ]. A phase I study is performed to evaluate the safety and the maximum tolerated dose of artesunate in patients with metastatic breast cancer, the oral administration of artesunate is safe and 2.

The tolerability and anti-proliferative properties of oral artesunate are also shown in patients with colorectal cancer [ ]. Moreover, a study of long term treatment with oral artesunate is performed in patients with metastatic breast cancer, 2. An ongoing phase II clinical trial is carried out to study the safety and effectiveness of neoadjuvant artesunate in patients with stage II or III colorectal cancer awaiting surgical treatment.

Wogonin Fig. It has various anti-cancer effects in many cancers, including lung, breast, head and neck, gastric and colorectal cancers, glioma, leukemia, lymphoma, and osteosarcoma, through the induction of apoptosis and cell cycle arrest, and inhibition of cell growth, migration, invasion, and angiogenesis [ , , , , , , , , , , ].

Wogonin can induce apoptosis and inhibit cell proliferation in human neuroblastoma SK-N-BE2 and IMR, NSCLC A, glioma U and U87, and hepatocellular carcinoma HepG2 and Bel cells [ , , , ]. It also induces cell cycle arrest in human colorectal cancer HCT, NSCLC A, chronic myelogenous leukemia imatinib-resistant K, and ovarian cancer A cells [ , , , ].

Besides, wogonin induces autophagy in human pancreatic cells Panc-1 and Colo, and nasopharyngeal carcinoma NPC-TW and NPC-TW cells [ , ]. However, inhibition of autophagy promotes wogonin-induced apoptosis in human nasopharyngeal carcinoma NPC-TW and NPC-TW cells [ ].

Mitochondrial dysfunction, oxidative stress and ER stress play important roles in wogonin-induced anti-cancer effects. Wogonin activates mitochondrial and ER stress-related pathways including the modulation of Bcl-2 family proteins, cytochrome c release, GRP78 and kDa glucose-regulated protein GRP94 accumulation, and caspase activation in human neuroblastoma SK-N-BE2 and IMR cells, and induces mitochondrial dysfunction through IRE1α-dependent pathway [ ].

ER stress markers and downstream pathways are also activated following wogonin treatment in human leukemia HL and osteosarcoma U2OS cells, including IRE1α, PERK-eIF2α, ATF-6, CHOP, GRP94 and GRP78 [ , ].

Wogonin also enhances ROS production in human glioma U and U87, pancreatic cancer Panc-1 and Colo, and NSCLC A cells [ , , ]. Wogonin has immunomodulatory effects in cancer cells. It enhances the recruitment of DCs, T and NK cells into the tumor tissues in gastric cancer MFC xenograft mice, and also down-regulates the level of B7-H1, an immunoglobulin-like immune suppressive molecule, to promote anti-tumor immunity [ ].

Moreover, immunization with wogonin-treated tumor cell vaccine effectively inhibits tumor growth in MFC xenograft mice [ ]. Targeting TNF receptor with wogonin is also suggested to be a potential strategy for the treatment of chronic lymphocytic leukemia [ ].

In order to enhance the accumulation and retention of wogonin in cancer cells, wogonin-conjugated Pt IV pro-drug is developed [ ]. It also further induces cell cycle arrest, enhances ROS production and apoptosis, and decreases mitochondrial membrane potential compared to wogonin in SGC cells [ ].

LW, a derivative of wogonin, inhibits cell proliferation and induces cell cycle arrest in human breast cancer MCF-7 and MDA-MB cells, and suppresses tumor growth in MCF-7 xenograft mice [ ]. A synthetic wogonin derivative, GL-V9, inhibits metastasis in human breast cancer MDA-MB and MCF-7 cells [ ], and induces apoptosis and cell cycle arrest in human hepatocellular carcinoma HepG2 and gastric cancer cells MGC cells [ , , ].

