Editing Experimental cancer treatment

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'''Experimental cancer treatments''' are [[Mainstream medicine|mainstream medical]] therapies intended to treat [[cancer]] by improving on, supplementing or replacing conventional methods ([[surgery]], [[chemotherapy]], [[Radiation therapy|radiation]], and [[immunotherapy]]).  However, researchers are [[Medical research|still trying to determine]] whether these treatments are safe and effective treatments.  Experimental cancer treatments are normally available only to people who participate in formal research programs, which are called [[Clinical trial|''clinical trials'']].  Occasionally, a seriously ill person may be able to access an experimental drug through an [[expanded access]] program.  Some of the treatments have [[Approved drug|regulatory approval]] for treating other conditions.  [[Health insurance]] and [[publicly funded health care]] programs normally refuse to pay for experimental cancer treatments.

The entries listed below vary between theoretical therapies to unproven controversial therapies. Many of these treatments are alleged to help against only specific forms of cancer. It is not a list of treatments widely available at hospitals.

==Studying cancer treatments==
{{See also|Drug discovery}}
The twin goals of research are to determine whether the treatment actually works (called [[efficacy]]) and whether it is sufficiently safe. Regulatory processes attempt to balance the potential benefits with the potential harms, so that people given the treatment are more likely to benefit from it than to be harmed by it.

Medical research for cancer begins much like research for any disease. In organized studies of new treatments for cancer, the [[pre-clinical development]] of drugs, devices, and techniques begins in laboratories, either with isolated cells or in small animals, most commonly rats or mice. In other cases, the proposed treatment for cancer is already in use for some other medical condition, in which case more is known about its safety and potential efficacy.

[[Clinical trial]]s are the study of treatments in humans. The first-in-human tests of a potential treatment are called [[Clinical trial#Phase I|Phase I]] studies. Early clinical trials typically enroll a very small number of patients, and the purpose is to identify major safety issues and the ''[[maximum tolerated dose]]'', which is the highest dose that does not produce serious or fatal [[adverse effect]]s. The dose given in these trials may be far too small to produce any useful effect. In most research, these early trials may involve healthy people, but cancer studies normally enroll only people with relatively severe forms of the disease in this stage of testing. On average, 95% of the participants in these early trials receive no benefit, but all are exposed to the risk of adverse effects.<ref>{{cite news | title = When Optimism Is Unrealistic
| author = Chen, Pauline W.
| date = 3 March 2011
| url = https://www.nytimes.com/2011/03/03/health/views/03chen.html
| work=The New York Times}}
</ref>  Most participants show signs of [[optimism bias]] (the irrational belief that they will beat the odds).

Later studies, called [[Clinical trial#Phase II|Phase II]] and [[Clinical trial#Phase III|Phase III]] studies, enroll more people, and the goal is to determine whether the treatment actually works. Phase III studies are frequently [[randomized controlled trial]]s, with the experimental treatment being compared to the current best available treatment rather than to a [[placebo]]. In some cases, the Phase III trial provides the best available treatment to all participants, in addition to some of the patients receiving the experimental treatment.

==Bacterial treatments==
[[Chemotherapy|Chemotherapeutic]] [[medication|drugs]] have a hard time penetrating tumors to kill them at their core because these cells may lack a good blood supply.<ref>{{Cite journal |last1=Boohaker |first1=R. J. |last2=Lee |first2=M. W. |last3=Vishnubhotla |first3=P. |last4=Perez |first4=J. L. M. |last5=Khaled |first5=A. R. |title=The Use of Therapeutic Peptides to Target and to Kill Cancer Cells |url=https://www.eurekaselect.com/article/44099 |journal=Current Medicinal Chemistry |date=2012 |language=en |volume=19 |issue=22 |pages=3794–3804 |doi=10.2174/092986712801661004 |pmc=4537071 |pmid=22725698}}</ref> Researchers have been using [[anaerobic bacteria]], such as ''[[Clostridium novyi]]'', to consume the interior of oxygen-poor tumours. These should then die when they come in contact with the tumor's oxygenated sides, meaning they would be harmless to the rest of the body. A major problem has been that bacteria do not consume all parts of the malignant tissue. However, combining the therapy with chemotherapeutic treatments can help to solve this problem.

