Zhou J, Vallejo J, Kluetz P, Anti-cancdr al. Cancer Centre in Vancouver and Princess Margaret Cancer Centre in Toronto. Qazi, A.

Anti-cancer research studies -

For example:. Does the treatment work for everyone with a specific illness? Or does it only work for some people? There are always many cancer clinical trials going on. This is because doctors and researchers are always trying to find new and better ways to treat cancer and to care for people diagnosed with cancer.

Clinical trials may be an option for treatment for anyone with cancer. Talk with your health care team about your treatment options. Learn more about how to find cancer clinical trials. First, talk with your cancer care doctor about whether or not treatment through a clinical trial is an option for you.

They can help you find clinical trials that are open to you see "How do doctors decide if I can be in a clinical trial? You can also see which clinical trials are searching for volunteers right now. There are many different online databases that can help you find this information.

There are also programs that will match you with a clinical trial. Learn more about how to find a cancer clinical trial. Each clinical trial follows a specific set of rules.

Doctors call these rules the "protocol. What questionnaires participants will be asked to complete to track how they are feeling and functioning.

There are 3 main phases of a clinical trial: phase I, phase II, and phase III. Doctors gather different information about the treatment in each phase. Clinical trial phases are different from cancer stages. Staging a tumor tell you how much cancer there is and how far it has spread.

Clinical trial phases describe different things doctors are studying about a new drug or treatment. You do not have to go through each phase of a clinical trial.

The phase only describes where the researchers are in the process of studying a new treatment or topic. Learn more about the phases of clinical trials. If you choose to join a clinical trial, the study's researchers will check if that specific clinical trial is right for you.

To decide who can join a specific clinical trial, they look for volunteers who have certain things in common. This may include:. Together, a study's requirements on who can or cannot join are called the eligibility criteria. For example, some clinical trials focus on how treatments affect adults age 65 and older.

If you are younger than 65, that study is not right for you. But you may be able to join a different one. Learn more about eligibility criteria for cancer clinical trials. When you decide to join a cancer clinical trial, the study's researchers and staff will provide you with many details about that clinical trial.

When you meet them about the clinical trial and throughout the clinical trial, make sure you:. Tell the research team if you have a new health problem.

It could be a side effect of the clinical trial treatment. It is important to let the research team know about any changes to your health during the clinical trial and later. This will help them keep you safe. Clinical trial volunteers may decide to stop participating in the study at any time, for any reason.

If you join a clinical trial, the doctor and other health care staff will check your health regularly during the clinical trial. Clinical trial staff include nurses, researchers, and other health care professionals. Before you start a clinical trial, the staff will answer any questions you have.

They will review all the clinical trial information with you. If you decide to join the clinical trial, they will help you join, called enrollment.

During the clinical trial, the research team will check your health regularly. They will tell you about any tests and procedures you need. The staff may check on you for several weeks, months, or even years.

They want to know how you are feeling, how well the treatment works, how long it works, and if it causes any problems. Learn more about patient safety during clinical trials.

In some clinical trials, the research team knows what treatment you get, but you do not. In other clinical trials, no one knows, including the research team, until the study is complete and all data are analyzed.

This can sometimes take years. And sometimes, everyone knows, including the patients. Talk with the research team ahead of time about the structure of the study you are interested in joining.

Sometimes, placebos are used during cancer clinical trials. A placebo is a drug or treatment that is not active.

It is sometimes called a "sugar pill. This means the participant will be receiving the standard of care for that type of cancer. When researchers use a placebo, they must:. Tell them if they will receive an experimental treatment at some point in the clinical trial, if not right away.

Learn more about how placebos are used in cancer clinical trials. You can join a clinical trial at any point during your cancer treatment. If you join one, you will receive the same level of care as with regular cancer treatment.

People join cancer clinical trials for many different reasons. For some, a clinical trial is the best treatment option available. Others are willing to face the added uncertainty of a clinical trial because standard treatments are not perfect and they are hoping for a better result.

Others volunteer for clinical trials because they know that these studies are a way to contribute to progress in treating cancer. Clinical trials need people of all ages. Right now, more children join clinical trials than adults.

About half of these adults live a long time after cancer. You can stop participating in a clinical trial at any time. This includes if your cancer gets worse while receiving treatment as part of a clinical trial.

If you decide to leave the clinical trial, you will discuss with your cancer care team your treatment options. Learn more about patient safety during cancer clinical trials. If you are in the United States, you may have concerns about whether or not your cancer care is covered by health insurance if you join a clinical trial.

Recent changes to the U. health care laws mean that most routine care costs from clinical trials are covered by most health insurance policies, including Medicaid. Other costs are covered by the study's researchers or sponsor.

Before deciding to join a cancer clinical trial, talk with the researchers and your insurance company to confirm what costs are covered and who will cover them. Learn more about health insurance coverage of clinical trials.

You may have many questions about what happens when a cancer clinical trial ends. For example, you may wonder if you can continue receiving the treatment or if there are additional clinical trials you can participate in.

What happens next depends on the type of trial you are participating in and the results of the study. But you should always be informed about your options before the clinical trial begins. It can take time for a drug that was studied in a clinical trial to be approved by the FDA and become available to the public.

Because of this, it is important to know what your options are after the clinical trial has ended. Sometimes, the manufacturer of the treatment makes the treatment available to clinical trial volunteers when the study is over.

Other times, the manufacturer can make the treatment available to purchase, though insurance may not cover this cost. In other cases, the drug or treatment tested during the clinical trial may not be available. The results showed that the drug was so effective that the results need to be presented right away.

It would be unfair to continue the clinical trial for the people in the control group receiving the current standard of care. Before you decide to participate in a clinical trial, ask what will happen if the trial has to end for any reason.

Ask how the information will be shared with you. You can watch a free series of educational videos on Cancer. The series is called Preparatory Education About Clinical Trials, or PRE-ACT. Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A.

Global cancer statistics GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in countries. CA Cancer J Clin. Article PubMed Google Scholar.

Baskar R, Lee KA, Yeo R, Yeoh K-W. Cancer and radiation therapy: current advances and future directions. Int J Med Sci. Article PubMed PubMed Central Google Scholar.

Palumbo MO, Kavan P, Miller WH, Panasci L, Assouline S, Johnson N, et al. Systemic cancer therapy: achievements and challenges that lie ahead. Front Pharmacol. Article PubMed PubMed Central CAS Google Scholar. Schuck A, Konemann S, Heinen K, Rube CE, Hesselmann S, Reinartz G, et al. Microscopic residual disease is a risk factor in the primary treatment of breast cancer.

Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft. Article Google Scholar. Jacobson LK, Johnson MB, Dedhia RD, Niknam-Bienia S, Wong AK. Impaired wound healing after radiation therapy: a systematic review of pathogenesis and treatment.

JPRAS Open. Formenti SC, Demaria S. Systemic effects of local radiotherapy. Lancet Oncol. Malhotra V, Perry MC. Classical chemotherapy: mechanisms, toxicities and the therapeutic window. Cancer Biol Ther.

PubMed Google Scholar. Hoelder S, Clarke PA, Workman P. Discovery of small molecule cancer drugs: successes, challenges and opportunities.

Mol Oncol. Article CAS PubMed PubMed Central Google Scholar. Hojjat-Farsangi M. Small-molecule inhibitors of the receptor tyrosine kinases: promising tools for targeted Cancer therapies. Int J Mol Sci.

Eck MJ, Manley PW. The interplay of structural information and functional studies in kinase drug design: insights from BCR-Abl. Curr Opin Cell Biol. Article CAS PubMed Google Scholar. Iqbal N, Iqbal N. Imatinib: a breakthrough of targeted therapy in Cancer. Chemother Res Pract. PubMed PubMed Central Google Scholar.

