Sierra Acai Company
Sierra Acai Company
Open 7 Days a Week
MonaVie Independent Distributor
Distributor Training
Shop Online
Enroll Now
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
Friends
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
14-September-2008 18:38:44 - Chemotherapy Chemotherapy, in its most general sense, refers to treatment of disease by chemicals that kill cells, specifically those of micro-organisms or cancer. In popular usage, it will usually refer to antineoplastic drugs used to treat cancer or the combination of these drugs into a standardized treatment regimen. In its non-oncological use, the term may also refer to antibiotics antibacterial chemotherapy. In that sense, the first modern chemotherapeutic agent was Paul Ehrlich's arsphenamine, an arsenic compound discovered in 1909 and used to treat syphilis. This was later followed by sulfonamides discovered by Domagk and penicillin discovered by Alexander Fleming. Other uses of cytostatic chemotherapy agents including the ones mentioned below are the treatment of autoimmune diseases such as multiple sclerosis and rheumatoid arthritis and the suppression of transplant rejections see immunosuppression and DMARDs. Contents 1 History 2 Principles 3 Treatment schemes 4 Types 4.1 Alkylating agents L01A 4.2 Anti-metabolites L01B 4.3 Plant alkaloids and terpenoids L01C 4.3.1 Vinca alkaloids L01CA 4.3.2 Podophyllotoxin L01CB 4.3.3 Taxanes L01CD 4.4 Topoisomerase inhibitors L01CB and L01XX 4.5 Antitumour antibiotics L01D 4.6 Monoclonal antibodies 4.7 Hormonal therapy 5 Dosage 6 Delivery 7 Newer and experimental approaches 7.1 Hematopoietic stem cell transplant approaches 7.2 Isolated infusion approaches 7.3 Targeted delivery mechanisms 7.4 Nanoparticles 8 Side-effects 8.1 Immunosuppression and myelosuppression 8.2 Nausea and vomiting 8.3 Other side effects 9 See also 10 References 11 External links History This section needs additional citations for verification. January 2008 Further information: History of cancer chemotherapy The use of chemical substances and drugs as medication dates back to the ancient Indian system of medicine called Ayurveda which uses many metals besides herbs for treatment of a large number of ailments. More recently, Persian physician, Muhammad ibn ZakarÄ«ya RÄ?zi Rhazes, in the 10th century, introduced the use of chemicals such as vitriol, copper, mercuric and arsenic salts, sal ammoniac, gold scoria, chalk, clay, coral, pearl, tar, bitumen and alcohol for medical purposes.1 The first drug used for cancer chemotherapy, however, dates back to the early 20th century, though it was not originally intended for that purpose. Mustard gas was used as a chemical warfare agent during World War I and was studied further during World War II. During a military operation in World War II, a group of people were accidentally exposed to mustard gas and were later found to have very low white blood cell counts2. It was reasoned that an agent that damaged the rapidly growing white blood cells might have a similar effect on cancer. Therefore, in the 1940s, several patients with advanced lymphomas cancers of certain white blood cells were given the drug by vein, rather than by breathing the irritating gas. Their improvement, although temporary, was remarkable.3 4 That experience led researchers to look for other substances that might have similar effects against cancer. As a result, many other drugs have been developed to treat cancer, and drug development since then has exploded into a multi-billion dollar industry. The targeted-therapy revolution has arrived, but the principles and limitations of chemotherapy discovered by the early researchers still apply. 5 Principles This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. January 2008 Cancer is the uncontrolled growth of cells coupled with malignant behavior: invasion and metastasis. Cancer is thought to be caused by the interaction between genetic susceptibility and environmental toxins. Broadly, most chemotherapeutic drugs work by impairing mitosis cell division, effectively targeting fast-dividing cells. As these drugs cause damage to cells they are termed cytotoxic. Some drugs cause cells to undergo apoptosis so-called programmed cell death. Unfortunately, scientists have yet to identify specific features of malignant and immune cells that would make them uniquely targetable barring some recent examples, such as the Philadelphia chromosome as targeted by imatinib. This means that other fast dividing cells such as those responsible for hair growth