Another strategy is to use anaerobic bacteria that have been transformed with an enzyme that can convert a non-toxic [[prodrug]] into a toxic drug. With the proliferation of the bacteria in the [[necrosis|necrotic]] and [[Hypoxia (medical)|hypoxic]] areas of the tumor, the enzyme is expressed solely in the tumor. Thus, a systemically applied prodrug is metabolised to the toxic drug only in the tumor. This has been demonstrated to be effective with the nonpathogenic anaerobe ''[[Clostridium sporogenes]]''.<ref name="Mengesha">{{cite book |author= Mengesha|year=2009|chapter=Clostridia in Anti-tumor Therapy |title=Clostridia: Molecular Biology in the Post-genomic Era|publisher=Caister Academic Press|isbn =  978-1-904455-38-7  }}</ref>

==Drug therapies==

===HAMLET (human alpha-lactalbumin made lethal to tumor cells)===
{{Main|HAMLET (human alpha-lactalbumin made lethal to tumor cells)}}
HAMLET (human alpha-lactalbumin made lethal to tumor cells) is a molecular complex derived from human [[breast milk]] that kills tumor cells by a process resembling programmed cell death ([[apoptosis]]). {{As of|2008}}, it had been tested in humans with skin [[papilloma]]s and [[bladder cancer]].<ref name=Hallgren>
{{cite book | vauthors = Hallgren O, Aits S, Brest P, Gustafsson L, Mossberg AK, Wullt B, Svanborg C | title = Bioactive Components of Milk | chapter = Apoptosis and Tumor Cell Death in Response to HAMLET (Human α-Lactalbumin Made Lethal to Tumor Cells) | volume = 606 | pages = 217–40 | year = 2008 | pmid = 18183931 | doi = 10.1007/978-0-387-74087-4_8 | isbn = 978-0-387-74086-7 | series = Advances in Experimental Medicine and Biology }}</ref>

===p53 activation therapy===
{{See also|Pramlintide}}
Several drug therapies are being developed based on [[p53]], the [[tumour suppressor gene]] that protects the cell in response to damage and stress. It is analogous to deciding what to do with a damaged car: p53 brings everything to a halt, and then decides whether to fix the cell or, if the cell is beyond repair, to destroy the cell. This protective function of p53 is disabled in most cancer cells, allowing them to multiply without check. Restoration of p53 activity in tumours (where possible) has been shown to inhibit tumour growth and can even shrink the tumour.<ref>{{cite journal | vauthors = Martins CP, Brown-Swigart L, Evan GI | title = Modeling the therapeutic efficacy of p53 restoration in tumors | journal = Cell | volume = 127 | issue = 7 | pages = 1323–34 | date = December 2006 | pmid = 17182091 | doi = 10.1016/j.cell.2006.12.007 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Ventura A, Kirsch DG, McLaughlin ME, Tuveson DA, Grimm J, Lintault L, Newman J, Reczek EE, Weissleder R, Jacks T | title = Restoration of p53 function leads to tumour regression in vivo | journal = Nature | volume = 445 | issue = 7128 | pages = 661–5 | date = February 2007 | pmid = 17251932 | doi = 10.1038/nature05541 | s2cid = 4373520 }}</ref><ref>{{cite journal | vauthors = Xue W, Zender L, Miething C, Dickins RA, Hernando E, Krizhanovsky V, Cordon-Cardo C, Lowe SW | title = Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas | journal = Nature | volume = 445 | issue = 7128 | pages = 656–60 | date = February 2007 | pmid = 17251933 | pmc = 4601097 | doi = 10.1038/nature05529 }}</ref>

As p53 protein levels are usually kept low, one could block its degradation and allow large amounts of p53 to accumulate, thus stimulating p53 activity and its antitumour effects. Drugs that utilize this mechanism include [[nutlin]] and MI-219, which are both in phase I [[clinical trials]].<ref>{{cite journal | vauthors = Brown CJ, Lain S, Verma CS, Fersht AR, Lane DP | title = Awakening guardian angels: drugging the p53 pathway | journal = Nature Reviews. Cancer | volume = 9 | issue = 12 | pages = 862–73 | date = December 2009 | pmid = 19935675 | doi = 10.1038/nrc2763 | s2cid = 205468654 }}</ref> {{As of|2009}}, there are also other drugs that are still in the preclinical stage of testing, such as RITA<ref>{{cite journal | vauthors = Issaeva N, Bozko P, Enge M, Protopopova M, Verhoef LG, Masucci M, Pramanik A, Selivanova G | title = Small molecule RITA binds to p53, blocks p53-HDM-2 interaction and activates p53 function in tumors | journal = Nature Medicine | volume = 10 | issue = 12 | pages = 1321–8 | date = December 2004 | pmid = 15558054 | doi = 10.1038/nm1146 | s2cid = 82043 }}</ref> and MITA.<ref>{{cite journal | vauthors = Hedström E, Issaeva N, Enge M, Selivanova G | title = Tumor-specific induction of apoptosis by a p53-reactivating compound | journal = Experimental Cell Research | volume = 315 | issue = 3 | pages = 451–61 | date = February 2009 | pmid = 19071110 | doi = 10.1016/j.yexcr.2008.11.009 }}</ref>