Lavanya V, Mohamed Adil AA, Ahmed N, Rishi AK, Jamal S. Small molecule inhibitors as emerging cancer therapeutics. Integr Cancer Sci Therap. Google Scholar. Lambert JM. Drug-conjugated monoclonal antibodies for the treatment of cancer. Curr Opin Pharmacol. Argyriou AA, Kalofonos HP.

Recent advances relating to the clinical application of naked monoclonal antibodies in solid tumors. Mol Med. Jacobs SA. CAS PubMed PubMed Central Google Scholar. van de Donk NWCJ, Dhimolea E. Brentuximab vedotin. Baron JM, Boster BL, Barnett CM. Ado-trastuzumab emtansine T-DM1 : a novel antibody-drug conjugate for the treatment of HER2-positive metastatic breast cancer.

J Oncol Pharm Pract. Hoffman LM, Gore L. Front Oncol. Chen X, Cai H. Monoclonal antibodies for Cancer therapy approved by FDA. MOJ Immunol. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Buchbinder EI, Desai A. CTLA-4 and PD-1 pathways: similarities, differences, and implications of their inhibition.

Am J Clin Oncol. Whiteside TL. The role of regulatory T cells in cancer immunology. Immunotargets Ther. Schlessinger J. Cell signaling by receptor tyrosine kinases. Carpenter G, King L Jr, Cohen S. Epidermal growth factor stimulates phosphorylation in membrane preparations in vitro. Lax I, Bellot F, Howk R, Ullrich A, Givol D, Schlessinger J.

EMBO J. Lemmon MA, Bu Z, Ladbury JE, Zhou M, Pinchasi D, Lax I, et al. Two EGF molecules contribute additively to stabilization of the EGFR dimer. Garrett TP, McKern NM, Lou M, Elleman TC, Adams TE, Lovrecz GO, et al.

Crystal structure of a truncated epidermal growth factor receptor extracellular domain bound to transforming growth factor alpha.

Markman B, Javier Ramos F, Capdevila J, Tabernero J. EGFR and KRAS in colorectal cancer. Adv Clin Chem. Lee JC, Vivanco I, Beroukhim R, Huang JH, Feng WL, DeBiasi RM, et al. Epidermal growth factor receptor activation in glioblastoma through novel missense mutations in the extracellular domain.

PLoS Med. Blume-Jensen P, Hunter T. Oncogenic kinase signalling. Lui VW, Grandis JR. EGFR-mediated cell cycle regulation. Anticancer Res. CAS PubMed Google Scholar. Huang PH, Xu AM, White FM. Oncogenic EGFR signaling networks in glioma. Sci Signal.

Article PubMed CAS Google Scholar. Midha A, Dearden S, McCormack R. EGFR mutation incidence in non-small-cell lung cancer of adenocarcinoma histology: a systematic review and global map by ethnicity mutMapII. Am J Cancer Res. Shigematsu H, Lin L, Takahashi T, Nomura M, Suzuki M, Wistuba II, et al.

Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers. J Natl Cancer Inst. Sonobe M, Manabe T, Wada H, Tanaka F.

Mutations in the epidermal growth factor receptor gene are linked to smoking-independent, lung adenocarcinoma. Br J Cancer.

Zhang X, Gureasko J, Shen K, Cole PA, Kuriyan J. An allosteric mechanism for activation of the kinase domain of epidermal growth factor receptor. Fujino S, Enokibori T, Tezuka N, Asada Y, Inoue S, Kato H, et al. A comparison of epidermal growth factor receptor levels and other prognostic parameters in non-small cell lung cancer.

Eur J Cancer. Cappuzzo F, Finocchiaro G, Rossi E, Janne PA, Carnaghi C, Calandri C, et al. EGFR FISH assay predicts for response to cetuximab in chemotherapy refractory colorectal cancer patients. Ann Oncol. Seshacharyulu P, Ponnusamy MP, Haridas D, Jain M, Ganti A, Batra SK. Targeting the EGFR signaling pathway in cancer therapy.

Expert Opin Ther Targets. Ciardiello F, Tortora G. EGFR antagonists in cancer treatment. N Engl J Med. Normanno N, Bianco C, De Luca A, Maiello MR, Salomon DS. Target-based agents against ErbB receptors and their ligands: a novel approach to cancer treatment.

Endocr Relat Cancer. Scheffler M, Di Gion P, Doroshyenko O, Wolf J, Fuhr U. Clinical pharmacokinetics of tyrosine kinase inhibitors: focus on 4-anilinoquinazolines. Clin Pharmacokinet. Pao W, Miller V, Zakowski M, Doherty J, Politi K, Sarkaria I, et al.

Proc Natl Acad Sci U S A. Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S, Okimoto RA, Brannigan BW, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib.

Paez JG, Janne PA, Lee JC, Tracy S, Greulich H, Gabriel S, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

Cohen MH, Williams GA, Sridhara R, Chen G, Pazdur R. FDA drug approval summary: gefitinib ZD Iressa tablets. Kazandjian D, Blumenthal GM, Yuan W, He K, Keegan P, Pazdur R. FDA approval of Gefitinib for the treatment of patients with metastatic EGFR mutation-positive non-small cell lung Cancer.

Clin Cancer Res. Mok TS, Wu YL, Thongprasert S, Yang CH, Chu DT, Saijo N, et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. Zhao H, Fan Y, Ma S, Song X, Han B, Cheng Y, et al. Final overall survival results from a phase III, randomized, placebo-controlled, parallel-group study of gefitinib versus placebo as maintenance therapy in patients with locally advanced or metastatic non-small-cell lung cancer INFORM; C-TONG J Thorac Oncol.

Thatcher N, Chang A, Parikh P, Rodrigues Pereira J, Ciuleanu T, von Pawel J, et al. Gefitinib plus best supportive care in previously treated patients with refractory advanced non-small-cell lung cancer: results from a randomised, placebo-controlled, multicentre study Iressa Survival Evaluation in Lung Cancer.

Hartmann JT, Haap M, Kopp HG, Lipp HP. Tyrosine kinase inhibitors - a review on pharmacology, metabolism and side effects. Curr Drug Metab. Segovia-Mendoza M, González-González ME, Barrera D, Díaz L, García-Becerra R. Efficacy and mechanism of action of the tyrosine kinase inhibitors gefitinib, lapatinib and neratinib in the treatment of HER2-positive breast cancer: preclinical and clinical evidence.

Cappuzzo F, Finocchiaro G, Metro G, Bartolini S, Magrini E, Cancellieri A, et al. Clinical experience with gefitinib: an update. Crit Rev Oncol Hematol. Herbst RS, LoRusso PM, Purdom M, Ward D. Dermatologic side effects associated with gefitinib therapy: clinical experience and management. Clin Lung Cancer.

Johnson DH. Gefitinib Iressa trials in non-small cell lung cancer. Lung Cancer. Stamos J, Sliwkowski MX, Eigenbrot C. Structure of the epidermal growth factor receptor kinase domain alone and in complex with a 4-anilinoquinazoline inhibitor.

J Biol Chem. Cohen MH, Johnson JR, Chen YF, Sridhara R, Pazdur R. FDA drug approval summary: erlotinib Tarceva tablets. Shepherd FA, Rodrigues Pereira J, Ciuleanu T, Tan EH, Hirsh V, Thongprasert S, et al. Erlotinib in previously treated non-small-cell lung cancer. Cappuzzo F, Ciuleanu T, Stelmakh L, Cicenas S, Szczesna A, Juhasz E, et al.

