Wikipedia

Experimental cancer treatment

(Redirected from Experimental cancer treatments)

Experimental cancer treatments are mainstream medical therapies intended to treat cancer by improving on, supplementing or replacing conventional methods (surgery, chemotherapy, radiation, and immunotherapy). However, researchers are 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 trials. Occasionally, a seriously ill person may be able to access an experimental drug through an expanded access program. Some of the treatments have 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 treatments for cancer

edit
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 trials are the study of treatments in humans. The first-in-human tests of a potential treatment are called 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 effects. 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.[1] Most participants show signs of optimism bias (the irrational belief that they will beat the odds).

Later studies, called Phase II and Phase III studies, enroll more people, and the goal is to determine whether the treatment actually works. Phase III studies are frequently randomized controlled trials, 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

edit

Chemotherapeutic drugs have a hard time penetrating tumors to kill them at their core because these cells may lack a good blood supply.[2] 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 necrotic and 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.[3]

Drug therapies

edit

HAMLET (human alpha-lactalbumin made lethal to tumor cells)

edit
Main article: 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 papillomas and bladder cancer.[4]

p53 activation therapy

edit
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.[5][6][7]

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.[8] As of 2009, there are also other drugs that are still in the preclinical stage of testing, such as RITA[9] and MITA.[10]

BI811283

edit

BI811283 is a small molecule inhibitor of the aurora B kinase protein being developed by Boehringer Ingelheim for use as an 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 tumors and Acute Myeloid Leukaemia.[11]

Itraconazole

edit

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.[12]

Selective androgen receptor modulators

edit

The majority of breast cancers 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.[13][14] 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.[14][15][16] 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.[17][14] In 2022, the FDA granted fast track designation to ostarine for AR+, ER+, HER2- metastatic breast cancer.[18] SARMs have also shown antitumor effects in prostate cancer.[19]

Gene therapy

edit
Further information: Virotherapy and Oncolytic virus

Introduction of tumor suppressor genes into rapidly dividing cells has been thought to slow down or arrest tumor growth. 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 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.[20][21]

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

Epigenetic options

edit
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 and chemotherapy, or could enhance the effects of these current treatments.[22] 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.[23] Epigenetics also has the factor of reversibility, a characteristic that other cancer treatments do not offer.[24]

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.[25]

Telomerase deactivation therapy

edit

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.[26]

A number of research groups have experimented with the use of telomerase inhibitors in animal models, and as of 2005 and 2006 phase I and II 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 (GRN163L).

Radiation therapies

edit

Photodynamic therapy

edit

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 Visudyne. The drug is triggered by light of a specific wavelength.

Hyperthermiatic therapy

edit
Further information: 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 and coagulation of cellular proteins, rapidly killing cells within a tumour.

More prolonged moderate heating to temperatures just a few degrees above normal (39.5 °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 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.[27]

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 nanoparticles, 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.[28]

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 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.[29][30][31]

Noninvasive cancer heat treatment

edit

Heat treatment involves using radio waves to heat up tiny metals that are implanted in cancerous tissue. Gold nanoparticles or carbon nanotubes are the most likely candidate. Promising preclinical trials have been conducted,[32][33] although clinical trials may not be held for another few years.[34]

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.[35][36] 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.[37] 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.[38]

Cold atmospheric plasma treatment

edit

Cold atmospheric plasma or CAP for short is an emerging modality for the treatment of solid tumors[39] Recently, cold atmospheric plasma (CAP) indicated promising anti-neoplastic effects on several tumors, e.g. melanoma, glioma, and pancreatic cancer cells [5, 6, 7], and therefore could be an efficient method for anti-cancer treatment in clinical urology in the future.[40] One example of an experimental technology utilizing Cold Atmospheric plasma is Theraphi Archived 23 August 2018 at the Wayback Machine

Electromagnetic treatments

edit

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.[41]

Complementary and alternative treatments

edit
Main article: Alternative cancer treatments

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.[42] Complementary medicine usually refers to methods and substances used along with conventional medicine, while alternative medicine refers to compounds used instead of conventional medicine.[43] CAM use is common among people with cancer.[44]

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.[45]