===BI811283===
[[BI811283]] is a [[small molecule]] [[Enzyme inhibitor|inhibitor]] of the [[aurora B kinase]] protein being developed by [[Boehringer Ingelheim]] for use as an [[Anti-cancer drug|anti-cancer agent]]. {{As of|2010}}, BI 811283 is currently in the early stages of [[clinical development]] and is undergoing first-in-human trials in patients with [[solid tumor]]s and [[Acute myeloid leukemia|Acute Myeloid Leukaemia]].<ref name="one">{{Cite journal | volume = 28 | issue = 15 Suppl e13632 | pages = e13632 | vauthors = Gürtler U, Tontsch-Grunt U, Jarvis M, Zahn SK, Boehmelt G, Quant J, Adolf GR, Solca F | title = Effect of BI 811283, a novel inhibitor of Aurora B kinase, on tumor senescence and apoptosis | journal = J. Clin. Oncol. | year = 2010 | doi = 10.1200/jco.2010.28.15_suppl.e13632 }}
</ref>

=== Itraconazole ===
[[Itraconazole]], sometimes abbreviated ITZ, is an [[antifungal medication]] used to treat a number of [[fungal infections]]. Recent research works suggest itraconazole (ITZ) could also be used in the treatment of cancer by inhibiting the [[hedgehog pathway]] in a similar way to [[Sonidegib]].<ref>{{Cite journal|last1=Li|first1=Ke|last2=Fang|first2=Dengyang|last3=Xiong|first3=Zuming|last4=Luo|first4=Runlan|date=2019-08-23|title=Inhibition of the hedgehog pathway for the treatment of cancer using Itraconazole|journal=OncoTargets and Therapy|volume=12|pages=6875–6886|doi=10.2147/OTT.S223119|issn=1178-6930|pmc=6711563|pmid=31692536 |doi-access=free }}</ref>