SATURN: A double-blind, randomized, phase III study of maintenance erlotinib versus placebo following nonprogression with first-line platinum-based chemotherapy in patients with advanced NSCLC. J Clin Oncol. Kiyohara Y, Yamazaki N, Kishi A. Erlotinib-related skin toxicities: treatment strategies in patients with metastatic non-small cell lung cancer.

J Am Acad Dermatol. Johnston SR, Leary A. Drugs Today Barc. Cameron D, Casey M, Oliva C, Newstat B, Imwalle B, Geyer CE. Lapatinib plus Capecitabine in women with HER-2—positive advanced breast Cancer: final survival analysis of a Phase III randomized trial.

Janne PA, Wang X, Socinski MA, Crawford J, Stinchcombe TE, Gu L, et al. Randomized phase II trial of erlotinib alone or with carboplatin and paclitaxel in patients who were never or light former smokers with advanced lung adenocarcinoma: CALGB trial.

Maemondo M, Inoue A, Kobayashi K, Sugawara S, Oizumi S, Isobe H, et al. Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR. Pao W, Miller VA, Politi KA, Riely GJ, Somwar R, Zakowski MF, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain.

Toyooka S, Kiura K, Mitsudomi T. EGFR mutation and response of lung cancer to gefitinib. Li D, Ambrogio L, Shimamura T, Kubo S, Takahashi M, Chirieac LR, et al. Wissner A, Overbeek E, Reich MF, Floyd MB, Johnson BD, Mamuya N, et al.

Synthesis and structure-activity relationships of 6,7-disubstituted 4-anilinoquinolinecarbonitriles. The design of an orally active, irreversible inhibitor of the tyrosine kinase activity of the epidermal growth factor receptor EGFR and the human epidermal growth factor receptor-2 HER J Med Chem.

Smaill JB, Showalter HD, Zhou H, Bridges AJ, McNamara DJ, Fry DW, et al. Tyrosine kinase inhibitors. Tsou HR, Overbeek-Klumpers EG, Hallett WA, Reich MF, Floyd MB, Johnson BD, et al. Optimization of 6,7-disubstituted arylamino quinolinecarbonitriles as orally active, irreversible inhibitors of human epidermal growth factor receptor-2 kinase activity.

Engelman JA, Zejnullahu K, Gale CM, Lifshits E, Gonzales AJ, Shimamura T, et al. PF, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib.

Cancer Res. Fry DW. Mechanism of action of erbB tyrosine kinase inhibitors. Exp Cell Res. Garuti L, Roberti M, Bottegoni G. Irreversible protein kinase inhibitors. Curr Med Chem. Wissner A, Fraser HL, Ingalls CL, Dushin RG, Floyd MB, Cheung K, et al.

Dual irreversible kinase inhibitors: quinazoline-based inhibitors incorporating two independent reactive centers with each targeting different cysteine residues in the kinase domains of EGFR and VEGFR Bioorg Med Chem.

Morabito A, Piccirillo MC, Falasconi F, De Feo G, Del Giudice A, Bryce J, et al. Vandetanib ZD , a dual inhibitor of vascular endothelial growth factor receptor VEGFR and epidermal growth factor receptor EGFR tyrosine kinases: current status and future directions.

Feldinger K, Kong A. Profile of neratinib and its potential in the treatment of breast cancer. Breast Cancer. Gonzales AJ, Hook KE, Althaus IW, Ellis PA, Trachet E, Delaney AM, et al. Antitumor activity and pharmacokinetic properties of PF, a second-generation irreversible pan-erbB receptor tyrosine kinase inhibitor.

Mol Cancer Ther. Rabindran SK, Discafani CM, Rosfjord EC, Baxter M, Floyd MB, Golas J, et al. Antitumor activity of HKI, an orally active, irreversible inhibitor of the HER-2 tyrosine kinase.

Wedge SR, Ogilvie DJ, Dukes M, Kendrew J, Chester R, Jackson JA, et al. ZD inhibits vascular endothelial growth factor signaling, angiogenesis, and tumor growth following oral administration.

Torrance CJ, Jackson PE, Montgomery E, Kinzler KW, Vogelstein B, Wissner A, et al. Combinatorial chemoprevention of intestinal neoplasia. Nat Med. Smaill JB, Rewcastle GW, Loo JA, Greis KD, Chan OH, Reyner EL, et al.

Irreversible inhibitors of the epidermal growth factor receptor: 4- phenylamino quinazoline- and 4- phenylamino pyrido[3,2-d]pyrimidineacrylamides bearing additional solubilizing functions.

Solca F, Dahl G, Zoephel A, Bader G, Sanderson M, Klein C, et al. Target binding properties and cellular activity of afatinib BIBW , an irreversible ErbB family blocker.

J Pharmacol Exp Ther. Smith S, Keul M, Engel J, Basu D, Eppmann S, Rauh D. Characterization of covalent-reversible EGFR inhibitors. ACS Omega. Nelson V, Ziehr J, Agulnik M, Johnson M. Afatinib: emerging next-generation tyrosine kinase inhibitor for NSCLC.

OncoTargets Therapy. Giaccone G, Wang Y. Strategies for overcoming resistance to EGFR family tyrosine kinase inhibitors. Cancer Treat Rev. Ninomiya T, Takigawa N, Ichihara E, Ochi N, Murakami T, Honda Y, et al. Afatinib prolongs survival compared with gefitinib in an epidermal growth factor receptor-driven lung cancer model.

Sequist LV, Yang JC, Yamamoto N, O'Byrne K, Hirsh V, Mok T, et al. Phase III study of afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations. Geater SL, Zhou C, Hu C-P, Feng JF, Lu S, Huang Y, et al. LUX-Lung 6: Patient-reported outcomes PROs from a randomized open-label, phase III study in first-line advanced NSCLC patients pts harboring epidermal growth factor receptor EGFR mutations.

Wu YL, Zhou C, Hu CP, Feng J, Lu S, Huang Y, et al. Afatinib versus cisplatin plus gemcitabine for first-line treatment of Asian patients with advanced non-small-cell lung cancer harbouring EGFR mutations LUX-lung 6 : an open-label, randomised phase 3 trial.

Yang JC, Wu YL, Schuler M, Sebastian M, Popat S, Yamamoto N, et al. Afatinib versus cisplatin-based chemotherapy for EGFR mutation-positive lung adenocarcinoma LUX-lung 3 and LUX-lung 6 : analysis of overall survival data from two randomised, phase 3 trials. Lin NU, Winer EP, Wheatley D, Carey LA, Houston S, Mendelson D, et al.

A phase II study of afatinib BIBW , an irreversible ErbB family blocker, in patients with HER2-positive metastatic breast cancer progressing after trastuzumab. Breast Cancer Res Treat. Kalous O, Conklin D, Desai AJ, O'Brien NA, Ginther C, Anderson L, et al.

Dacomitinib PF , an irreversible pan-HER inhibitor, inhibits proliferation of HER2-amplified breast cancer cell lines resistant to trastuzumab and lapatinib. Wu YL, Cheng Y, Zhou X, Lee KH, Nakagawa K, Niho S, et al. Dacomitinib versus gefitinib as first-line treatment for patients with EGFR-mutation-positive non-small-cell lung cancer ARCHER : a randomised, open-label, phase 3 trial.

Thornton K, Kim G, Maher VE, Chattopadhyay S, Tang S, Moon YJ, et al. Vandetanib for the treatment of symptomatic or progressive medullary thyroid cancer in patients with unresectable locally advanced or metastatic disease: U.