Moreover, targeting cancer cells specifically is an important strategy in cancer therapy, so wogonin-loaded liposomes are synthesized [ ]. These liposomes accumulate in the liver and prolong its retention time and exert better inhibitory effects than wogonin in human hepatocellular carcinoma HepG2 cells.

The combination therapy has been widely used to enhance the anti-cancer effects of wogonin. The combined treatment of wogonin and oxaliplatin synergistically inhibits cell growth in human gastric cancer BGC cells and BGC xenograft zebrafish, through nitrosative stress and disruption of mitochondrial membrane potential [ ].

Wogonin also suppresses sorafenib-induced autophagy to exacerbate apoptosis in human hepatocellular carcinoma Hep3B and Bel cells [ ], and augments cisplatin-induced apoptosis through H 2 O 2 accumulation in human NSCLC A and cervical cancer HeLa cells [ ]. As wogonin has various anti-cancer activities, it is currently under phase I clinical trial to test the safety and efficacy as an anti-cancer drug in China [ ].

β - Elemene Fig. Chen et C. Ling, Rhizoma zedoariae , and Curcuma Zedoary. It has various pharmacological effects including anti-oxidative, anti-inflammatory and anti-cancer activities [ , , ]. It exerts anti-cancer effects in many cancers, such as lung, gastric, cervical, breast and bladder cancers, osteosarcoma, through apoptosis, inhibition of cell proliferation, migration and invasion, angiogenesis [ , , , , , , ].

It up-regulates insulin-like growth factor-binding protein 1 IGFBP1 to induce a reciprocal interaction between microRNA p and FoxO3a, which leads to the inhibition of cell growth in human NSCLC A and H cells [ ].

Moreover, it induces protective autophagy in human gastric cells MGC and SGC, and NSCLC A cells, as autophagy inhibition promotes β-elemene-induced anti-tumor effects [ , ]. However, autophagy inhibition attenuates β-elemene-induced apoptosis in human NSCLC cisplatin-resistant SPC-A-1 cells [ ].

β-Elemene can also inhibit cell migration and invasion in human cervical cancer SiHa, murine breast cancer 4T1 and melanoma B16F10 cells [ , , ], whilst it inhibits cell growth and metastasis through angiogenesis suppression in murine melanoma B16F10 cells [ ]. β-Elemene exerts anti-tumor effects through phosphatase and tensin homolog PTEN up-regulation and Akt suppression in human primary bladder cancer cells [ ].

β-elemene-induced apoptosis is also shown to be through mitochondrial-related pathways, including p21 and Bax up-regulation, caspase-9 activation, Bcl-2 and survivin down-regulation [ ].

ER stress also plays a role in β-elemene-induced apoptosis. β-Elemene up-regulates ER stress markers to induce apoptosis in human NSCLC A cells, including PERK, IRE1α, ATF-6, ATF-4 and CHOP [ ].

Moreover, it also enhances ROS production in human NSCLC A cells [ ], and up-regulates HIF-1α expression via ROS to induce apoptosis in human osteosarcoma MG63 and Saos-2 cells [ ].

β-Elemene has immunomodulatory effects in cancer and immune cells. It inhibits LPS-induced IL-6, TNF-α, IL-1β and IL secretion, as well as inducible nitric oxide synthase in murine RAW M2 macrophages are regarded as tumor-associated macrophages, which can promote tumorigenesis [ ].

β-Elemene can induce the polarization of M2 to M1 macrophages, and can also suppress M2 macrophage-treated conditioned medium-induced cell proliferation, migration and invasion in mouse lung cancer Lewis cells [ ]. β-Elemene has poor water solubility, low oral bioavailability and severe phlebitis, so different delivery systems have been developed to solve these issues [ , , ].

β-Elemene-loaded nanostructured lipid carriers are synthesized to enhance the intravenous delivery of β-elemene, and have higher bioavailiabity [ ]. They inhibit tumor growth compared to β-elemene in hepatocellular carcinoma H22 xenograft mice.