and for replacement of the intestinal epithelium lining are also often affected. However, some drugs have a better side-effect profile than others, enabling doctors to adjust treatment regimens to the advantage of patients in certain situations. As chemotherapy affects cell division, tumors with high growth fractions such as acute myelogenous leukemia and the aggressive lymphomas, including Hodgkin's disease are more sensitive to chemotherapy, as a larger proportion of the targeted cells are undergoing cell division at any time. Malignancies with slower growth rates, such as indolent lymphomas, tend to respond to chemotherapy much more modestly. Drugs affect younger tumors i.e. more differentiated more effectively, because mechanisms regulating cell growth are usually still preserved. With succeeding generations of tumor cells, differentiation is typically lost, growth becomes less regulated, and tumors become less responsive to most chemotherapeutic agents. Near the center of some solid tumors, cell division has effectively ceased, making them insensitive to chemotherapy. Another problem with solid tumors is the fact that the chemotherapeutic agent often does not reach the core of the tumor. Solutions to this problem include radiation therapy both brachytherapy and teletherapy and surgery. Over time, cancer cells become more resistant to chemotherapy treatments. Recently, scientists have identified small pumps on the surface of cancer cells that actively move chemotherapy from inside the cell to the outside. Research on p-glycoprotein and other such chemotherapy efflux pumps, is currently ongoing. Medications to inhibit the function of p-glycoprotein are undergoing testing as of June, 2007 to enhance the efficacy of chemotherapy. Treatment schemes This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. January 2008 There are a number of strategies in the administration of chemotherapeutic drugs used today. Chemotherapy may be given with a curative intent or it may aim to prolong life or to palliate symptoms. Combined modality chemotherapy is the use of drugs with other cancer treatments, such as radiation therapy or surgery. Most cancers are now treated in this way. Combination chemotherapy is a similar practice which involves treating a patient with a number of different drugs simultaneously. The drugs differ in their mechanism and side effects. The biggest advantage is minimising the chances of resistance developing to any one agent. In neoadjuvant chemotherapy preoperative treatment initial chemotherapy is aimed for shrinking the primary tumour, thereby rendering local therapy surgery or radiotherapy less destructive or more effective. Adjuvant chemotherapy postoperative treatment can be used when there is little evidence of cancer present, but there is risk of recurrence. This can help reduce chances of resistance developing if the tumour does develop. It is also useful in killing any cancerous cells which have spread to other parts of the body. This is often effective as the newly growing tumours are fast-dividing, and therefore very susceptible. Palliative chemotherapy is given without curative intent, but simply to decrease tumor load and increase life expectancy. For these regimens, a better toxicity profile is generally expected. All chemotherapy regimens require that the patient be capable of undergoing the treatment. Performance status is often used as a measure to determine whether a patient can receive chemotherapy, or whether dose reduction is required. Types This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. January 2008 The majority of chemotherapeutic drugs can be divided in to alkylating agents, antimetabolites, anthracyclines, plant alkaloids, topoisomerase inhibitors, and other antitumour agents. All of these drugs affect cell division or DNA synthesis and function in some way. Some newer agents don't directly interfere with DNA. These include monoclonal antibodies and the new tyrosine kinase inhibitors e.g. imatinib mesylate Gleevec or Glivec, which directly targets a molecular abnormality in certain types of cancer chronic myelogenous leukemia, gastrointestinal stromal tumors. In addition, some drugs may be used which modulate tumor cell behaviour without directly attacking those cells. Hormone treatments fall into this category of adjuvant therapies. Where available, Anatomical Therapeutic Chemical Classification System codes are provided for the major categories. Alkylating agents L01A Main article: Alkylating antineoplastic