===Selective androgen receptor modulators===
The majority of [[breast cancer]]s are [[androgen receptor]] (AR) positive and SARMs may help treat these cancers, although promising results have only been obtained with cancers that are both [[estrogen receptor]] (ER) positive and AR positive.<ref name=Solomon>{{cite journal |last1=Solomon |first1=Zachary J. |last2=Mirabal |first2=Jorge Rivera |last3=Mazur |first3=Daniel J. |last4=Kohn |first4=Taylor P. |last5=Lipshultz |first5=Larry I. |last6=Pastuszak |first6=Alexander W. |title=Selective Androgen Receptor Modulators: Current Knowledge and Clinical Applications |journal=Sexual Medicine Reviews |date=2019 |volume=7 |issue=1 |pages=84–94 |doi=10.1016/j.sxmr.2018.09.006|pmid=30503797 |pmc=6326857 }}</ref><ref name="Dai">{{cite journal |last1=Dai |first1=Charles |last2=Ellisen |first2=Leif W |title=Revisiting Androgen Receptor Signaling in Breast Cancer |journal=The Oncologist |date=2023 |volume=28 |issue=5 |pages=383–391 |doi=10.1093/oncolo/oyad049 |pmid=36972361 |pmc=10166165 |url=https://academic.oup.com/oncolo/article/28/5/383/7087214}}</ref> [[Anabolic androgenic steroids]] (AAS) were historically used successfully to treat AR positive breast cancer, but were phased out after the development of anti-estrogen therapies, due to androgenic side effects and concerns about [[aromatization]] to estrogen.  SARMs have some of the same therapeutic effects as AAS, but fewer side effects, and they cannot be aromatized.<ref name="Dai" /><ref name =trans>{{cite journal |last1=Christiansen |first1=Andrew R. |last2=Lipshultz |first2=Larry I. |last3=Hotaling |first3=James M. |last4=Pastuszak |first4=Alexander W. |title=Selective androgen receptor modulators: the future of androgen therapy? |journal=Translational Andrology and Urology |date=March 2020 |volume=9 |issue=Suppl 2 |pages=S135–S148 |doi=10.21037/tau.2019.11.02 |pmid=32257854 |pmc=7108998 |issn=2223-4683 |doi-access=free }}</ref><ref name=Narayanan>{{cite journal |last1=Narayanan |first1=Ramesh |last2=Coss |first2=Christopher C. |last3=Dalton |first3=James T. |title=Development of selective androgen receptor modulators (SARMs) |journal=Molecular and Cellular Endocrinology |date=2018 |volume=465 |pages=134–142 |doi=10.1016/j.mce.2017.06.013|pmid=28624515 |pmc=5896569 }}</ref> Although a trial on AR positive [[triple negative breast cancer]] was ended early due to lack of efficacy, ostarine showed benefits in some patients with ER+, AR+ [[metastatic]] breast cancer in a phase II study. In patients with more than 40 percent AR positivity as determined by [[immunohistochemistry]], the [[clinical benefit rate]] (CBR) was 80 percent and the [[objective response rate]] (ORR) was 48 percent—which was considered promising given that the patients had advanced disease and had been heavily pretreated.<ref>{{cite journal |last1=Palmieri |first1=Carlo |last2=Linden |first2=Hannah M. |last3=Birrell |first3=Stephen |last4=Lim |first4=Elgene |last5=Schwartzberg |first5=Lee S. |last6=Rugo |first6=Hope S. |last7=Cobb |first7=Patrick Wayne |last8=Jain |first8=Kirti |last9=Vogel |first9=Charles L. |last10=O'Shaughnessy |first10=Joyce |last11=Johnston |first11=Stephen R. D. |last12=Getzenberg |first12=Robert H. |last13=Barnette |first13=K. Gary |last14=Steiner |first14=Mitchell S. |last15=Brufsky |first15=Adam |last16=Overmoyer |first16=Beth |title=Efficacy of enobosarm, a selective androgen receptor (AR) targeting agent, correlates with the degree of AR positivity in advanced AR+/estrogen receptor (ER)+ breast cancer in an international phase 2 clinical study. |journal=Journal of Clinical Oncology |date=2021 |volume=39 |issue=15_suppl |pages=1020 |doi=10.1200/JCO.2021.39.15_suppl.1020 |s2cid=236407030 |url=https://ascopubs.org/doi/abs/10.1200/JCO.2021.39.15_suppl.1020 |language=en |issn=0732-183X}}</ref><ref name="Dai"/> In 2022, the FDA granted [[Fast track (FDA)|fast track designation]] to ostarine for AR+, [[Estrogen receptor|ER]]+, [[HER2]]- [[metastatic]] breast cancer.<ref>{{cite web |title=FDA Grants Fast Track Designation to Enobosarm in AR+, ER+, HER2- Metastatic Breast Cancer |url=https://www.cancernetwork.com/view/fda-grants-fast-track-designation-to-enobosarm-in-ar-er-her2--metastatic-breast-cancer |website=Cancer Network |access-date=27 August 2023 |language=en |date=10 January 2022}}</ref> SARMs have also shown antitumor effects in prostate cancer.<ref>{{cite journal |last1=Nyquist |first1=Michael D. |last2=Ang |first2=Lisa S. |last3=Corella |first3=Alexandra |last4=Coleman |first4=Ilsa M. |last5=Meers |first5=Michael P. |last6=Christiani |first6=Anthony J. |last7=Pierce |first7=Cordell |last8=Janssens |first8=Derek H. |last9=Meade |first9=Hannah E. |last10=Bose |first10=Arnab |last11=Brady |first11=Lauren |last12=Howard |first12=Timothy |last13=De Sarkar |first13=Navonil |last14=Frank |first14=Sander B. |last15=Dumpit |first15=Ruth F. |last16=Dalton |first16=James T. |last17=Corey |first17=Eva |last18=Plymate |first18=Stephen R. |last19=Haffner |first19=Michael C. |last20=Mostaghel |first20=Elahe A. |last21=Nelson |first21=Peter S. |title=Selective androgen receptor modulators activate the canonical prostate cancer androgen receptor program and repress cancer growth |journal=The Journal of Clinical Investigation |date=2021 |volume=131 |issue=10 |pages=e146777 |doi=10.1172/JCI146777 |pmid=33998604 |pmc=8121509 |issn=0021-9738}}</ref>