ETME, a novel β-elemene derivative, synergizes with arsenic trioxide to induce cell cycle arrest and apoptosis in human hepatocellular carcinoma SMMC cells, which is dependent on p53 [ ]. Another β-elemene derivative, 13,bis cis-3,5-dimethylpiperazinyl -β-elemene IIi , is shown to inhibit cell proliferation in human gastric cancer SGC and cervical cancer HeLa cells, and inhibit tumor growth in sarcoma S xenograft mice [ ].

It also induces autophagy in human breast cancer MCF-7 cells, so it can be a potential anti-tumor agent. The combination therapy is commonly used to enhance the efficacy of β-elemene for cancer treatment.

β-Elemene when combined with cisplatin synergistically enhances apoptosis and inhibits cell proliferation in human gingival squamous cell carcinoma YD cells and YD xenograft mice [ ].

β-Elemene potentiates the anti-proliferation effect of gefitinib as well as the induction of apoptosis and autophagy in human glioblastoma multiforme U and U87MG cells, through inhibiting EGFR signaling pathway [ ]. CEP Fig. With the presence of a 1-benzylisoquinoline moiety on alkyl chain, CEP belongs to a class of compounds called biscoclaurine alkaloids that have attracted significant attentions to pharmacologists and clinicians due to their resemblance to polypeptides [ ].

CEP is widely used in Japan for the treatment of many acute and chronic diseases [ ]. It exhibits anti-malarial, anti-viral, anti-inflammatory, anti-metastatic, and anti-cancer activities in various cell lines and animal models [ , , , ].

Among its anti-cancer activities, CEP exhibits multiple pharmacological actions, including apoptosis and radiation sensitization, inhibition of angiogenesis and metastasis, and reversing MDR [ , , , , , , , , , , , , , ].

CEP induces apoptosis and cell cycle arrest in many types of cancer cells [ , , , , ]. In contrast, the inhibition of autophagy is an effective treatment for NSCLC, and CEP is identified as a novel autophagic inhibitor in human NSCLC NCI-H cells [ ]. It inhibits autophagy by preventing autophagosome—lysosome fusion and inhibiting lysosomal cathepsin B and cathepsin D maturation.

Therefore, this suggests that autophagy plays a dual role in cancer via different signaling routes. Moreover, CEP is suggested to be a potential anti-angiogenic agent, it blocks angiogenesis in endothelial cells, zebrafish and xenograft mice by inhibiting cholesterol trafficking [ ].

It can also suppress metastasis in a highly metastatic tumor, cholangiocarcinoma, and markedly inhibit cell migration in human cholangiocarcinoma KKU-M and KKU-M cells [ ]. CEP has anti-tumor action mainly by inducing apoptosis and ROS production [ , , ].

ROS is shown to be an important factor to determine cell fate, and it can be regulated by p21 [ ]. CEP efficiently inhibits the growth of pmutated colorectal cancer cells that are often resistant to commonly used chemotherapeutic agents [ ].

Similarly, CEP triggers apoptosis via ROS production and reducing mitochondrial membrane potential, thus inducing caspase-3 and PARP activation in human NSCLC H and A cells [ ]. It also exerts anti-tumor activity through ROS production and JNK activation in human choroidal melanoma MEL cells and xenograft mice [ ].

In addition, CEP is also a potential anti-cancer drug for ovarian cancer by markedly increasing p21 expression and decreasing cyclins A and D levels in human ovarian cancer CaOV-3 and OVCAR3 cells [ ]. CEP also plays an important role in immunity.

It is shown to reduce IL-6 and TNF-α secretion in LPS-stimulated DCs, and inhibits LPS-stimulated DC maturation and antigen uptake by DCs [ ].

CEP-treated DCs becomes a poor stimulator of allogeneic T cell activation and reduces IFN-γ production [ ]. Therefore, it is suggested that CEP may have potential to be a cancer immunomodulatory agent.