agent Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. Cisplatin and carboplatin, as well as oxaliplatin are alkylating agents. Other agents are mechlorethamine, cyclophosphamide, chlorambucil. They work by chemically modifying a cell's DNA. Anti-metabolites L01B Main article: antimetabolite Anti-metabolites masquerade as purine azathioprine, mercaptopurine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the S phase of the cell cycle, stopping normal development and division. They also affect RNA synthesis. Due to their efficiency, these drugs are the most widely used cytostatics. Plant alkaloids and terpenoids L01C These alkaloids are derived from plants and block cell division by preventing microtubule function. Microtubules are vital for cell division and without them it can not occur. The main examples are vinca alkaloids and taxanes. Vinca alkaloids L01CA Vinca alkaloids bind to specific sites on tubulin, inhibiting the assembly of tubulin into microtubules M phase of the cell cycle. They are derived from the Madagascar periwinkle, Catharanthus roseus formerly known as Vinca rosea. The vinca alkaloids include: Vincristine Vinblastine Vinorelbine Vindesine Podophyllotoxin L01CB Podophyllotoxin is a plant-derived compound used to produce two other cytostatic drugs, etoposide and teniposide. They prevent the cell from entering the G1 phase the start of DNA replication and the replication of DNA the S phase. The exact mechanism of its action is not yet known. The substance has been primarily obtained from the American Mayapple Podophyllum peltatum. Recently it has been discovered that a rare Himalayan Mayapple Podophyllum hexandrum contains it in a much greater quantity, but as the plant is endangered, its supply is limited. Studies have been conducted to isolate the genes involved in the substance's production, so that it could be obtained recombinantively. Taxanes L01CD The prototype taxane is the natural product paclitaxel, originally known as Taxol and first derived from the bark of the Pacific Yew tree. Docetaxel is a semi-synthetic analogue of paclitaxel. Taxanes enhance stability of microtubules, preventing the separation of chromosomes during anaphase. Topoisomerase inhibitors L01CB and L01XX Topoisomerases are essential enzymes that maintain the topology of DNA. Inhibition of type I or type II topoisomerases interferes with both transcription and replication of DNA by upsetting proper DNA supercoiling. Some type I topoisomerase inhibitors include camptothecins: irinotecan and topotecan. Examples of type II inhibitors include amsacrine, etoposide, etoposide phosphate, and teniposide. These are semisynthetic derivatives of epipodophyllotoxins, alkaloids naturally occurring in the root of American Mayapple Podophyllum peltatum. Antitumour antibiotics L01D See main article: antineoplastic The most important immunosuppressant from this group is dactinomycin, which is used in kidney transplantations. Monoclonal antibodies Monoclonal antibodies work by targeting tumour specific antigens, thus enhancing the host's immune response to tumour cells to which the agent attaches itself. Examples are trastuzumab Herceptin, cetuximab, and rituximab Rituxan or Mabthera. Bevacizumab Avastin is a monoclonal antibody that does not directly attack tumor cells but instead blocks the formation of new tumor vessels. Hormonal therapy Several malignancies respond to hormonal therapy. Strictly speaking, this is not chemotherapy. Cancer arising from certain tissues, including the mammary and prostate glands, may be inhibited or stimulated by appropriate changes in hormone balance. Steroids often dexamethasone can inhibit tumour growth or the associated edema tissue swelling, and may cause regression of lymph node malignancies. Dexamethasone is also an antiemetic, so it may be used with cytotoxic chemotherapy even if it has no direct effect on the cancer. Prostate cancer is often sensitive to finasteride, an agent that blocks the peripheral conversion of testosterone to dihydrotestosterone. Breast cancer cells often highly express the estrogen and/or progesterone receptor. Inhibiting the production with aromatase inhibitors or action with tamoxifen of these hormones can often be used as an adjunct to therapy. Gonadotropin-releasing hormone agonists GnRH, such as goserelin possess a paradoxical negative feedback effect followed by inhibition of the release of FSH follicle-stimulating hormone and LH luteinizing hormone, when given continuously. Some other tumours are also hormone dependent, although the specific mechanism