Food and Drug Administration drug approval summary. Kim ES, Herbst RS, Wistuba II, Lee JJ, Blumenschein GR Jr, Tsao A, et al. The BATTLE trial: personalizing therapy for lung cancer. Cancer Discov. Natale RB, Thongprasert S, Greco FA, Thomas M, Tsai CM, Sunpaweravong P, et al.

Phase III trial of vandetanib compared with erlotinib in patients with previously treated advanced non-small-cell lung cancer. Yu HA, Riely GJ. Second generation epidermal growth factor receptor tyrosine kinase inhibitors in lung cancers.

J Natl Compr Canc Netw. Chan A, Delaloge S, Holmes FA, Moy B, Iwata H, Harvey VJ, et al. Neratinib after trastuzumab-based adjuvant therapy in patients with HER2-positive breast cancer ExteNET : a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial.

Gandhi L, Bahleda R, Tolaney SM, Kwak EL, Cleary JM, Pandya SS, et al. Phase I study of Neratinib in combination with Temsirolimus in patients with human epidermal growth factor receptor 2—dependent and other solid tumors.

Modjtahedi H, Cho BC, Michel MC, Solca F. A comprehensive review of the preclinical efficacy profile of the ErbB family blocker afatinib in cancer.

Article CAS Google Scholar. Butterworth S, Finlay MRV, Ward RA, Kadambar VK, Chandrashekar RC, Murugan A, et al. Google Patents; Kobayashi S, Boggon TJ, Dayaram T, Janne PA, Kocher O, Meyerson M, et al.

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. Tang ZH, Lu JJ. Osimertinib resistance in non-small cell lung cancer: mechanisms and therapeutic strategies. Cancer Lett. Walter AO, Sjin RT, Haringsma HJ, Ohashi K, Sun J, Lee K, et al. Discovery of a mutant-selective covalent inhibitor of EGFR that overcomes TM-mediated resistance in NSCLC.

Sequist LV, Soria JC, Goldman JW, Wakelee HA, Gadgeel SM, Varga A, et al. Rociletinib in EGFR-mutated non-small-cell lung cancer. Kim ES. Olmutinib: first global approval. Hotz B, Keilholz U, Fusi A, Buhr HJ, Hotz HG.

In vitro and in vivo antitumor activity of cetuximab in human gastric cancer cell lines in relation to epidermal growth factor receptor EGFR expression and mutational phenotype.

Gastric Cancer. Chung CH, Mirakhur B, Chan E, Le Q-T, Berlin J, Morse M, et al. Cetuximab-induced anaphylaxis and IgE specific for galactose-α-1,3-galactose.

Freeman DJ, Bush T, Ogbagabriel S, Belmontes B, Juan T, Plewa C, et al. Activity of panitumumab alone or with chemotherapy in non-small cell lung carcinoma cell lines expressing mutant epidermal growth factor receptor.

Messersmith WA, Hidalgo M. Panitumumab, a monoclonal anti epidermal growth factor receptor antibody in colorectal cancer: another one or the one? Liu M, Zhang H, Jimenez X, Ludwig D, Witte L, Bohlen P, et al.

Identification and characterization of a fully human antibody directed against epidermal growth factor receptor for cancer therapy. Genova C, Hirsch FR. Clinical potential of necitumumab in non-small cell lung carcinoma.

OncoTargets Ther. Martinelli E, De Palma R, Orditura M, De Vita F, Ciardiello F. Anti-epidermal growth factor receptor monoclonal antibodies in cancer therapy.

Clin Exp Immunol. Patel D, Lahiji A, Patel S, Franklin M, Jimenez X, Hicklin DJ, et al. Monoclonal antibody cetuximab binds to and down-regulates constitutively activated epidermal growth factor receptor vIII on the cell surface.

Cohen MH, Chen H, Shord S, Fuchs C, He K, Zhao H, et al. Approval summary: Cetuximab in combination with cisplatin or carboplatin and 5-fluorouracil for the first-line treatment of patients with recurrent locoregional or metastatic squamous cell head and neck cancer.

Karapetis CS, Khambata-Ford S, Jonker DJ, O'Callaghan CJ, Tu D, Tebbutt NC, et al. K-ras mutations and benefit from cetuximab in advanced colorectal cancer.

Di Nicolantonio F, Martini M, Molinari F, Sartore-Bianchi A, Arena S, Saletti P, et al. Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer.

Amado RG, Wolf M, Peeters M, Van Cutsem E, Siena S, Freeman DJ, et al. Wild-type KRAS is required for Panitumumab efficacy in patients with metastatic colorectal Cancer.

Fitzgerald TL, Lertpiriyapong K, Cocco L, Martelli AM, Libra M, Candido S, et al. Roles of EGFR and KRAS and their downstream signaling pathways in pancreatic cancer and pancreatic cancer stem cells. Adv Biol Regul. Lievre A, Bachet JB, Le Corre D, Boige V, Landi B, Emile JF, et al.

KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer. Cohenuram M, Saif MW. Panitumumab the first fully human monoclonal antibody: from the bench to the clinic. Anti-Cancer Drugs. Brinkmeyer JK, Moore DC. Necitumumab for the treatment of squamous cell non-small cell lung cancer.

Paz-Ares L, Mezger J, Ciuleanu TE, Fischer JR, von Pawel J, Provencio M, et al. Necitumumab plus pemetrexed and cisplatin as first-line therapy in patients with stage IV non-squamous non-small-cell lung cancer INSPIRE : an open-label, randomised, controlled phase 3 study. Niu G, Chen X. Vascular endothelial growth factor as an anti-angiogenic target for Cancer therapy.

Curr Drug Targets. Yu Y, Lee P, Ke Y, Zhang Y, Yu Q, Lee J, et al. A humanized anti-VEGF rabbit monoclonal antibody inhibits angiogenesis and blocks tumor growth in xenograft models. PLoS One. Ferrara N, Hillan KJ, Novotny W. Bevacizumab Avastin , a humanized anti-VEGF monoclonal antibody for cancer therapy.

Biochem Biophys Res Commun. Presta LG, Chen H, Connor SJ, Chisholm V, Meng YG, Krummen L, et al. Humanization of an anti-vascular endothelial growth factor monoclonal antibody for the therapy of solid tumors and other disorders. Ellis LM, Hicklin DJ. VEGF-targeted therapy: mechanisms of anti-tumour activity.

Nat Rev Cancer. Zhang F, Tang Z, Hou X, Lennartsson J, Li Y, Koch AW, et al. VEGF-B is dispensable for blood vessel growth but critical for their survival, and VEGF-B targeting inhibits pathological angiogenesis.

Proc Natl Acad Sci. Ferrara N, Gerber H-P, LeCouter J. The biology of VEGF and its receptors. Carmeliet P. VEGF as a Key Mediator of Angiogenesis in Cancer.

Battinelli EM, Markens BA, Kulenthirarajan RA, Machlus KR, Flaumenhaft R, Italiano JE. Anticoagulation inhibits tumor cell—mediated release of platelet angiogenic proteins and diminishes platelet angiogenic response.

Rak J, Mitsuhashi Y, Bayko L, Filmus J, Shirasawa S, Sasazuki T, et al. Hanson J, Gorman J, Reese J, Fraizer G. Regulation of vascular endothelial growth factor, VEGF, gene promoter by the tumor suppressor, WT1.

Front Biosci. Tian T, Nan K-J, Wang S-H, Liang X, Lu C-X, Guo H, et al. PTEN regulates angiogenesis and VEGF expression through phosphatase-dependent and -independent mechanisms in HepG2 cells. Hurwitz H, Saini S. Bevacizumab in the treatment of metastatic colorectal Cancer: safety profile and Management of Adverse Events.

