Prescription drugs derived from the Artemisia annua plant show very limited benefit in improving cancer treatment outcomes.

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This section does not replicate the other information on this topic but provides additional details or context most relevant to professionals.

Mode of action: interaction with iron

Artemisinin’s anticancer activity is believed to occur when it comes in contact with iron. Cancer cells concentrate iron for use in cellular division (the malaria parasite also collects high concentrations of iron). Artemisinin’s contact with iron triggers the release of free radicals between cells that destroy cancer cells. Because of this “ferroptosis” effect, iron is often administered several hours before artemisinin to enhance targeting the cancer cells while sparing normal cells.1Hu Y, Guo N et al. The potential mechanisms by which artemisinin and its derivatives induce ferroptosis in the treatment of cancer. Oxidative Medicine and Cellular Longevity. 2022 Jan 4;2022:1458143; Crespo-Ortiz MP, Wei MQ. Antitumor activity of artemisinin and its derivatives: from a well-known antimalarial agent to a potential anticancer drug. Journal of Biomedicine and Biotechnology. 2012;2012:247597. In addition, several other pathways for the anti-cancer modes of action of artesunate and artemisinin derivatives have been studied. These include growth inhibition through cell cycle arrest, apoptosis of cancer cells, inhibition of angiogenesis, disruption of cell migration and modulation of nuclear receptor responsiveness.2Firestone GL, Sundar SN. Anticancer activities of artemisinin and its bioactive derivatives. Expert Reviews in Molecular Medicine. 2009 Oct 30;11:e32.

Preclinical evidence

Notable preclinical evidence is listed here; clinical evidence is in How can artemisinin-based drugs help you? What the research says ›