is still unclear. Dosage This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. January 2008 Dosage of chemotherapy can be difficult: if the dose is too low, it will be ineffective against the tumor, while at excessive doses the toxicity side-effects, neutropenia will be intolerable to the patient. This has led to the formation of detailed dosing schemes in most hospitals, which give guidance on the correct dose and adjustment in case of toxicity. In immunotherapy, they are in principle used in smaller dosages than in the treatment of malignant diseases. In most cases, the dose is adjusted for the patient's body surface area, a measure that correlates with blood volume. The BSA is usually calculated with a mathematical formula or a nomogram, using a patient's weight and height, rather than by direct measurement. Delivery This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. January 2008 Most chemotherapy is delivered intravenously, although there are a number of agents that can be administered orally e.g. melphalan, busulfan, capecitabine. In some cases, isolated limb perfusion often used in melanoma, or isolated infusion of chemotherapy into the liver or the lung have been used. The main purpose of these approaches is to deliver a very high dose of chemotherapy to tumour sites without causing overwhelming systemic damage. Depending on the patient, the cancer, the stage of cancer, the type of chemotherapy, and the dosage, intravenous chemotherapy may be given on either an inpatient or outpatient basis. For continuous, frequent or prolonged intravenous chemotherapy administration, various systems may be surgically inserted into the vasculature to maintain access. Commonly used systems are the Hickman line, the Port-a-Cath or the PICC line. These have a lower infection risk, are much less prone to phlebitis or extravasation, and abolish the need for repeated insertion of peripheral cannulae. Harmful and lethal toxicity from chemotherapy limits the dosage of chemotherapy that can be given. Some tumours can be destroyed by sufficiently high doses of chemotheraputic agents. Unfortunately, these high doses cannot be given because they would be fatal to the patient. Newer and experimental approaches This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. January 2008 Hematopoietic stem cell transplant approaches Stem cell harvesting and autologous or allogeneic stem cell transplant has been used to allow for higher doses of chemotheraputic agents where dosages are primarily limited by hematopoietic damage. Years of research in treating solid tumors, particularly breast cancer, with hematopoeitic stem cell transplants, has yielded little proof of efficacy. Hematological malignancies such as myeloma, lymphoma, and leukemia remain the main indications for stem cell transplants. Isolated infusion approaches Isolated limb perfusion often used in melanoma, or isolated infusion of chemotherapy into the liver or the lung have been used to treat some tumours. The main purpose of these approaches is to deliver a very high dose of chemotherapy to tumor sites without causing overwhelming systemic damage. These approaches can help control solitary or limited metastases, but they are by definition not systemic and therefore do not treat distributed metastases or micrometastases. Targeted delivery mechanisms Specially targeted delivery vehicles aim to increase effective levels of chemotherapy for tumor cells while reducing effective levels for other cells. This should result in an increased tumor kill and/or reduced toxicity. Specially targeted delivery vehicles have a differentially higher affinity for tumor cells by interacting with tumor specific or tumour associated antigens. In addition to their targeting component, they also carry a payload - whether this is a traditional chemotherapeutic agent, or a radioisotope or an immune stimulating factor. Specially targeted delivery vehicles vary in their stability, selectivity and choice of target, but in essence they all aim to increase the maximum effective dose that can be delivered to the tumor cells. Reduced systemic toxicity means that they can also be used in sicker patients, and that they can carry new chemotherapeutic agents that would have been far too toxic to deliver via traditional systemic approaches. Nanoparticles Nanoparticles have emerged as a useful vehicle for poorly-soluble agents such as paclitaxel. Protein-bound paclitaxel e.g. Abraxane or nab-paclitaxel was approved by the US FDA in January 2005 for the treatment of refractory