==Gene therapy==
{{Further|Virotherapy|Oncolytic virus}}

Introduction of [[tumor suppressor gene]]s into rapidly dividing cells has been thought to slow down or arrest tumor growth. [[Adenoviridae|Adenoviruses]] are a commonly utilized vector for this purpose. Much research has focused on the use of adenoviruses that cannot reproduce, or reproduce only to a limited extent, within the patient to ensure safety via the avoidance of [[lytic cycle|cytolytic]] destruction of noncancerous cells infected with the vector. However, new studies focus on adenoviruses that can be permitted to reproduce, and destroy cancerous cells in the process, since the adenoviruses' ability to infect normal cells is substantially impaired, potentially resulting in a far more effective treatment.<ref>{{cite journal | vauthors = Rein DT, Breidenbach M, Curiel DT | title = Current developments in adenovirus-based cancer gene therapy | journal = Future Oncology | volume = 2 | issue = 1 | pages = 137–43 | date = February 2006 | pmid = 16556080 | pmc = 1781528 | doi = 10.2217/14796694.2.1.137 }}</ref><ref>{{cite journal | vauthors = Kanerva A, Lavilla-Alonso S, Raki M, Kangasniemi L, Bauerschmitz GJ, Takayama K, Ristimäki A, Desmond RA, Hemminki A | title = Systemic therapy for cervical cancer with potentially regulatable oncolytic adenoviruses | journal = PLOS ONE | volume = 3 | issue = 8 | pages = e2917 | date = August 2008 | pmid = 18698374 | pmc = 2500220 | doi = 10.1371/journal.pone.0002917 | bibcode = 2008PLoSO...3.2917K | doi-access = free }}</ref>

Another use of gene therapy is the introduction of [[enzyme]]s into these cells that make them susceptible to particular chemotherapy agents; studies with introducing [[thymidine kinase]] in [[glioma]]s, making them susceptible to [[aciclovir]], are in their experimental stage.

==Epigenetic options==
{{See also|Epigenetics}}
[[Epigenetics]] is the study of heritable changes in gene activity that are not caused by changes in the DNA sequence, often a result of environmental or dietary damage to the [[histone]] receptors within the cell. Current research has shown that epigenetic pharmaceuticals could be a putative replacement or adjuvant therapy for currently accepted treatment methods such as [[radiation therapy|radiation]] and [[chemotherapy]], or could enhance the effects of these current treatments.<ref name="pmid20664922">{{cite journal | vauthors = Wang LG, Chiao JW | title = Prostate cancer chemopreventive activity of phenethyl isothiocyanate through epigenetic regulation (review) | journal = International Journal of Oncology | volume = 37 | issue = 3 | pages = 533–9 | date = September 2010 | pmid = 20664922 | doi = 10.3892/ijo_00000702 | doi-access = free }}</ref> It has been shown that the epigenetic control of the proto-onco regions and the tumor suppressor sequences by conformational changes in histones directly affects the formation and progression of cancer.<ref name="IglesiasLinares2010">{{cite journal | vauthors = Iglesias-Linares A, Yañez-Vico RM, González-Moles MA | title = Potential role of HDAC inhibitors in cancer therapy: insights into oral squamous cell carcinoma | journal = Oral Oncology | volume = 46 | issue = 5 | pages = 323–9 | date = May 2010 | pmid = 20207580 | doi = 10.1016/j.oraloncology.2010.01.009 }}</ref> Epigenetics also has the factor of reversibility, a characteristic that other cancer treatments do not offer.<ref name="Li2005">{{cite journal | vauthors = Li LC, Carroll PR, Dahiya R | title = Epigenetic changes in prostate cancer: implication for diagnosis and treatment | journal = Journal of the National Cancer Institute | volume = 97 | issue = 2 | pages = 103–15 | date = January 2005 | pmid = 15657340 | doi = 10.1093/jnci/dji010 | doi-access = free }}</ref>

Some investigators, like [[Randy Jirtle]], PhD, of Duke University Medical Center, think epigenetics may ultimately turn out to have a greater role in disease than genetics.<ref>{{cite news |first=Laura |last=Beil |title=Medicine's New Epicenter? Epigenetics: New field of epigenetics may hold the secret to flipping cancer's "off" switch. |date=Winter 2008 |publisher=CURE (Cancer Updates, Research and Education) |url=http://www.curetoday.com/index.cfm/fuseaction/article.show/id/2/article_id/949 |access-date=20 January 2014 |archive-url=https://web.archive.org/web/20090529011629/http://www.curetoday.com/index.cfm/fuseaction/article.show/id/2/article_id/949 |archive-date=29 May 2009 |url-status=dead }}</ref>

==Telomerase deactivation therapy==
Because most malignant cells rely on the activity of the protein [[telomerase]] for their immortality, it has been proposed that a drug that inactivates telomerase might be effective against a broad spectrum of malignancies. At the same time, most healthy tissues in the body express little if any telomerase, and would function normally in its absence. Currently, [[inositol hexaphosphate]], which is available over-the-counter, is undergoing testing in cancer research due to its telomerase-inhibiting abilities.<ref>{{cite journal | vauthors = Jagadeesh S, Banerjee PP | title = Inositol hexaphosphate represses telomerase activity and translocates TERT from the nucleus in mouse and human prostate cancer cells via the deactivation of Akt and PKCalpha | journal = Biochemical and Biophysical Research Communications | volume = 349 | issue = 4 | pages = 1361–7 | date = November 2006 | pmid = 16979586 | doi = 10.1016/j.bbrc.2006.09.002 }}</ref>

A number of research groups have experimented with the use of [[telomerase inhibitor]]s in [[animal model]]s, and as of 2005 and 2006 phase I and II [[Clinical trial|human clinical trials]] are underway. [[Geron Corporation]] is currently conducting two clinical trials involving telomerase inhibitors. One uses a vaccine ([[GRNVAC1]]) and the other uses a lipidated oligonucleotide ([[Imetelstat|GRN163L]]).