Improving treatment outcomes

Cancer as a whole
  • Artesunate enhanced the anticancer activity of doxorubicin, temozolomide, and erlotinib and sensitized tumor cells to cisplatin in preclinical studies.3Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Dihydroartemisinin (DHA) enhanced anticancer activity of doxorubicin, cisplatin, carboplatin, temozolomide, gemcitabine, cytarabine, and dexamethasone in preclinical studies.4Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Ethacrynic acid and L-buthionine sulfoximine sensitized MSV-HL13 cells to artesunate in preclinical studies.5Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
Brain cancer
  • Artesunate and dihydroartemisinin (DHA) each sensitized glioblastoma cells to radiotherapy in preclinical trials.6Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artemether enhanced the anticancer activity of VCAM1 shRNA against glioblastoma cells in preclinical trials.7Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artemisone enhanced the anticancer activity of oxaliplatin against glioma cells in preclinical trials.8Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
Breast cancer 
  • Artemisone enhanced the anticancer activity of either oxaliplatin, gemcitabine, or thalidomide against breast cancer cells in preclinical trials.9Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artesunate enhanced apoptosis in MCF-7 breast cancer cells in vitro via lysosome-dependent mitochondrial outer membrane permeabilization.10Hamacher-Brady A, Stein HA et al. Artesunate activates mitochondrial apoptosis in breast cancer cells via iron-catalyzed lysosomal reactive oxygen species production. Journal of Biological Chemistry. 2011 Feb 25;286(8):6587-601.
  • Resistance to artesunate was induced in highly metastatic breast cancer cell line (MDA-MB-231) but not in a cell line that was less tumorogenic (MDA-MB-468) in preclinical trials.11Bachmeier B, Fichtner I et al. Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells. PLOS ONE. 2011;6(5):e20550.
  • Anticancer activity in breast cancer cell lines treated with artemisinin derivatives12Kumar MS, Yadav TT, Khair RR, Peters GJ, Yergeri MC. Combination therapies of artemisinin and its derivatives as a viable approach for future cancer treatment. Current Pharmaceutical Design. 2019;25(31):3323–3338.
Cervical cancer
  • Artesunate sensitized cervical cancer cells to radiotherapy in preclinical trials.13Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artesunate enhanced the anticancer activity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) against cervical cancer cells in preclinical studies.14Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • DHA enhanced the anticancer activity of PARK7 siRNA or p8 siRNA against cervical cancer cells in preclinical trials.15Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
Colorectal cancer
  • Dihydroartemisinin (DHA) enhanced the anticancer activity of VCAM1 shRNA or p8 siRNA against colon cancer cells in preclinical trials.16Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artemisone enhanced the anticancer activity of either oxaliplatin, gemcitabine, or thalidomide against colon cancer cells in preclinical trials.17Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • DHA exerted an anticancer effect against several CRC cell lines and restored cancer cell sensitivity to 5-FU in a p53 knockout CRC HCT116 cell line in preclinical studies.18Yao Z, Bhandari A et al. Dihydroartemisinin potentiates antitumor activity of 5-fluorouracil against a resistant colorectal cancer cell line. Biochemical and Biophysical Research Communications. 2018;501(3):636–642.
  • Many artemisinin derivatives have been synthesized and show cytotoxic activity against HCT116 and WM-266-4 CRC cell lines in vitro.19Wang LL, Kong L et al. Design and synthesis of novel artemisinin derivatives with potent activities against colorectal cancer in vitro and in vivo. European Journal of Medicinal Chemistry. 2019;182:111665.
  • Synthesized thymoquinone-artemisinin hybrid drugs selectively decreased the viability of HCT116 and HT29 CRC cell lines in vitro. The hybrid labeled 7a performed better than 5-fluorouracil at suppressing these cell lines in vitro.20Fröhlich T, Ndreshkjana B et al. Synthesis of novel hybrids of thymoquinone and artemisinin with high activity and selectivity against colon cancer. ChemMedChem. 2017;12(3):226–234.
  • Artesunate inhibited proliferation of HCT116 CRC cell lines in vitro and in vivo (in mice) by inducing apoptosis and autophagy. When autophagy was pharmacologically blocked, apoptosis was increased even further.21Jiang F, Zhou JY, Zhang D, Liu MH, Chen YG. Artesunate induces apoptosis and autophagy in HCT116 colon cancer cells, and autophagy inhibition enhances the artesunate‑induced apoptosis. International Journal of Molecular Medicine. 2018;42(3):1295–1304.
  • Dihydroartemisinin (DHA) reduced viability of HCT116 CRC cell lines in vitro. The study suggests the mechanisms include G1 cell cycle arrest, apoptotic cell death, accumulation of reactive oxygen species (ROS).22Lu M, Sun L, Zhou J, Yang J. Dihydroartemisinin induces apoptosis in colorectal cancer cells through the mitochondria-dependent pathway. Tumor Biology. 2014;35(6):5307–5314.