breast cancer, and allows reduced use of the Cremophor vehicle usually found in paclitaxel. Nanoparticles made of magnetic material can also be used to concentrate agents at tumour sites using an externally applied magnetic field. Side-effects This section needs additional citations for verification. January 2008 The treatment can be physically exhausting for the patient. Current chemotherapeutic techniques have a range of side effects mainly affecting the fast-dividing cells of the body. Important common side-effects include dependent on the agent: Pain Nausea and vomiting Diarrhea or constipation Anemia Malnutrition Hair loss Memory loss Depression of the immune system, hence potentially lethal infections and sepsis Weight loss or gain Hemorrhage Secondary neoplasms Cardiotoxicity Hepatotoxicity Nephrotoxicity Ototoxicity Immunosuppression and myelosuppression Virtually all chemotherapeutic regimens can cause depression of the immune system, often by paralysing the bone marrow and leading to a decrease of white blood cells, red blood cells and platelets. The latter two, when they occur, are improved with blood transfusion. Neutropenia a decrease of the neutrophil granulocyte count below 0.5 x 109/litre can be improved with synthetic G-CSF granulocyte-colony stimulating factor, e.g. filgrastim, lenograstim, Neupogen, Neulasta. In very severe myelosuppression, which occurs in some regimens, almost all the bone marrow stem cells cells which produce white and red blood cells are destroyed, meaning allogenic or autologous bone marrow cell transplants are necessary. In autologous BMTs, cells are removed from the patient before the treatment, multiplied and then re-injected afterwards; in allogenic BMTs the source is a donor. However, some patients still develop diseases because of this interference with bone marrow. Nausea and vomiting Nausea and vomiting caused by chemotherapy; stomach upset may trigger a strong urge to vomit, or forcefully eliminate what is in the stomach. Stimulation of the vomiting center results in the coordination of responses from the diaphragm, salivary glands, cranial nerves, and gastrointestinal muscles to produce the interruption of respiration and forced expulsion of stomach contents known as retching and vomiting. The vomiting center is stimulated directly by afferent input from the vagal and splanchnic nerves, the pharynx, the cerebral cortex, cholinergic and histamine stimulation from the vestibular system, and efferent input from the chemoreceptor trigger zone CTZ. The CTZ is in the area postrema, outside the blood-brain barrier, and is thus susceptible to stimulation by substances present in the blood or cerebral spinal fluid. The neurotransmitters dopamine and serotonin stimulate the vomiting center indirectly via stimulation of the CTZ. The 5-HT3 inhibitors are the most effective antiemetics and constitute the single greatest advance in the management of nausea and vomiting in patients with cancer. These drugs are designed to block one or more of the signals that cause nausea and vomiting. The most sensitive signal during the first 24 hours after chemotherapy appears to be 5-HT3. Blocking the 5-HT3 signal is one approach to preventing acute emesis vomiting, or emesis that is severe, but relatively short-lived. Approved 5-HT3 inhibitors include: Dolasetron Anzemet, Granisetron Kytril, and Ondansetron Zofran. The newest 5-HT3 inhibitor, palonosetron Aloxi, also prevents delayed nausea and vomiting, which occurs during the 2-5 days after treatment. Another drug to control nausea in cancer patients became available in 2005. The substance P inhibitor aprepitant marketed as Emend has been shown to be effective in controlling the nausea of cancer chemotherapy. The results of two large controlled trials were published in 2005, describing the efficacy of this medication in over 1,000 patients.6 Some studies7 and patient groups claim that the use of cannabinoids derived from marijuana during chemotherapy greatly reduces the associated nausea and vomiting, and enables the patient to eat. Some synthetic derivatives of the active substance in marijuana Tetrahydrocannabinol or THC such as Marinol may be practical for this application. Natural marijuana, known as medical cannabis is also used and recommended by some oncologists, though its use is regulated and not legal everywhere.8 Other side effects In particularly large tumors, such as large lymphomas, some patients develop tumor lysis syndrome from the rapid breakdown of malignant cells. Although prophylaxis