Semin Oncol. Morabito A, De Maio E, Di Maio M, Normanno N, Perrone F. Tyrosine kinase inhibitors of vascular endothelial growth factor receptors in clinical trials: current status and future directions.

Kamba T, McDonald DM. Mechanisms of adverse effects of anti-VEGF therapy for cancer. Escudier B, Eisen T, Stadler WM, Szczylik C, Oudard S, Siebels M, et al. Sorafenib in advanced clear-cell renal-cell carcinoma. Llovet JM, Ricci S, Mazzaferro V, Hilgard P, Gane E, Blanc JF, et al.

Sorafenib in advanced hepatocellular carcinoma. Brose MS, Nutting CM, Jarzab B, Elisei R, Siena S, Bastholt L, et al. Sorafenib in radioactive iodine-refractory, locally advanced or metastatic differentiated thyroid cancer: a randomised, double-blind, phase 3 trial.

Boudou-Rouquette P, Ropert S, Mir O, Coriat R, Billemont B, Tod M, et al. Chu D, Lacouture ME, Fillos T, Wu S. Risk of hand-foot skin reaction with sorafenib: a systematic review and meta-analysis. Acta Oncol. Lacouture ME, Wu S, Robert C, Atkins MB, Kong HH, Guitart J, et al. Evolving strategies for the management of hand-foot skin reaction associated with the multitargeted kinase inhibitors sorafenib and sunitinib.

Lipworth AD, Robert C, Zhu AX. Hand-foot syndrome hand-foot skin reaction, palmar-plantar erythrodysesthesia : focus on sorafenib and sunitinib. Gong L, Giacomini MM, Giacomini C, Maitland ML, Altman RB, Klein TE.

PharmGKB summary: Sorafenib pathways. Pharmacogenet Genomics. Weiner LM, Dhodapkar MV, Ferrone S. Monoclonal Antibodies for Cancer Immunotherapy. Heist RS, Duda DG, Sahani DV, Ancukiewicz M, Fidias P, Sequist LV, et al. Improved tumor vascularization after anti-VEGF therapy with carboplatin and nab-paclitaxel associates with survival in lung cancer.

Willett CG, Boucher Y, di Tomaso E, Duda DG, Munn LL, Tong RT, et al. Direct evidence that the VEGF-specific antibody bevacizumab has antivascular effects in human rectal cancer. Ellis LM. Mechanisms of action of bevacizumab as a component of therapy for metastatic colorectal Cancer. Wang L-L, Hu R-C, Dai A-G, Tan S-X.

Bevacizumab induces A cell apoptosis through the mechanism of endoplasmic reticulum stress in vitro. Int J Clin Exp Pathol. Antitumor effect of the angiogenesis inhibitor bevacizumab is dependent on susceptibility of tumors to hypoxia-induced apoptosis.

Biochem Pharmacol. Saltz LB, Clarke S, Diaz-Rubio E, Scheithauer W, Figer A, Wong R, et al. Bevacizumab in combination with oxaliplatin-based chemotherapy as first-line therapy in metastatic colorectal cancer: a randomized phase III study. Johnson DH, Fehrenbacher L, Novotny WF, Herbst RS, Nemunaitis JJ, Jablons DM, et al.

Randomized Phase II trial comparing bevacizumab plus carboplatin and paclitaxel with carboplatin and paclitaxel alone in previously untreated locally advanced or metastatic non-small-cell lung Cancer.

Wheler JJ, Janku F, Falchook GS, Jackson TL, Fu S, Naing A, et al. Phase I study of anti-VEGF monoclonal antibody bevacizumab and histone deacetylase inhibitor valproic acid in patients with advanced cancers.

Cancer Chemother Pharmacol. Kreisl TN, Kim L, Moore K, Duic P, Royce C, Stroud I, et al. Phase II trial of single-agent bevacizumab followed by bevacizumab plus irinotecan at tumor progression in recurrent glioblastoma. Escudier B, Pluzanska A, Koralewski P, Ravaud A, Bracarda S, Szczylik C, et al.

Bevacizumab plus interferon alfa-2a for treatment of metastatic renal cell carcinoma: a randomised, double-blind phase III trial. Fuh KC, Secord AA, Bevis KS, Huh W, ElNaggar A, Blansit K, et al. Comparison of bevacizumab alone or with chemotherapy in recurrent ovarian cancer patients.

Gynecol Oncol. Cohen MH, Gootenberg J, Keegan P, Pazdur R. Kabbinavar FF, Schulz J, McCleod M, Patel T, Hamm JT, Hecht JR, et al. Addition of bevacizumab to bolus fluorouracil and leucovorin in first-line metastatic colorectal cancer: results of a randomized phase II trial.

Fuchs CS, Tomasek J, Yong CJ, Dumitru F, Passalacqua R, Goswami C, et al. Ramucirumab monotherapy for previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma REGARD : an international, randomised, multicentre, placebo-controlled, phase 3 trial.

Wilke H, Muro K, Van Cutsem E, Oh S-C, Bodoky G, Shimada Y, et al. Ramucirumab plus paclitaxel versus placebo plus paclitaxel in patients with previously treated advanced gastric or gastro-oesophageal junction adenocarcinoma RAINBOW : a double-blind, randomised phase 3 trial.

Garon EB, Ciuleanu T-E, Arrieta O, Prabhash K, Syrigos KN, Goksel T, et al. Ramucirumab plus docetaxel versus placebo plus docetaxel for second-line treatment of stage IV non-small-cell lung cancer after disease progression on platinum-based therapy REVEL : a multicentre, double-blind, randomised phase 3 trial.

Vennepureddy A, Singh P, Rastogi R, Atallah JP, Terjanian T. Evolution of ramucirumab in the treatment of cancer - a review of literature. Clarke JM, Hurwitz HI. Targeted inhibition of VEGF receptor 2: an update on ramucirumab.

Expert Opin Biol Ther. Van Cutsem E, Tabernero J, Lakomy R, Prenen H, Prausová J, Macarulla T, et al. Addition of Aflibercept to fluorouracil, Leucovorin, and irinotecan improves survival in a Phase III randomized trial in patients with metastatic colorectal Cancer previously treated with an Oxaliplatin-based regimen.

Cook KM, Figg WD. Angiogenesis inhibitors — current strategies and future prospects. Tang PA, Moore MJ. Aflibercept in the treatment of patients with metastatic colorectal cancer: latest findings and interpretations.

Ther Adv Gastroenterol. Bibeau F, Goldman-Levy G, Artru P, Desrame J, Lledo G, Mithieux F, et al. PPathologic response of liver metastases from colorectal cancer after chemotherapy and aflibercept: initial report of 23 cases from 9 patients.

Article PubMed Central Google Scholar. Tannock IF, Fizazi K, Ivanov S, Karlsson CT, Fléchon A, Skoneczna I, et al. Aflibercept versus placebo in combination with docetaxel and prednisone for treatment of men with metastatic castration-resistant prostate cancer VENICE : a phase 3, double-blind randomised trial.

Gaya A, Tse V. A preclinical and clinical review of aflibercept for the management of cancer. Haller JA, Boyer DS, Heier JS, Brown DM, Clark L, RVEGF V. Invest Ophthalmol Vis Sci. Li L, Ma BBY. Colorectal cancer in Chinese patients: current and emerging treatment options. Bordonaro R, Sobrero AF, Frassineti L, Ciuffreda L, Aprile G, Thomas AL, et al.

Gotlieb WH, Amant F, Advani S, Goswami C, Hirte H, Provencher D, et al. Intravenous aflibercept for treatment of recurrent symptomatic malignant ascites in patients with advanced ovarian cancer: a phase 2, randomised, double-blind, placebo-controlled study.