==Radiation therapies==

===Photodynamic therapy===
[[Photodynamic therapy]] (PDT) is generally a non-invasive treatment using a combination of light and a photosensitive drug, such as 5-ALA, Foscan, Metvix, [[padeliporfin]] (Tookad, WST09, WST11), Photofrin, or [[Verteporfin|Visudyne]]. The drug is triggered by light of a specific wavelength.

===Hyperthermiatic therapy===
{{Further|Hyperthermia therapy}}

Localized and whole-body application of heat has been proposed as a technique for the treatment of malignant tumours. Intense heating will cause [[denaturation (biochemistry)|denaturation]] and coagulation of [[cell (biology)|cellular]] [[protein]]s, rapidly killing cells within a tumour.

More prolonged moderate heating to temperatures just a few degrees above normal (39.5&nbsp;°C) can cause more subtle changes. A mild heat treatment combined with other stresses can cause cell death by [[apoptosis]]. There are many biochemical consequences to the [[heat shock protein|heat shock response]] within the cell, including slowed cell division and increased sensitivity to ionizing [[radiation therapy]]. The purpose of overheating the tumor cells is to create a lack of oxygen so that the heated cells become overacidified, which leads to a lack of nutrients in the tumor. This in turn disrupts the metabolism of the cells so that cell death (apoptosis) can set in. In certain cases chemotherapy or radiation that has previously not had any effect can be made effective. Hyperthermia alters the cell walls by means of so-called heat shock proteins. The cancer cells then react very much more effectively to the cytostatics and radiation. If hyperthermia is used conscientiously it has no serious side effects.<ref>Dr med Peter Wolf, 2008, Innovations in biological cancer therapy, a guide for patients and their relatives, p 31-32</ref>

There are many techniques by which heat may be delivered. Some of the most common involve the use of focused [[ultrasound]] (FUS or [[HIFU]]), [[microwave]] heating, [[induction heating]], [[magnetic hyperthermia]], and direct application of heat through the use of heated saline pumped through catheters. Experiments with carbon nanotubes that selectively bind to cancer cells have been performed. Lasers are then used that pass harmlessly through the body, but heat the nanotubes, causing the death of the cancer cells. Similar results have also been achieved with other types of [[nanoparticle]]s, including gold-coated nanoshells and nanorods that exhibit certain degrees of 'tunability' of the absorption properties of the nanoparticles to the wavelength of light for irradiation. The success of this approach to cancer treatment rests on the existence of an 'optical window' in which biological tissue (i.e., healthy cells) are completely transparent at the wavelength of the laser light, while nanoparticles are highly absorbing at the same wavelength. Such a 'window' exists in the so-called near-infrared region of the electromagnetic spectrum. In this way, the laser light can pass through the system without harming healthy tissue, and only diseased cells, where the nanoparticles reside, get hot and are killed.

[[Magnetic Hyperthermia]] makes use of magnetic nanoparticles, which can be injected into tumours and then generate heat when subjected to an alternating magnetic field.<ref>[http://www.physics.org/featuredetail.asp?id=44 Hyperthermia - Cancer therapy hots up] on physics.org</ref>

