Chemotherapy
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225790364
2008-07-15T12:24:33Z
Jfdwolff
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unsourced - clearly not a widely used treatment and hence not to be added here
'''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 [[chemotherapy regimen|standardized treatment regimen]].
In its non-[[Oncology|oncological]] use, the term may also refer to [[antibiotic]]s (''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 [[Sulfonamide (medicine)|sulfonamides]] discovered by [[Gerhard Domagk|Domagk]] and [[penicillin]] discovered by [[Alexander Fleming]].
Other uses of cytostatic chemotherapy agents (including the ones mentioned below) are the treatment of [[autoimmune disease]]s such as [[multiple sclerosis]] and [[rheumatoid arthritis]] and the suppression of [[transplant rejection]]s (see [[immunosuppression]] and [[DMARD]]s).
==History==
{{Refimprovesect|date=January 2008}}
{{see|History of cancer chemotherapy}}
The use of [[chemical substance]]s and drugs as [[medication]] dates back to the ancient [[India]]n system of medicine called [[Ayurveda]] which uses many metals besides herbs for treatment of a large number of ailments. More recently, [[Islamic medicine|Persian physician]], [[Muhammad ibn Zakarīya Rāzi]] (Rhazes), in the 10th century, introduced the use of chemicals such as [[Sulfuric acid|vitriol]], [[copper]], [[mercuric]] and [[arsenic]] [[salt]]s, [[sal ammoniac]], [[gold]] [[scoria]], [[chalk]], [[clay]], [[coral]], [[pearl]], [[tar]], [[bitumen]] and [[alcohol]] for medical purposes.<ref>[http://www.muslimheritage.com/uploads/The_Valuable_Contributions_of_al-Razi_in_the_History_of_Pharmacy.pdf The Valuable Contribution of al-Razi (Rhazes) to the History of Pharmacy], FSTC.</ref>
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 counts<ref>{{cite journal |author=Hirsch J |title=An anniversary for cancer chemotherapy |journal=JAMA |volume=296 |issue=12 |pages=1518–20 |year=2006 |month=September |pmid=17003400 |doi=10.1001/jama.296.12.1518}}</ref>. 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.<ref>{{cite journal | author =Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman A,
McLennan MT. | title = Nitrogen mustard therapy | journal = JAMA| volume = 132 | issue = | pages = 26–32 | year = 1946}}</ref> <ref>{{cite journal | author =Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman A, McLennan MT. | title = Landmark article Sept. 21, 1946: Nitrogen mustard therapy. Use of methyl-bis(beta-chloroethyl)amine hydrochloride and tris(beta-chloroethyl)amine 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| journal = JAMA| volume = 251 | issue = 17 | pages = 2255–61 | year = 1984 | pmid=6368885}}</ref> 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. <ref>{{cite journal | author =Joensuu H. | title = Systemic chemotherapy for cancer: from weapon to treatment| journal = Lancet Oncol.| volume = 9| issue = 3 | pages = 304 | year = 2008| pmid=18308256 | doi = 10.1016/S1470-2045(08)70075-5}}</ref>
==Principles==
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[[Cancer]] is the uncontrolled growth of [[cell (biology)|cell]]s 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 [[intestine|intestinal]] [[epithelium]] (lining) are also often affected. However, some drugs have a better [[Adverse effect (medicine)|side-effect]] profile than others, enabling [[physician|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 [[lymphoma]]s, 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 [[sealed source radiotherapy|brachytherapy]] and [[external beam radiotherapy|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==
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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|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]]'' (''post''operative 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==
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The majority of chemotherapeutic drugs can be divided in to [[alkylating antineoplastic agent|alkylating agent]]s, [[antimetabolite]]s, [[anthracycline]]s, plant [[alkaloid]]s, [[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|imatinib mesylate]]'' (''Gleevec'' or ''Glivec''), which directly targets a molecular abnormality in certain types of cancer ([[chronic myelogenous leukemia]], [[gastrointestinal stromal tumor]]s).
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|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|antimetabolite}}
[[Anti-metabolite]]s 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 [[alkaloid]]s are derived from [[plant]]s 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 alkaloid]]s and [[taxane]]s.
==== 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 still has to be elucidated.
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 [[genetic engineering|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 [[chromosome]]s during [[anaphase]].
===Topoisomerase inhibitors (L01CB and L01XX) ===
[[Topoisomerase]]s are essential [[enzyme]]s that maintain the [[topology]] of DNA. Inhibition of type I or type II topoisomerases interferes with both [[Transcription (genetics)|transcription]] and [[DNA replication|replication]] of DNA by upsetting proper DNA [[supercoil]]ing.