  • Orally administered artesunate reduced pre-neoplastic changes comparable to aspirin in rats treated with dimethylhydrazine (DMH) to induce colon carcinogenesis. It could not be determined if a control group was included in the study.23Verma S, Das P, Kumar VL. Chemoprevention by artesunate in a preclinical model of colorectal cancer involves down regulation of β-catenin, suppression of angiogenesis, cellular proliferation and induction of apoptosis. Chemico-Biological Interactions. 2017;278:84–91.
  • Artesunate significantly inhibited HCT116 CRC cell viability in a dose dependent manner. The study suggested that the mechanisms of action included suppressing the fatty acid biosynthetic pathway and activating the mitochondrial apoptosis pathway.24Chen X, Wong YK et al. Artesunate activates the intrinsic apoptosis of HCT116 cells through the suppression of fatty acid synthesis and the NF-κB pathway. Molecules. 2017;22(8):1272.
  • 10-(4-phenyl-1H-1,2,3- triazol)-artemisinin (5a) controlled acquired drug resistance and recovered the anticancer effect of paclitaxel on cancer cells in vitro.25Lee DH, Hasanuzzaman M et al. 10-phenylpyrazole artemisinin is a novel P-glycoprotein inhibitor that suppresses the overexpression and function of P-glycoprotein. Current Pharmaceutical Design. 2018;24(46):5590–5597.
  • Anticancer activity in colorectal cancer cell lines treated with artemisinin derivatives26Kumar MS, Yadav TT, Khair RR, Peters GJ, Yergeri MC. Combination therapies of artemisinin and its derivatives as a viable approach for future cancer treatment. Current Pharmaceutical Design. 2019;25(31):3323–3338.
Endometrial cancer
Endothelial cancer
  • Artesunate enhanced cytotoxic activity of captopril against HUVEC endothelial cells in preclinical studies28Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
Gastric cancer
  • Artesunate inhibited the growth of gastric cancer cell lines SGC-7901, BGC-823, and AGS but had no effect on GES-1 cells in vitro and caused a dose dependent tumor regression in mice.29Zhou X, Sun WJ et al. Artesunate inhibits the growth of gastric cancer cells through the mechanism of promoting oncosis both in vitro and in vivo. Anticancer Drugs. 2013 Oct;24(9):920-7.
Leukemia
  • DHA had a synergistic interaction with 6PGD inhibitors Physcion and S3 against leukemia cells in preclinical studies.30Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70. 
  • Artesunate inhibited growth of leukemia cells when used with arsenic trioxide in preclinical studies.31Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70. 
  • Dihydroartemisinin (DHA) had a synergistic interaction with 6PGD inhibitors physcion and S3 against leukemia cells in preclinical studies32Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70. 
  • DHA had an additive interaction with sodium salicylate against leukemia cells in preclinical studies.33Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70. 
  • DHA enhanced the anticancer action of vitamin C and vitamin D3 against leukemia cells in preclinical studies.34Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70. 
  • Anticancer activity in leukemia cell lines treated with artemisinin derivatives35Kumar MS, Yadav TT, Khair RR, Peters GJ, Yergeri MC. Combination therapies of artemisinin and its derivatives as a viable approach for future cancer treatment. Current Pharmaceutical Design. 2019;25(31):3323–3338.
Liver cancer
  • Dihydroartemisinin (DHA) increased efficacy of gemcitabine against human hepatoma cells.36Hou J, Wang D, Zhang R, Wang H. Experimental therapy of hepatoma with artemisinin and its derivatives: in vitro and in vivo activity, chemosensitization, and mechanisms of action. Clinical Cancer Research. 2008 Sep 1;14(17):5519-30.
  • DHA enhanced the anticancer activity of p8 siRNA against liver cancer cells in preclinical trials.37Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artesunate inhibited solid tumor growth in vivo and increased survival of mice bearing H22 ascitic liver tumors. There was also evidence of cytotoxicity to human hepatocarcinoma SMMC-7721 cell line in vitro.38Wang Q, Wu LM, Li AY, Zhao Y, Wang NP. [Experimental studies of antitumor effect of artesunate on liver cancer]. [Article in Chinese]. Zhongguo Zhong Yao Za Zhi. 2001 Oct;26(10):707-8, 720.
  • Artesunate downregulated vascular endothelial growth factor and placental growth factor expression and reduced viability in HepG2 and BWTG3 cell lines in vitro. It also decreased vessel density and tumor burden in mice (in vivo).39in vitroVandewynckel YP, Laukens D et al. Therapeutic effects of artesunate in hepatocellular carcinoma: repurposing an ancient antimalarial agent. European Journal of Gastroenterology and Hepatology. 2014 Aug;26(8):861-70.
  • Anticancer activity in hepatocellular carcinoma cell lines treated with artemisinin derivatives40Kumar MS, Yadav TT, Khair RR, Peters GJ, Yergeri MC. Combination therapies of artemisinin and its derivatives as a viable approach for future cancer treatment. Current Pharmaceutical Design. 2019;25(31):3323–3338.
Lung cancer