Rougier P, Riess H, Manges R, Karasek P, Humblet Y, Barone C, et al. Randomised, placebo-controlled, double-blind, parallel-group phase III study evaluating aflibercept in patients receiving first-line treatment with gemcitabine for metastatic pancreatic cancer.

Sasich LD, Sukkari SR. The US FDAs withdrawal of the breast cancer indication for Avastin bevacizumab. Saudi Pharmaceutical J. Yarden Y. The EGFR family and its ligands in human cancer. Moasser MM. The oncogene HER2; its signaling and transforming functions and its role in human cancer pathogenesis.

Vu T, Claret FX. Trastuzumab: updated mechanisms of action and resistance in breast Cancer. Slamon DJ, Godolphin W, Jones LA, Holt JA, Wong SG, Keith DE, et al. Slamon DJ, Leyland-Jones B, Shak S, Fuchs H, Paton V, Bajamonde A, et al.

Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast Cancer that overexpresses HER2. Hudis CA. Trastuzumab — mechanism of action and use in clinical practice. Zazo S, González-Alonso P, Martín-Aparicio E, Chamizo C, Cristóbal I, Arpí O, et al. Carter P, Presta L, Gorman CM, Ridgway JB, Henner D, Wong WL, et al.

Humanization of an anti-pHER2 antibody for human cancer therapy. Arnould L, Gelly M, Penault-Llorca F, Benoit L, Bonnetain F, Migeon C, et al.

Trastuzumab-based treatment of HER2-positive breast cancer: an antibody-dependent cellular cytotoxicity mechanism? Clynes RA, Towers TL, Presta LG, Ravetch JV. Inhibitory fc receptors modulate in vivo cytoxicity against tumor targets. Junttila TT, Akita RW, Parsons K, Fields C, Lewis Phillips GD, Friedman LS, et al.

Cancer Cell. Baselga J. Phase I and II clinical trials of trastuzumab. Vogel CL, Cobleigh MA, Tripathy D, Gutheil JC, Harris LN, Fehrenbacher L, et al.

Efficacy and safety of trastuzumab as a single agent in first-line treatment of HER2-overexpressing metastatic breast cancer. Breast Cancer Res. Zhang H, Wang Y, Wu Y, Jiang X, Tao Y, Yao Y, et al. Therapeutic potential of an anti-HER2 single chain antibody-DM1 conjugates for the treatment of HER2-positive cancer.

Signal Transduct Target Ther. Junttila TT, Li G, Parsons K, Phillips GL, Sliwkowski MX. Trastuzumab-DM1 T-DM1 retains all the mechanisms of action of trastuzumab and efficiently inhibits growth of lapatinib insensitive breast cancer. Krop I, Winer EP.

Trastuzumab emtansine: a novel antibody-drug conjugate for HER2-positive breast cancer. Patel TA, Ensor J, Creamer S, Rodriguez AA, Niravath PA, Darcourt JG, et al. Care Multicenter randomized open label phase II trial of neoadjuvant trastuzumabemtansine T-DM1 in combination with lapatinib and nab-paclitaxel compared with paclitaxel, trastuzumab and pertuzumab in HER 2 neu over-expressed breast cancer patients TEAL study.

Verma S, Miles D, Gianni L, Krop IE, Welslau M, Baselga J, et al. Trastuzumab emtansine for HER2-positive advanced breast cancer. Dillon RL, Chooniedass S, Premsukh A, Adams GP, Entwistle J, MacDonald GC, et al. Trastuzumab-deBouganin conjugate overcomes multiple mechanisms of T-DM1 drug resistance.

J Immunother. Capelan M, Pugliano L, De Azambuja E, Bozovic I, Saini KS, Sotiriou C, et al. Pertuzumab: new hope for patients with HER2-positive breast cancer. Scheuer W, Friess T, Burtscher H, Bossenmaier B, Endl J, Hasmann M.

Strongly enhanced antitumor activity of Trastuzumab and Pertuzumab combination treatment on HER2-positive human xenograft tumor models. Baselga J, Cortes J, Kim SB, Im SA, Hegg R, Im YH, et al. Pertuzumab plus trastuzumab plus docetaxel for metastatic breast cancer.

Geyer CE, Forster J, Lindquist D, Chan S, Romieu CG, Pienkowski T, et al. Lapatinib plus capecitabine for HER2-positive advanced breast cancer. Mechanisms of lapatinib resistance in HER2-driven breast cancer.

Medina PJ, Goodin S. Lapatinib: a dual inhibitor of human epidermal growth factor receptor tyrosine kinases. Clin Ther. Cameron D, Casey M, Press M, Lindquist D, Pienkowski T, Romieu CG, et al.

A phase III randomized comparison of lapatinib plus capecitabine versus capecitabine alone in women with advanced breast cancer that has progressed on trastuzumab: updated efficacy and biomarker analyses.

Hallberg B, Palmer RH. The role of the ALK receptor in cancer biology. Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology. Chia PL, Mitchell P, Dobrovic A, John T.

Prevalence and natural history of ALK positive non-small-cell lung cancer and the clinical impact of targeted therapy with ALK inhibitors. Clin Epidemiol.

Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S, et al.

The aim of the International Institute of AAnti-cancer Research Anti-cancer research studies is to Improve endurance for basketball an independent platform for Anti-cxncer cooperation stuies the fight against cancer. The IIAR will advance, protect and support throughout the world the ideals of freedom, peace, health, scientific knowledge, equality, welfare and mutual respect among communities in science and life. This site provides information on the aims and activities of the IIAR, including current cancer research projects and invitations for cooperation. Editorial office: Bay Avenue, Highlands, NJUSA. Mailing address: Anticancer Research USA, Inc.

Anti-cancer research studies -

It cannot be given by the National Cancer Institute. Information about using the images in this summary, along with many other images related to cancer can be found in Visuals Online. Visuals Online is a collection of more than 3, scientific images.

The information in these summaries should not be used to make decisions about insurance reimbursement. More information on insurance coverage is available on Cancer. gov on the Managing Cancer Care page. More information about contacting us or receiving help with the Cancer.

gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer. Complementary and alternative medicine CAM —also called integrative medicine—includes a broad range of healing philosophies, approaches, and therapies.

A therapy is generally called complementary when it is used in addition to conventional treatments; it is often called alternative when it is used instead of conventional treatment.

Conventional treatments are those that are widely accepted and practiced by the mainstream medical community. Depending on how they are used, some therapies can be considered either complementary or alternative. Complementary and alternative therapies are used in an effort to prevent illness, reduce stress, prevent or reduce side effects and symptoms, or control or cure disease.

Unlike conventional treatments for cancer, complementary and alternative therapies are often not covered by insurance companies. Patients should check with their insurance provider to find out about coverage for complementary and alternative therapies.

Cancer patients considering complementary and alternative therapies should discuss this decision with their doctor, nurse, or pharmacist as they would any type of treatment. Some complementary and alternative therapies may affect their standard treatment or may be harmful when used with conventional treatment.

It is important that the same scientific methods used to test conventional therapies are used to test CAM therapies. The National Cancer Institute and the National Center for Complementary and Integrative Health NCCIH are sponsoring a number of clinical trials research studies at medical centers to test CAM therapies for use in cancer.

Conventional approaches to cancer treatment have generally been studied for safety and effectiveness through a scientific process that includes clinical trials with large numbers of patients. Less is known about the safety and effectiveness of complementary and alternative methods.

Few CAM therapies have been tested using demanding scientific methods. A small number of CAM therapies that were thought to be purely alternative approaches are now being used in cancer treatment—not as cures, but as complementary therapies that may help patients feel better and recover faster.