is available and is often initiated in patients with large tumors, this is a dangerous side-effect which can lead to death if left untreated. A proportion of patients report fatigue or non-specific neurocognitive problems, such as an inability to concentrate; this is sometimes called post-chemotherapy cognitive impairment, colloquially referred to as chemo brain by patients' groups.9 Specific chemotherapeutic agents are associated with organ-specific toxicities, including cardiovascular disease e.g., doxorubicin, interstitial lung disease e.g., bleomycin and occasionally secondary neoplasm e.g. MOPP therapy for Hodgkin's disease. See also Cancer Gene therapy Experimental cancer treatments Chemotherapy regimens National Comprehensive Cancer Network Safe Handling of Hazardous Drugs References ^ The Valuable Contribution of al-Razi Rhazes to the History of Pharmacy, FSTC. ^ Hirsch J September 2006. An anniversary for cancer chemotherapy. JAMA 296 12: 1518-20. doi:10.1001/jama.296.12.1518. PMID 17003400. ^ Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman A, McLennan MT. 1946. Nitrogen mustard therapy. JAMA 132: 26-32. ^ Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman A, McLennan MT. 1984. Landmark article Sept. 21, 1946: Nitrogen mustard therapy. Use of methyl-bisbeta-chloroethylamine hydrochloride and trisbeta-chloroethylamine hydrochloride for Hodgkin's disease, lymphosarcoma, leukemia and certain allied and miscellaneous disorders. By Louis S. Goodman, Maxwell M. Wintrobe, William Dameshek, Morton J. Goodman, Alfred Gilman and Margaret T. McLennan. JAMA 251 17: 2255-61. PMID 6368885. ^ Joensuu H. 2008. Systemic chemotherapy for cancer: from weapon to treatment. Lancet Oncol. 9 3: 304. doi:10.1016/S1470-20450870075-5. PMID 18308256. ^ Gralla R, de Wit R, Herrstedt J, Carides A, Ianus J, Guoguang-Ma J, Evans J, Horgan K 2005. Antiemetic efficacy of the neurokinin-1 antagonist, aprepitant, plus a 5HT3 antagonist and a corticosteroid in patients receiving anthracyclines or cyclophosphamide in addition to high-dose cisplatin: analysis of combined data from two Phase III randomized clinical trials. Cancer 104 4: 864-8. doi:10.1002/cncr.21222. PMID 15973669. ^ Tramer MR, Carroll D, Campbell FA, Reynolds DJ, Moore RA, McQuay HJ. Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review. BMJ 2001;323:16-21. PMID 11440936. ^ Frequently Asked Questions - Medical Marihuana ^ Tannock IF, Ahles TA, Ganz PA, Van Dam FS June 2004. Cognitive impairment associated with chemotherapy for cancer: report of a workshop. J. Clin. Oncol. 22 11: 2233-9. doi:10.1200/JCO.2004.08.094. PMID 15169812. External links American Cancer Society - Chemotherapy Cancerbackup - Understanding Chemotherapy The leukemia and lymphoma society Chemotherapy.com Educational and support information about chemotherapy and associated side effects v d e Chemotherapeutic agents/Antineoplastic agents L01 Purine+pyrimidine/ Ribonucleotides/ Deoxyribonucleotides Antimetabolites Folic acid Aminopterin, Methotrexate, Pemetrexed, Raltitrexed Purine Cladribine, Clofarabine, Fludarabine, Mercaptopurine, Pentostatin, Thioguanine Pyrimidine Cytarabine, Decitabine, Fluorouracil/Capecitabine, Floxuridine, Gemcitabine, Enocitabine, Sapacitabine DNA Alkylating/alkylating-like Nitrogen mustards Chlorambucil, Chlormethine, Cyclophosphamide, Ifosfamide, Melphalan, Bendamustine, Trofosfamide, Uramustine Nitrosoureas Carmustine, Fotemustine, Lomustine, Nimustine, Prednimustine, Ranimustine, Semustine, Streptozocin Platinum alkylating-like Carboplatin, Cisplatin, Nedaplatin, Oxaliplatin, Triplatin tetranitrate, Satraplatin Alkyl sulfonates Busulfan, Mannosulfan, Treosulfan Hydrazines Procarbazine Triazenes Dacarbazine, Temozolomide Aziridines Carboquone, ThioTEPA, Triaziquone, Triethylenemelamine Spindle poisons/mitotic inhibitors Taxanes Docetaxel, Larotaxel, Ortataxel, Paclitaxel, Tesetaxel · Vinca alkaloids Vinblastine, Vincristine, Vinflunine, Vindesine, Vinorelbine · Ixabepilone Cytotoxic/antitumor antibiotics Anthracyclines Aclarubicin, Daunorubicin, Doxorubicin, Epirubicin, Idarubicin, Amrubicin, Pirarubicin, Valrubicin, Zorubicin Anthracenediones Mitoxantrone, Pixantrone Streptomyces Actinomycin, Bleomycin, Mitomycin, Plicamycin · Hydroxyurea Topoisomerase inhibitors Camptotheca Camptothecin, Topotecan, Irinotecan, Rubitecan, Belotecan · Podophyllum Etoposide, Teniposide Other Altretamine · Amsacrine · Bexarotene · Estramustine · Irofulven · Trabectedin Cellular CI monoclonal antibodies Receptor tyrosine kinase Cetuximab, Panitumumab, Trastuzumab · CD20 Rituximab, Tositumomab · other Alemtuzumab, Bevacizumab, Edrecolomab, Gemtuzumab Tyrosine kinase inhibitors Axitinib · Bosutinib · Cediranib · Dasatinib · Erlotinib · Gefitinib · Imatinib · Lapatinib · Lestaurtinib · Nilotinib · Semaxanib · Sorafenib · Sunitinib · Vandetanib Cyclin-dependent kinase inhibitors Alvocidib · Seliciclib Other Fusion protein Aflibercept · Denileukin diftitox Other/ungrouped Photosensitizers Aminolevulinic acid/Methyl aminolevulinate · Efaproxiral · Porphyrin derivatives Porfimer sodium, Talaporfin, Temoporfin, Verteporfin Other Retinoids Alitretinoin, Tretinoin · Anagrelide · Arsenic trioxide · Asparaginase/Pegaspargase · Atrasentan · Bortezomib · Carmofur · Celecoxib · Demecolcine · Elesclomol · Elsamitrucin · Etoglucid · Lonidamine · Lucanthone · Masoprocol · Mitobronitol · Mitoguazone · Mitotane · Oblimersen · Omacetaxine · Sitimagene ceradenovec · Tegafur · Testolactone · Tiazofurine · Tipifarnib · Vorinostat v d e Pathology: Tumor, Neoplasm, Cancer, and Oncology C00-D48, 140-239 Benign tumors Hyperplasia - Cyst - Pseudocyst - Hamartoma - Benign tumor Malignant progression Dysplasia - Carcinoma in situ - Cancer - Metastasis Topography Oral - Head/Neck - Nasopharyngeal - digestive system - Respiratory system - Bone - Skin - Blood - Urogenital - Nervous system - Endocrine system Histology Carcinoma - Sarcoma - Papilloma - Adenoma Misc. Tumor suppressor genes/oncogenes - Staging/grading - Carcinogenesis - Carcinogen - Research - Paraneoplastic syndrome - List of oncology-related terms v d e Major drug groups Gastrointestinal tract/metabolism A stomach acid Antacids, H2 antagonists, Proton pump inhibitors Antiemetics Laxatives Antidiarrhoeals/Antipropulsives Anti-obesity drugs Anti-diabetics Vitamins Dietary minerals Blood and blood forming organs B Antithrombotics Anticoagulants, Antiplatelets, Thrombolytics Antihemorrhagics Cardiovascular system C cardiac therapy/antianginals Cardiac glycosides, Antiarrhythmics, Cardiac stimulant Antihypertensives Diuretics Vasodilators Beta blockers renin-angiotensin system ACE inhibitors, Angiotensin II receptor antagonists, Renin inhibitors Antihyperlipidemics Skin D Emollients Cicatrizant Antipruritics Reproductive system G Hormonal contraception Fertility agents SERMs Sex hormones Endocrine system H Corticosteroids Sex hormones Thyroid hormones Antithyroid agent Infections and infestations J, P Antibiotics Antivirals Vaccines Antifungals Antiparasitic Antiprotozoals, Anthelmintics Malignant and immune disease L Anticancer agents Immunostimulators Immunosuppressants Muscles, bones, and joints M Anabolic steroids Anti-inflammatories NSAID Antirheumatics Corticosteroids Muscle relaxants Brain and nervous system N Anesthetics General, Local Analgesics Anticonvulsants Mood stabilizers Psycholeptic Anxiolytics, Antipsychotics, Hypnotics/Sedatives Psychoanaleptic Antidepressants, Stimulants/Psychostimulants Respiratory system R Bronchodilators Decongestants H1 antagonists Other ATC V Antidotes Contrast media Radiopharmaceuticals Dressing Retrieved from http://en..org/wiki/Chemotherapy Categories: Cancer treatments | Chemotherapeutic agents | OncologyHidden category: Articles needing additional references from January 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Türkçe БеларуÑ?каÑ? тарашкевіца БългарÑ?ки Català Česky Dansk Deutsch Ελληνικά Español Euskara Ù?ارسی Français í•œêµì–´ Bahasa Indonesia Italiano עברית Lietuvių Bahasa Melayu Nederlands 日本語 ‪Norsk bokmÃ¥l‬ Polski Português РуÑ?Ñ?кий Simple English SlovenÅ¡Ä?ina СрпÑ?ки / Srpski Suomi Svenska Türkçe УкраїнÑ?ька ä¸æ–‡ This page was last modified on 4 September 2008, at 22:56
39 Reasons to Drink Acai Juice Every Day
What is MonaVie - Watch the 8-minute video
Discovering MonaVie Video
The Power of You Video
Effects of MonaVie Active on Antioxidant Capacity in Humans
Log into your Wholesale MonaVie Account
So many of us do not eat a balanced diet, get enough sleep, have too much stress, or are impacted with toxins and pollutants. Drinking 2 ounces of MonaVie twice a day will help your body detoxify as well as build your immune system. Its the smartest thing you can do for yourself, so start today. Buying MonaVie through our company guarantees you support 7 days a week and, if you would like to share MonaVie with your family and friends we will guide you from start to finish.
1. Click on Enroll Now (30 - 55% off retail price)
2. Pay $39 for your Wholesale ID number.
3. NO minimum order required.
4. MonaVie is delivered to your door in 3 to 5 days.