  • Artesunate and dihydroartemisinin (DHA) each sensitized lung cancer cells to radiotherapy in preclinical trials.41Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artemisone enhanced the anticancer activity of either oxaliplatin or gemcitabine against pancreatic cancer cells in preclinical trials.42Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artesunate, DHA, and other artemisinin derivatives led to lower colony formation, less proliferation, greater apoptosis, and other anticancer activity in preclinical studies.43Cheong DHJ, Tan DWS, Wong FWS, Tran T. Anti-malarial drug, artemisinin and its derivatives for the treatment of respiratory diseases. Pharmacological Research. 2020 Aug;158:104901. 
Lymphoma
  • Artesunate enhanced anticancer activity of rituximab against B-cell lymphoma cells in preclinical studies.44Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
Oral squamous cell carcinoma
  • Artemisinin promotes apoptosis in HPV 16 immortalized and transformed human gingival epithelial (IHGK) cells.45Yamachika E, Habte T, Oda D. Artemisinin: an alternative treatment for oral squamous cell carcinoma. Anticancer Research. 2004 Jul-Aug;24(4):2153-60.
Ovarian cancer
  • Dihydroartemisinin (DHA) enhanced the anticancer activity of p8 siRNA against ovarian cancer cells in preclinical trials.46Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artesunate and DHA both inhibited SKOV3 and epithelial ovarian cancer (EOC) cell growth via G2/M cell cycle arrest, induced autophagy and disruption of the NF-kappaB signaling pathway in EOC cells in vitro.47Li B, Bu S, Sun J, Guo Y, Lai D. Artemisinin derivatives inhibit epithelial ovarian cancer cells via autophagy-mediated cell cycle arrest. Acta Biochimica et Biophysica Sinica (Shanghai). 2018 Dec 1;50(12):1227-1235.
  • DHA significantly inhibited proliferation, migration, and invasion of ovarian cancer cells and induced apoptosis in vitro but had few effects on cell proliferation and apoptosis in human ovarian surface epithelial cells.48Liu Y, Gao S et al. Dihydroartemisinin induces apoptosis and inhibits proliferation, migration, and invasion in epithelial ovarian cancer via inhibition of the hedgehog signaling pathway. Cancer Medicine. 2018 Nov;7(11):5704-5715.
  • DHA directly targets platelet-derived growth factor receptor-alpha (PDGFR𝛼) to inhibit ovarian cancer cell growth and metastasis.49Li X, Ba Q et al. Dihydroartemisinin selectively inhibits PDGFRα-positive ovarian cancer growth and metastasis through inducing degradation of PDGFRα protein. Cell Discovery. 2017 Nov 21;3:17042.
  • Artesunate treatment showed strong induction of reactive oxygen species (ROS) and reduced proliferation of ovarian cancer cells in vitro and a decrease of tumor growth in a mouse model of ovarian cancer (in vivo).50Greenshields AL, Shepherd TG, Hoskin DW. Contribution of reactive oxygen species to ovarian cancer cell growth arrest and killing by the anti-malarial drug artesunate. Molecular Carcinogenesis. 2017 Jan;56(1):75-93.
  • DHA enhanced toxicity to human ovarian cancer cells without appreciable toxicity to normal cells when conjugated with the chemotherapy drug melphalan in ARS4.51Li X, Zhou Y et al. Preclinical efficacy and safety assessment of artemisinin-chemotherapeutic agent conjugates for ovarian cancer. EBioMedicine. 2016 Dec;14:44-54.
  • Combined treatment of DHA and Curcumin synergistically decreased cell viability, arrested cell cycle, and promoted apoptosis in SKOV3 cells in vitro. The combined DHA-curcumin treatment also significantly inhibited tumor growth in mice (in vivo).52Zhao J, Pan Y et al. Dihydroartemisinin and curcumin synergistically induce apoptosis in SKOV3 cells via upregulation of MiR-124 targeting midkine. Cell Physiology and Biochemistry. 2017;43(2):589-601.
Pancreatic cancer
  • Artesunate inhibited growth of pancreatic cancer cells when used with triptolide in preclinical studies.53Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70. 
  • Dihydroartemisinin (DHA) enhanced the anticancer activity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) against prostate cancer cells in preclinical studies.54Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artemisone enhanced the anticancer activity of either oxaliplatin, gemcitabine, or thalidomide against pancreatic cancer cells in preclinical trials.55Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
  • Artesunate produced dose-dependent tumor regression in vivo in a pancreatic cancer xenografts model in mice that was comparable to gemcitabine. In vitro, artesunate demonstrated loss of mitochondrial membrane potential, cell lysis and other cytotoxic activity against Panc-1, BxPC-3 and CFPAC-1 pancreatic cancer cell lines.56Du JH, Zhang HD, Ma ZJ, Ji KM. Artesunate induces oncosis-like cell death in vitro and has antitumor activity against pancreatic cancer xenografts in vivo. Cancer Chemotherapy and Pharmacology. 2010 Apr;65(5):895-902.
Prostate cancer
  • Dihydroartemisinin (DHA) enhanced the anticancer activity of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) against prostate cancer cells in preclinical studies.57Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70.
Renal cell carcinoma
Sarcoma
  • Artesunate inhibited growth of osteosarcoma cells when used with allicin in preclinical studies.59Efferth T. Cancer combination therapies with artemisinin-type drugs. Biochemical Pharmacology. 2017 Sep 1;139:56-70. 
Artesunate combined with other therapies