One example is acupuncture. According to a panel of experts at a National Institutes of Health NIH meeting in November , acupuncture has been found to help control nausea and vomiting caused by chemotherapy and pain related to surgery.

However, some approaches, such as the use of laetrile, have been studied and found not to work and to possibly cause harm. The NCI Best Case Series Program which was started in , is one way CAM approaches that are being used in practice are being studied.

OCCAM carefully reviews these materials to see if any seem worth further research. When considering complementary and alternative therapies, patients should ask their health care provider the following questions:.

National Center for Complementary and Integrative Health NCCIH. The National Center for Complementary and Integrative Health NCCIH at the National Institutes of Health NIH facilitates research and evaluation of complementary and alternative practices, and provides information about a variety of approaches to health professionals and the public.

NCCIH and the NIH National Library of Medicine NLM jointly developed CAM on PubMed , a free and easy-to-use search tool for finding CAM-related journal citations.

As a subset of the NLM's PubMed bibliographic database, CAM on PubMed features more than , references and abstracts for CAM-related articles from scientific journals.

This database also provides links to the websites of over 1, journals, allowing users to view full-text articles. A subscription or other fee may be required to access full-text articles. Office of Cancer Complementary and Alternative Medicine.

The NCI Office of Cancer Complementary and Alternative Medicine OCCAM coordinates the activities of the NCI in the area of complementary and alternative medicine CAM.

OCCAM supports CAM cancer research and provides information about cancer-related CAM to health providers and the general public via the NCI website.

National Cancer Institute NCI Cancer Information Service. residents may call the Cancer Information Service CIS , NCI's contact center, toll free at CANCER Monday through Friday from am to pm.

A trained Cancer Information Specialist is available to answer your questions. The Food and Drug Administration FDA regulates drugs and medical devices to ensure that they are safe and effective. The Federal Trade Commission FTC enforces consumer protection laws. Publications available from the FTC include:.

Medicinal Mushrooms PDQ® —Patient Version On This Page Introduction Questions and Answers About Turkey Tail and Polysaccharide-K PSK Questions and Answers About Reishi About This PDQ Summary General CAM Information Evaluation of CAM Therapies Questions to Ask Your Health Care Provider About CAM To Learn More About CAM Introduction Go to Health Professional Version.

How it is given or taken. Reviews of laboratory and animal studies. Results of clinical trials studies in humans. Side effects. Food and Drug Administration FDA information. What is turkey tail? What is PSK? How is PSK given or taken? Have any laboratory or animal studies been done using PSK?

Have any studies of PSK been done in people? Gastric cancer Studies show that the use of PSK as adjuvant therapy in patients with gastric stomach cancer may help repair immune cell damage caused by chemotherapy and strengthen the immune system.

Studies of PSK as adjuvant therapy for gastric cancer include the following: A randomized clinical trial in Japan done between and included patients who had surgery for gastric cancer. After surgery, patients received chemotherapy with or without PSK. On average, the patients who received chemotherapy and PSK lived longer than those who received chemotherapy alone.

In , a study in Japan followed patients who had successful surgery for gastric cancer and were given chemotherapy with or without PSK. Patients who received chemotherapy and PSK were less likely to have recurrent cancer and lived longer than those who did not.

Treatment with PSK caused few side effects. The researchers thought the study showed that PSK and chemotherapy should be given to gastric cancer patients after surgery to remove the cancer. A review published in combined results from 8 randomized controlled trials in 8, patients who had surgery to remove gastric cancers.

After surgery, patients in the trials were given chemotherapy with or without PSK. The results suggest that receiving chemotherapy and PSK helped patients live longer after surgery. Emodin inhibits breast cancer growth by blocking the tumor-promoting feedforward loop between cancer cells and macrophages.

Cancer Ther. James, M. Curcumin inhibits cancer stem cell phenotypes in ex vivo models of colorectal liver metastases, and is clinically safe and tolerable in combination with FOLFOX chemotherapy.

Joo, J. Kanai, M. A phase I study investigating the safety and pharmacokinetics of highly bioavailable curcumin Theracurmin in cancer patients. Cancer Chemother. Kim, M.

Carcinogenesis 35 3 , — Kim, D. HS, a resveratrol analogue, downregulates the expression of hypoxia-induced HIF-1 and VEGF and inhibits tumor growth of human breast cancer cells in a nude mouse xenograft model.

Kimura, Y. Resveratrol isolated from polygonum cuspidatum root prevents tumor growth and metastasis to lung and tumor-induced neovascularization in Lewis lung carcinoma-bearing mice.

Kiselev, V. A new promising way of maintenance therapy in advanced ovarian cancer: a comparative clinical study. BMC Cancer 18 1 , Kong, Y. Pterostilbene induces apoptosis and cell cycle arrest in diffuse large B-cell lymphoma cells. Kotsakis, A. A multicentre phase II trial of cabazitaxel in patients with advanced non-small-cell lung cancer progressing after docetaxel-based chemotherapy.

Cancer 7 , — Kumar, N. Randomized, placebo-controlled trial evaluating the safety of one-year administration of green tea catechins. Oncotarget 7 43 , — Kunnumakkara, A. Curcumin mediates anticancer effects by modulating multiple cell signaling pathways.

Lond 15 , — Kuppusamy, P. Concomitant activation of ETS-like transcription factor-1 and death Receptor-5 via extracellular signal-regulated kinase in withaferin a-mediated inhibition of hepatocarcinogenesis in mice.

Lee, W. Phytoagents for cancer management: regulation of nucleic acid oxidation, ROS, and related mechanisms. Cell Longev , Li, X. Synergistic apoptotic effect of crocin and cisplatin on osteosarcoma cells via caspase induced apoptosis.

Li, J. Lin, W. Lin, C. Berberine-targeted miR chemosensitizes oral carcinomas stem cells. Oncotarget 8 46 , — Lu, L. Combination of baicalein and docetaxel additively inhibits the growth of non-small cell lung cancer in vivo. Modern Med. Lu, W. Licochalcone A attenuates glioma cell growth in vitro and in vivo through cell cycle arrest.

Food Funct. Madunic, J. Apigenin: A dietary flavonoid with diverse anticancer properties. Mahammedi, H. The new combination docetaxel, prednisone and curcumin in patients with castration-resistant prostate cancer: a pilot phase II study.

Oncology 90 2 , 69— Mahata, S. Berberine modulates AP-1 activity to suppress HPV transcription and downstream signaling to induce growth arrest and apoptosis in cervical cancer cells.

Cancer 10, Mao, L. Berberine decelerates glucose metabolism via suppression of mTORdependent HIF1alpha protein synthesis in colon cancer cells. Martin, A. Oncotarget 8 42 , — Martino, E.

Vinca alkaloids and analogues as anti-cancer agents: Looking back, peering ahead. Mock, C. Recent Advances of Curcumin and its Analogues in Breast Cancer Prevention and Treatment. RSC Adv. Mostofa, A.

Thymoquinone as a potential adjuvant therapy for cancer treatment: evidence from preclinical studies. Mundy, C. Tiotropium bromide. Drug Discovery 3 8 , — Nakamura, K.

Curcumin down-regulates AR gene expression and activation in prostate cancer cell lines. Newman, D. Natural Products as Sources of New Drugs from to The influence of natural products upon drug discovery.

Nussbaumer, S. Analysis of anticancer drugs: a review. Talanta 85 5 , — Odeh, L. Synergistic effect of thymoquinone and melatonin against breast cancer implanted in mice. Ogbonna, J. Oudard, S. Cabazitaxel versus docetaxel as first-line therapy for patients with metastatic castration-resistant prostate cancer: a randomized phase III trial-firstana.