One of the challenges in thermal therapy is delivering the appropriate amount of heat to the correct part of the patient's body. A great deal of current research focuses on precisely positioning heat delivery devices (catheters, microwave, and ultrasound applicators, etc.) using ultrasound or [[magnetic resonance imaging]], as well as of developing new types of nanoparticles that make them particularly efficient absorbers while offering little or no concerns about toxicity to the circulation system. Clinicians also hope to use advanced imaging techniques to monitor heat treatments in real time—heat-induced changes in [[biological tissue|tissue]] are sometimes perceptible using these imaging instruments. In [[magnetic hyperthermia]] or magnetic fluid hyperthermia method, it will be easier to control temperature distribution by controlling the velocity of [[ferrofluid]] injection and size of [[magnetic nanoparticles]].<ref>{{cite journal | vauthors = Javidi M, Heydari M, Attar MM, Haghpanahi M, Karimi A, Navidbakhsh M, Amanpour S | title = Cylindrical agar gel with fluid flow subjected to an alternating magnetic field during hyperthermia | journal = International Journal of Hyperthermia | volume = 31 | issue = 1 | pages = 33–9 | date = February 2015 | pmid = 25523967 | doi = 10.3109/02656736.2014.988661 | s2cid = 881157 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Javidi M, Heydari M, Karimi A, Haghpanahi M, Navidbakhsh M, Razmkon A | title = Evaluation of the effects of injection velocity and different gel concentrations on nanoparticles in hyperthermia therapy | journal = Journal of Biomedical Physics & Engineering | volume = 4 | issue = 4 | pages = 151–62 | date = December 2014 | pmid = 25599061 | pmc = 4289522 }}</ref><ref>{{cite journal |doi=10.1142/S0219519415500888 | volume=15 | issue=5 | journal=[[Journal of Mechanics in Medicine and Biology]] | pages=1550088| year=2015 | last1=Heydari | first1=Morteza | last2=Javidi | first2=Mehrdad | last3=Attar | first3=Mohammad Mahdi | last4=Karimi | first4=Alireza | last5=Navidbakhsh | first5=Mahdi | last6=Haghpanahi | first6=Mohammad | last7=Amanpour | first7=Saeid | title=Magnetic Fluid Hyperthermia in a Cylindrical Gel Contains Water Flow }}</ref>

===Noninvasive cancer heat treatment===
Heat treatment involves using radio waves to heat up tiny metals that are implanted in cancerous tissue. [[Gold nanoparticle]]s or [[carbon nanotube]]s are the most likely candidate. Promising preclinical trials have been conducted,<ref name="Studies on using radio waves against cancer are advancing">
{{cite news |title=Research on local man's cancer treatment idea shows it has promise
| author = David Templeton |newspaper=Pittsburgh Post-Gazette |date=18 January 2007 |access-date=4 November 2007 |url=http://www.post-gazette.com/pg/07018/754702-114.stm}}</ref><ref>{{cite journal | vauthors = Gannon CJ, Cherukuri P, Yakobson BI, Cognet L, Kanzius JS, Kittrell C, Weisman RB, Pasquali M, Schmidt HK, Smalley RE, Curley SA | title = Carbon nanotube-enhanced thermal destruction of cancer cells in a noninvasive radiofrequency field | journal = Cancer | volume = 110 | issue = 12 | pages = 2654–65 | date = December 2007 | pmid = 17960610 | doi = 10.1002/cncr.23155 | s2cid = 15680068 }}</ref> although clinical trials may not be held for another few years.<ref name="The cure to cancer could be in your radio!">{{cite news |year=2007 |title=The cure to cancer could be in your radio! |publisher=Winknews.com |access-date=1 November 2007 |url=http://www.winknews.com/features/health/10949561.html |archive-date=2 November 2007 |archive-url=https://web.archive.org/web/20071102225618/http://www.winknews.com/features/health/10949561.html |url-status=dead }}</ref>

Another method that is entirely non-invasive referred to as [[Tumor Treating Fields]] has already reached clinical trial stage in many countries. The concept applies an [[electric field]] through a tumour region using electrodes external to the body. Successful trials have shown the process effectiveness to be greater than chemotherapy and there are no side-effects and only negligible time spent away from normal daily activities.<ref>{{cite journal | vauthors = Pless M, Weinberg U | title = Tumor treating fields: concept, evidence and future | journal = Expert Opinion on Investigational Drugs | volume = 20 | issue = 8 | pages = 1099–106 | date = August 2011 | pmid = 21548832 | doi = 10.1517/13543784.2011.583236 | s2cid = 903933 }}</ref><ref>{{Cite web |year=2012 |title=Tumour Treating Fields explained | publisher= ted.com |access-date=31 January 2012 |url=http://www.ted.com/talks/bill_doyle_treating_cancer_with_electric_fields.html}}</ref> This treatment is still in very early development stages for many types of cancer.