Targeting P-gp using P-gp inhibitors is one of the main strategies to reverse MDR, and cepharanthine hydrochloride CEH , a salt form of CEP, is suggested to be a potent P-gp inhibitor [ ].

CEH exhibits MDR reversal potency in various cancer cells [ , , , ]. CEH can reverse MDR-mediated cisplatin resistance in esophageal squamous cell carcinoma [ ].

It increases the sensitivity of the cells and induces apoptosis via c-Jun activation, thus down-regulating P-gp and enhancing p21 levels. In addition, by reversing MDR, CEH induces cell cycle arrest and apoptosis in human nasopharyngeal carcinoma CNE-1 and CNE-2 cells [ ].

In addition to chemotherapy, CEP may act as a radiosensitizer. Radiotherapy in the presence of CEP exhibits significant enhancement of tumor responses in human oral squamous cell carcinoma [ ].

This pre-clinical data indicates that CEP has the potential to be used in clinical settings in combination with radiotherapy to treat oral squamous cell carcinoma.

Moreover, paclitaxel and CEP co-loaded nano-particles also enhance the anti-cancer effects in human gastric cancer MKN45 cells and xenograft mice, suggesting that these nano-particles could be a potential formulation for gastric cancer [ ].

In addition, CEP enhances the anti-cancer effects of dacomitinib in human NSCLC NCI-H cells and NCI-H xenograft mice [ ], and cisplatin in lung and breast xenograft mice [ ].

Although CEP has not yet been translated into clinical use for the treatment of cancer, the pharmacological activities and pre-clinical data support its significant clinical potential for anti-cancer therapy. Chinese herbal medicine has played, and still plays, an important role in human health care in China and other Asian countries.

Chinese herbal medicine is also recognized worldwide as a rich source for the discovery of novel drugs in the past decades. Table 1 illustrates the experimental models and conditions, pharmacological effects, as well as mechanistic actions of the natural compounds derived from Chinese herbal medicine.

Despite the unique anti-cancer beneficial features of many compounds derived from Chinese herbal medicine, their clinical applications are disproportionally limited. As of , only preliminary clinical studies have been performed with artemisinins, emodin, cucurbitacins, tanshiones, shikonin, and CEP in various cancers, without any approved clinical applications.

The phase I safety studies of UA-liposomes, oridonin derivative HAO , and wogonin were evaluated in patients with advanced solid tumors. The phase II clinical trials of berberine hydrochloride, ginsenoside Rg3, and artesunate are being conducted in patients with cancer.

EGCG was shown to have potential anti-cancer effects in a phase III clinical trial. Based on our critical review of those clinical studies, we conclude that Chinese herbal medicine is a promising source and could be used as a complementary approach for cancer therapy.

We believe that as the evidence for safety and efficacy continues to develop, this will improve the understanding about the mechanistic actions and clinical potential of these compounds. Chinese herbal medicine will also serve as a huge community from which many promising compounds will be developed for clinical use.

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Anti-inflammatory activities of Sigesbeckia glabrescens Makino: combined in vitro and in silico investigations.

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Curcuminoids induce reactive oxygen species and autophagy to enhance apoptosis in human oral cancer cells. Am J Chin Med. Article CAS PubMed Google Scholar. Wang N, Tan HY, Li L, Yuen MF, Feng Y. Berberine and Coptidis Rhizoma as potential anticancer agents: recent updates and future perspectives.

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Int J Biol Macromol. 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.

Types of alternative therapy There are many types of alternative therapy. These include: amygdalin Laetrile ® , Vitamin B17 Essiac ® Vitaltea ® , Flor-essence ® cannabis oil or CBD oil metabolic therapy diets that claim to treat cancer megavitamin therapy.

Amygdalin Laetrile®, vitamin B17 Amygdalin is a compound found in bitter almonds, peach stones and apricot stones. Why some people use laetrile Many websites that sell Laetrile claim it can slow or stop the growth of cancer.