Paller, C. A phase I study of muscadine grape skin extract in men with biochemically recurrent prostate cancer: safety, tolerability, and dose determination.

Prostate 75 14 , — Muscadine grape skin extract MPX in men with biochemically recurrent prostate cancer: a randomized, multicenter, placebo-controlled clinical trial.

Pastorelli, D. Phytosome complex of curcumin as complementary therapy of advanced pancreatic cancer improves safety and efficacy of gemcitabine: Results of a prospective phase II trial. Pezzani, R. Synergistic effects of plant derivatives and conventional chemotherapeutic agents: an update on the cancer perspective.

Kaunas 55 4 , Pooladanda, V. Nimbolide epigenetically regulates autophagy and apoptosis in breast cancer. In Vitro 51, — Prasad, S. Ursolic acid inhibits growth and metastasis of human colorectal cancer in an orthotopic nude mouse model by targeting multiple cell signaling pathways: chemosensitization with capecitabine.

Ursolic acid inhibits the growth of human pancreatic cancer and enhances the antitumor potential of gemcitabine in an orthotopic mouse model through suppression of the inflammatory microenvironment. Oncotarget 7 11 , — Qazi, A.

Anticancer activity of a broccoli derivative, sulforaphane, in barrett adenocarcinoma: potential use in chemoprevention and as adjuvant in chemotherapy. Saha, A. Phila 7 6 , — Sharma, R.

Phase I clinical trial of oral curcumin: biomarkers of systemic activity and compliance. Short, N. A phase II study of omacetaxine mepesuccinate for patients with higher-risk myelodysplastic syndrome and chronic myelomonocytic leukemia after failure of hypomethylating agents.

Skroza, N. Clinical utility of ingenol mebutate in the management of actinic keratosis: perspectives from clinical practice. Risk Manag 14, — Su, J. Su, X. Anticancer activity of sulforaphane: the epigenetic mechanisms and the Nrf2 signaling pathway. Subramani, R. Nimbolide inhibits pancreatic cancer growth and metastasis through ROS-mediated apoptosis and inhibition of epithelial-to-mesenchymal transition.

Suman, S. Withaferin-A suppress AKT induced tumor growth in colorectal cancer cells. Oncotarget 7 12 , — Tao, Y. Baicalin, the major component of traditional Chinese medicine Scutellaria baicalensis induces colon cancer cell apoptosis through inhibition of oncomiRNAs.

Taverna, S. Curcumin inhibits in vitro and in vivo chronic myelogenous leukemia cells growth: a possible role for exosomal disposal of miR Oncotarget 6 26 , — Thangapazham, R. Green tea polyphenols and its constituent Epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and.

In vivo. Tozer, G. The biology of the combretastatins as tumour vascular targeting agents. Tsai, J. Oncotarget 6 30 , — Tsang, C. Berberine suppresses Id-1 expression and inhibits the growth and development of lung metastases in hepatocellular carcinoma.

Acta 3 , — van Agtmael, M. Artemisinin drugs in the treatment of malaria: from medicinal herb to registered medication. Trends Pharmacol. Wang, Y. The specific anti-cancer activity of green tea - -epigallocatechingallate EGCG.

Amino Acids 22 2 , — Wang, T. Alpinumisoflavone suppresses tumour growth and metastasis of clear-cell renal cell carcinoma. Enhancement of anti-tumor activity of ursolic acid by nanostructured lipid carriers.

China Nanomed. Wani, M. Plant antitumor agents. the isolation and structure of taxol, a novel antileukemic and antitumor agent from taxus brevifolia. Wen, W. Pterostilbene, a natural phenolic compound, synergizes the antineoplastic effects of megestrol acetate in endometrial cancer.

Wilken, R. Curcumin: A review of anti-cancer properties and therapeutic activity in head and neck squamous cell carcinoma. Wu, W. Prostate cancer xenograft inhibitory activity and pharmacokinetics of decursinol, a metabolite of angelica gigas pyranocoumarins, in mouse models.

Wu, J. Licochalcone A suppresses hexokinase 2-mediated tumor glycolysis in gastric cancer via downregulation of the Akt signaling pathway. Wu, X. Glycyrrhizin suppresses the growth of human NSCLC cell line HCC by downregulating HMGB1 level.

Xu, Y. Yallapu, M. Ovarian Res. Yan, X-B. Apigenin inhibits proliferation of human chondrosarcoma cells via cell cycle arrest and mitochondrial apoptosis induced by ROS generation-an in vitro and in vivo study. Youn, D. Berberine improves benign prostatic hyperplasia via suppression of 5 alpha reductase and extracellular signal-regulated kinase in vivo and in vitro.

Zhang, Y. Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine. Zhang, J. Single oral dose pharmacokinetics of decursin and decursinol angelate in healthy adult men and women.

PloS One 10 2 , e Zhang, B. Alpinumisoflavone radiosensitizes esophageal squamous cell carcinoma through inducing apoptosis and cell cycle arrest.

Pharmacotherapy 95, — Zhang, W. Dicumarol inhibits PDK1 and targets multiple malignant behaviors of ovarian cancer cells. PloS One 12 6 , e Ursolic acid enhances the therapeutic effects of oxaliplatin in colorectal cancer by inhibition of drug resistance.

Cancer Sci. Zhao, G. Zhao, Y. Pharmacotherapy 95, 18— Zhu, W. Trans-resveratrol alters mammary promoter hypermethylation in women at increased risk for breast cancer. Cancer 64 3 , — Thymoquinone inhibits proliferation in gastric cancer via the STAT3 pathway in vivo and in vitro.

World J. Citation: Choudhari AS, Mandave PC, Deshpande M, Ranjekar P and Prakash O Phytochemicals in Cancer Treatment: From Preclinical Studies to Clinical Practice. Received: 13 September ; Accepted: 10 December ; Published: 28 January Copyright © Choudhari, Mandave, Deshpande, Ranjekar and Prakash.

This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY. The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

This can bring hope if other treatment options do not work or are not available. Clinical trials are something you volunteer to do, not something you have to do. Learn all that you can before you decide to take part. Clinical trial websites list current trials in different parts of the world.

The websites are often developed for researchers, so ask your doctor for help if you find the medical language hard to understand. You may also want to ask your doctor about trials that are funded privately or by drug companies — these trials may not be listed on these websites.

Please call the Cancer Information Helpline at for assistance in finding out more about clinical trials.

a Includes 12 trials without Type diabetes blood sugar levels researcj but with immature outcome data. Hilal Anti-cwncerGonzalez-Velez MPrasad V. Limitations in Clinical Trials Leading to Anticancer Sports nutrition for endurance sports Approvals by the Studes Type diabetes blood sugar levels reseaech Drug Administration. JAMA Intern Med. Question How often are anticancer drugs approved by the US Food and Drug Administration FDA based on clinical trials with the following limitations: nonrandomized design, lack of demonstrated survival advantage, inappropriate use of crossover, or the use of suboptimal control arms? Findings In this observational study, trials leading to anticancer drug approvals between June 30,and July 31,were reviewed. Researchers found Anti-cancsr when they stkdies cancer studkes into immune cells, they were able to Anti-cancer research studies other immune cells how to attack cancer. March 1, Type diabetes blood sugar levels Red pepper quesadilla Christopher Vaughan. Ravi Majeti and his colleagues programmed mouse leukemia cells so that some of them could be induced to transform themselves into cells that attacked the cancer from which the cells were derived. Steve Fisch. Some cities fight gangs with ex-members who educate kids and starve gangs of new recruits. The research was published March 1 in Cancer Discovery.