[[High-intensity focused ultrasound]] (HIFU) is still in investigatory phases in many places around the world.<ref name="Steven Mo, Constantin-C Coussios, Len Seymour & Robert Carlisle 2012 1525">{{cite journal | vauthors = Mo S, Coussios CC, Seymour L, Carlisle R | title = Ultrasound-enhanced drug delivery for cancer | journal = Expert Opinion on Drug Delivery | volume = 9 | issue = 12 | pages = 1525–38 | date = December 2012 | pmid = 23121385 | doi = 10.1517/17425247.2012.739603 | s2cid = 31178343 }}</ref> In China it has CFDA approval and over 180 treatment centres have been established in China, Hong Kong, and Korea. HIFU has been successfully used to treat cancer to destroy tumours of the bone, brain, breast, liver, pancreas, rectum, kidney, testes, and prostate. Several thousand patients have been treated with various types of tumours. HIFU has CE approval for palliative care for bone metastasis. Experimentally, palliative care has been provided for cases of advanced pancreatic cancer. High-energy therapeutic ultrasound could increase higher-density anti-cancer drug load and nanomedicines to target tumor sites by 20x fold higher than traditional target cancer therapy.<ref>{{cite journal | vauthors = Mo S, Carlisle R, Laga R, Myers R, Graham S, Cawood R, Ulbrich K, Seymour L, Coussios CC | title = Increasing the density of nanomedicines improves their ultrasound-mediated delivery to tumours | journal = Journal of Controlled Release | volume = 210 | issue = 10 | pages = 10–8 | date = July 2015 | pmid = 25975831 | doi = 10.1016/j.jconrel.2015.05.265 | doi-access = free }}</ref>

== Cold atmospheric plasma treatment ==
Cold atmospheric plasma or CAP for has been proposed for the treatment of solid tumors.<ref>{{cite journal | vauthors = Babington P, Rajjoub K, Canady J, Siu A, Keidar M, Sherman JH | title = Use of cold atmospheric plasma in the treatment of cancer | journal = Biointerphases | volume = 10 | issue = 2 | pages = 029403 | date = June 2015 | pmid = 25791295 | doi = 10.1116/1.4915264 }}</ref>

==Electromagnetic treatments==
[[Tumor Treating Fields]] is a novel FDA-approved cancer treatment therapy that uses alternating electric field to disturb the rapid cell division exhibited by cancer cells.<ref>{{cite journal | vauthors = Davies AM, Weinberg U, Palti Y | title = Tumor treating fields: a new frontier in cancer therapy | journal = Annals of the New York Academy of Sciences | volume = 1291 | issue = 1 | pages = 86–95 | date = July 2013 | pmid = 23659608 | doi = 10.1111/nyas.12112 | bibcode = 2013NYASA1291...86D | s2cid = 33153055 }}</ref>

==Complementary and alternative treatments==
{{Main|Alternative cancer treatments}}

[[Alternative medicine|Complementary and alternative medicine]] (CAM) treatments are the diverse group of medical and healthcare systems, practices, and products that are not part of conventional medicine and have not been proven to be effective.<ref name="mnalt">{{cite journal | vauthors = Cassileth BR, Deng G | title = Complementary and alternative therapies for cancer | journal = The Oncologist | volume = 9 | issue = 1 | pages = 80–9 | year = 2004 | pmid = 14755017 | doi = 10.1634/theoncologist.9-1-80 | doi-access = free }}</ref> ''Complementary medicine'' usually refers to methods and substances used along with conventional medicine, while ''alternative medicine'' refers to compounds used instead of conventional medicine.<ref>[http://nccih.nih.gov/health/whatiscam/#2 What Is CAM?] [[National Center for Complementary and Integrative Health]]. retrieved 3 February 2008.</ref> CAM use is common among people with cancer.<ref name="Richardson2000">{{cite journal | vauthors = Richardson MA, Sanders T, [[J. Lynn Palmer|Palmer JL]], Greisinger A, Singletary SE | title = Complementary/alternative medicine use in a comprehensive cancer center and the implications for oncology | journal = Journal of Clinical Oncology | volume = 18 | issue = 13 | pages = 2505–14 | date = July 2000 | pmid = 10893280 | doi = 10.1200/JCO.2000.18.13.2505 }}</ref>

Most complementary and alternative medicines for cancer have not been rigorously studied or tested. Some alternative treatments that have been proven ineffective continue to be marketed and promoted.<ref name="pmid15061600">{{cite journal | vauthors = Vickers A | title = Alternative cancer cures: "unproven" or "disproven"? | journal = CA: A Cancer Journal for Clinicians | volume = 54 | issue = 2 | pages = 110–8 | year = 2004 | pmid = 15061600 | doi = 10.3322/canjclin.54.2.110 | citeseerx = 10.1.1.521.2180 | s2cid = 35124492 }}</ref>

== References ==
{{Reflist|30em}}

== External links ==
* [http://www.quackwatch.org/01QuackeryRelatedTopics/cancer.html "Questionable Cancer Therapies"]
* [https://clinicaltrials.gov/ct2/results?term=cancer&Search=Search clinicaltrials.gov]

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{{emerging technologies|topics=yes|biomed=yes}}

{{DEFAULTSORT:Experimental Cancer Treatment}}
[[Category:Experimental cancer treatments| ]]