Optimizing body terrain

Body weight
  • Less weight loss and less severe histopathologic liver changes in liver cirrhosis-induced rats treated with artesunate compared to liver cirrhosis induced rats not treated with artesunate.61Chen YX, Lai LN et al. Effect of artesunate supplementation on bacterial translocation and dysbiosis of gut microbiota in rats with liver cirrhosis. World Journal of Gastroenterology. 2016 Mar 14;22(10):2949-59.
Immune function
  • Fewer parasitic lesions in chicks treated with artemisinin62Allen PC, Lydon J, Danforth HD. Effects of components of Artemisia annua on coccidia infections in chickens. Poultry Science. 1997 Aug;76(8):1156-63.
Inflammation
  • Lower markers of inflammation among cell lines and animals treated with artesunate, dihydroartemisinin (DHA), or other artemisinin derivatives in preclinical studies63Cheong DHJ, Tan DWS, Wong FWS, Tran T. Anti-malarial drug, artemisinin and its derivatives for the treatment of respiratory diseases. Pharmacological Research. 2020 Aug;158:104901. 
  • Lower levels of inflammation among cell lines and animals treated with artesunate in preclinical studies64Cheong DHJ, Tan DWS, Wong FWS, Tran T. Anti-malarial drug, artemisinin and its derivatives for the treatment of respiratory diseases. Pharmacological Research. 2020 Aug;158:104901. 
  • Artemisinin attenuated renal function decline and reduced tubulointerstitial inflammation and fibrosis in subtotal nephrectomized rats. In vitro, artemisinin pretreatment prevented activation of inflammasomes and NF-kappaB in human kidney 2 (HK-2) cells that were induced to inflammatory injury with Ang II.65Wen Y, Pan MM et al. Artemisinin attenuates tubulointerstitial inflammation and fibrosis via the NF-κB/NLRP3 pathway in rats with 5/6 subtotal nephrectomy. Journal of Cellular Biochemistry. 2019 Mar;120(3):4291-4300.
  • Improved markers of inflammation among mice pretreated with artesunate for 7 days before inducing inflammation by injection of the inflammatory substance lipopolysaccharide (LPS) compared to mice not pretreated with artesunate before injection with LPS.66Mancuso RI, Azambuja JH, Olalla Saad ST. Artesunate strongly modulates myeloid and regulatory T cells to prevent LPS-induced systemic inflammation. Biomedicine & Pharmacotherapy. 2021 Nov;143:112211.
Oxidation
  • Artesunate likely induces apoptosis through expression of reactive oxygen species in the presence of iron.67Tsuda K, Miyamoto L et al. Mechanisms of the pH- and oxygen-dependent oxidation activities of artesunate. Biological and Pharmaceutical Bulletin. 2018;41(4):555-563.
  • Lower levels of oxidation among cell lines and animals treated with artesunate, dihydroartemisinin (DHA), or other artemisinin derivatives in preclinical studies68Cheong DHJ, Tan DWS, Wong FWS, Tran T. Anti-malarial drug, artemisinin and its derivatives for the treatment of respiratory diseases. Pharmacological Research. 2020 Aug;158:104901. 