* 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 [[epipodophyllotoxin]]s, alkaloids naturally occurring in the root of [[American Mayapple|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 transplantation]]s.
===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.
* [[Steroid]]s (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 inhibitor]]s) 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==
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''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==
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Most chemotherapy is [[Route of administration|delivered]] [[intravenous]]ly, 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==
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===[[Stem cell transplant|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 [[micrometastasis|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==
{{Refimprovesect|date=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):
<div style="-moz-column-count:3; column-count:3;">
* [[Pain]]
* [[Nausea]] and [[vomiting]]
* [[Diarrhea]] or [[constipation]]
* [[Anemia]]
* [[Malnutrition]]
* [[Alopecia|Hair loss]]
* [[Memory loss]]
* Depression of the [[immune system]], hence (potentially lethal) [[infection]]s and [[sepsis]]
* Weight loss or gain
* [[Hemorrhage]]
* [[Secondary neoplasms]]
* [[Cardiotoxicity]]
* [[Hepatotoxicity]]
* [[Nephrotoxicity]]
* [[Ototoxicity]]
</div>
===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 cell]]s, [[red blood cell]]s and [[platelet]]s. The latter two, when they occur, are improved with [[blood transfusion]]. [[Neutropenia]] (a decrease of the [[neutrophil granulocyte]] count below 0.5 x 10<sup>9</sup>/[[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 cell]]s (cells which produce [[white blood cells|white]] and [[red blood cell]]s) are destroyed, meaning ''allogenic'' or ''[[autologous]]'' [[bone marrow transplant|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-HT<sub>3</sub> inhibitors are the most effective [[antiemetic]]s 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-HT<sub>3</sub>. Blocking the 5-HT<sub>3</sub> signal is one approach to preventing acute emesis (vomiting), or emesis that is severe, but relatively short-lived. Approved 5-HT<sub>3</sub> inhibitors include: [[Dolasetron]] (Anzemet), [[Granisetron]] (Kytril), and [[Ondansetron]] (Zofran). The newest 5-HT<sub>3</sub> 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.<ref>{{cite journal |author=Gralla R, de Wit R, Herrstedt J, Carides A, Ianus J, Guoguang-Ma J, Evans J, Horgan K |title=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 |journal=Cancer |volume=104 |issue=4 |pages=864–8 |year=2005 |pmid=15973669 | doi = 10.1002/cncr.21222 <!--Retrieved from PMID by DOI bot-->}}</ref>
Some studies<ref>Tramer MR, Carroll D, Campbell FA, Reynolds DJ, Moore RA, McQuay HJ. ''Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative [[systematic review]].'' [[British Medical Journal|BMJ]] 2001;323:16-21. PMID 11440936.</ref> and patient groups claim that the use of [[cannabinoid]]s derived from [[Cannabis|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 everywhere legal.<ref>http://www.hc-sc.gc.ca/dhp-mps/marihuana/about-apropos/faq_e.html</ref>
===Other side effects===
In particularly large tumors, such as large [[lymphoma]]s, 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.<ref name="pmid15169812">{{cite journal |author=Tannock IF, Ahles TA, Ganz PA, Van Dam FS |title=Cognitive impairment associated with chemotherapy for cancer: report of a workshop |journal=J. Clin. Oncol. |volume=22 |issue=11 |pages=2233–9 |year=2004 |month=June |pmid=15169812 |doi=10.1200/JCO.2004.08.094 |url=http://www.jco.org/cgi/pmidlookup?view=long&pmid=15169812}}</ref>
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 (medicine)|MOPP]] therapy for Hodgkin's disease).
== See also ==
* [[Cancer]]
* [[Gene therapy]]
* [[Experimental cancer treatment]]s
* [[Chemotherapy regimens]]
* [[National Comprehensive Cancer Network]]
* [[Hazardous drugs#Safe handling|Safe Handling of Hazardous Drugs]]
== References ==
{{reflist}}
== External links ==
* [http://www.cancer.org/docroot/ETO/content/ETO_1_2X_Chemotherapy_What_It_Is_How_It_Helps.asp American Cancer Society - Chemotherapy]
* [http://www.cancerbackup.org.uk/treatments/chemotherapy Cancerbackup - Understanding Chemotherapy]
* [http://www.leukemia-lymphoma.org/all_page?item_id=225865 The leukemia and lymphoma society]
* [http://www.chemotherapy.com/ Chemotherapy.com Educational and support information about chemotherapy and associated side effects]
{{Chemotherapeutic agents}}
{{Tumors}}
{{Major Drug Groups}}
[[Category:Cancer treatments]]
[[Category:Chemotherapeutic agents| ]]
[[Category:Oncology]]
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