Helpful links for professionals

Bora KS, Sharma A. The genus Artemisia: a comprehensive review. Pharmaceutical Biology. 2011 Jan;49(1):101-9.

Zyad A, Tilaoui M, Jaafari A, Oukerrou MA, Mouse HA. More insights into the pharmacological effects of artemisinin. Phytotherapy Research. 2017 Nov 28.

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Authors

Andrew Jackson, ND

Research Associate
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Andrew Jackson, ND, serves as a CancerChoices research associate. As a naturopathic physician practicing in Kirkland, Washington, he teaches critical evaluation of the medical literture at Bastyr University in Kenmore, Washington. His great appreciation of scientific inquiry and the scientific process has led him to view research with a critical eye.

Andrew Jackson, ND Research Associate

Nancy Hepp, MS

Lead Researcher
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Ms. Hepp is a researcher and communicator who has been writing and editing educational content on varied health topics for more than 20 years. She serves as lead researcher and writer for CancerChoices and also served as the first program manager. Her graduate work in research and cognitive psychology, her master’s degree in instructional design, and her certificate in web design have all guided her in writing and presenting information for a wide variety of audiences and uses. Nancy’s service as faculty development coordinator in the Department of Family Medicine at Wright State University also provided experience in medical research, plus insights into medical education and medical care from the professional’s perspective.

Nancy Hepp, MS Lead Researcher

Reviewer

Laura Pole, MSN, RN, OCNS

Senior Clinical Consultant
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Laura Pole is senior clinical consultant for CancerChoices. Laura is an oncology clinical nurse specialist who has been providing integrative oncology clinical care, navigation, consultation, and education services for over 40 years. She is the co-creator and co-coordinator of the Integrative Oncology Navigation Training at Smith Center for Healing and the Arts in Washington, DC. Laura also manages the “Media Watch Cancer News That You Can Use” listserv for Smith Center/Commonweal. In her role as a palliative care educator and consultant, Laura has served as statewide Respecting Choices Faculty for the Virginia POST (Physician Orders for Scope of Treatment) Collaborative as well as provided statewide professional education on palliative and end-of-life care for the Virginia Association for Hospices and Palliative Care.

For CancerChoices, Laura curates content and research, networks with clinical and organizational partners, brings awareness and education of integrative oncology at professional and patient conferences and programs, and translates research into information relevant to the patient experience as well as clinical practice.

Laura sees her work with CancerChoices as a perfect alignment of all her passions, knowledge and skills in integrative oncology care. She is honored to serve you.

Laura Pole, MSN, RN, OCNS Senior Clinical Consultant

Last update: May 9, 2024

Last full literature review: October 2022

CancerChoices provides information about integrative in cancer care, a patient-centered approach combining the best of conventional care, self care and evidence-informed complementary care in an integrated plan cancer care. We review complementaryin cancer care, complementary care involves the use of therapies intended to enhance or add to standard conventional treatments; examples include supplements, mind-body approaches such as yoga or psychosocial therapy, and acupuncture therapies and self-care lifestyle actions and behaviors that may impact cancer outcomes; examples include eating health-promoting foods, limiting alcohol, increasing physical activity, and managing stress practices to help patients and professionals explore and integrate the best combination of conventionalthe cancer care offered by conventionally trained physicians and most hospitals; examples are chemotherapy, surgery, and radiotherapy and complementary therapies and practices for each person.

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