References

edit
  1. ^ Chen, Pauline W. (3 March 2011). "When Optimism Is Unrealistic". The New York Times.
  2. ^ Boohaker RJ, Lee MW, Vishnubhotla P, Perez JL, Khaled AR (2012). "The Use of Therapeutic Peptides to Target and to Kill Cancer Cells". Current Medicinal Chemistry. 19 (22): 3794–3804. doi:10.2174/092986712801661004. PMC 4537071. PMID 22725698.
  3. ^ Mengesha (2009). "Clostridia in Anti-tumor Therapy". Clostridia: Molecular Biology in the Post-genomic Era. Caister Academic Press. ISBN 978-1-904455-38-7.
  4. ^ Hallgren O, Aits S, Brest P, Gustafsson L, Mossberg AK, Wullt B, Svanborg C (2008). "Apoptosis and Tumor Cell Death in Response to HAMLET (Human α-Lactalbumin Made Lethal to Tumor Cells)". Bioactive Components of Milk. Advances in Experimental Medicine and Biology. Vol. 606. pp. 217–40. doi:10.1007/978-0-387-74087-4_8. ISBN 978-0-387-74086-7. PMID 18183931.
  5. ^ Martins CP, Brown-Swigart L, Evan GI (December 2006). "Modeling the therapeutic efficacy of p53 restoration in tumors". Cell. 127 (7): 1323–34. doi:10.1016/j.cell.2006.12.007. PMID 17182091.
  6. ^ Ventura A, Kirsch DG, McLaughlin ME, Tuveson DA, Grimm J, Lintault L, Newman J, Reczek EE, Weissleder R, Jacks T (February 2007). "Restoration of p53 function leads to tumour regression in vivo". Nature. 445 (7128): 661–5. doi:10.1038/nature05541. PMID 17251932. S2CID 4373520.
  7. ^ Xue W, Zender L, Miething C, Dickins RA, Hernando E, Krizhanovsky V, Cordon-Cardo C, Lowe SW (February 2007). "Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas". Nature. 445 (7128): 656–60. doi:10.1038/nature05529. PMC 4601097. PMID 17251933.
  8. ^ Brown CJ, Lain S, Verma CS, Fersht AR, Lane DP (December 2009). "Awakening guardian angels: drugging the p53 pathway". Nature Reviews. Cancer. 9 (12): 862–73. doi:10.1038/nrc2763. PMID 19935675. S2CID 205468654.
  9. ^ Issaeva N, Bozko P, Enge M, Protopopova M, Verhoef LG, Masucci M, Pramanik A, Selivanova G (December 2004). "Small molecule RITA binds to p53, blocks p53-HDM-2 interaction and activates p53 function in tumors". Nature Medicine. 10 (12): 1321–8. doi:10.1038/nm1146. PMID 15558054. S2CID 82043.
  10. ^ Hedström E, Issaeva N, Enge M, Selivanova G (February 2009). "Tumor-specific induction of apoptosis by a p53-reactivating compound". Experimental Cell Research. 315 (3): 451–61. doi:10.1016/j.yexcr.2008.11.009. PMID 19071110.
  11. ^ Gürtler U, Tontsch-Grunt U, Jarvis M, Zahn SK, Boehmelt G, Quant J, Adolf GR, Solca F (2010). "Effect of BI 811283, a novel inhibitor of Aurora B kinase, on tumor senescence and apoptosis". J. Clin. Oncol. 28 (15 Suppl e13632): e13632. doi:10.1200/jco.2010.28.15_suppl.e13632.
  12. ^ Li K, Fang D, Xiong Z, Luo R (23 August 2019). "Inhibition of the hedgehog pathway for the treatment of cancer using Itraconazole". OncoTargets and Therapy. 12: 6875–6886. doi:10.2147/OTT.S223119. ISSN 1178-6930. PMC 6711563. PMID 31692536.
  13. ^ Solomon ZJ, Mirabal JR, Mazur DJ, Kohn TP, Lipshultz LI, Pastuszak AW (2019). "Selective Androgen Receptor Modulators: Current Knowledge and Clinical Applications". Sexual Medicine Reviews. 7 (1): 84–94. doi:10.1016/j.sxmr.2018.09.006. PMC 6326857. PMID 30503797.
  14. ^ a b c Dai C, Ellisen LW (2023). "Revisiting Androgen Receptor Signaling in Breast Cancer". The Oncologist. 28 (5): 383–391. doi:10.1093/oncolo/oyad049. PMC 10166165. PMID 36972361.
  15. ^ Christiansen AR, Lipshultz LI, Hotaling JM, Pastuszak AW (March 2020). "Selective androgen receptor modulators: the future of androgen therapy?". Translational Andrology and Urology. 9 (Suppl 2): S135–S148. doi:10.21037/tau.2019.11.02. ISSN 2223-4683. PMC 7108998. PMID 32257854.
  16. ^ Narayanan R, Coss CC, Dalton JT (2018). "Development of selective androgen receptor modulators (SARMs)". Molecular and Cellular Endocrinology. 465: 134–142. doi:10.1016/j.mce.2017.06.013. PMC 5896569. PMID 28624515.
  17. ^ Palmieri C, Linden HM, Birrell S, Lim E, Schwartzberg LS, Rugo HS, Cobb PW, Jain K, Vogel CL, O'Shaughnessy J, Johnston SR, Getzenberg RH, Barnette KG, Steiner MS, Brufsky A, Overmoyer B (2021). "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 of Clinical Oncology. 39 (15_suppl): 1020. doi:10.1200/JCO.2021.39.15_suppl.1020. ISSN 0732-183X. S2CID 236407030.
  18. ^ "FDA Grants Fast Track Designation to Enobosarm in AR+, ER+, HER2- Metastatic Breast Cancer". Cancer Network. 10 January 2022. Retrieved 27 August 2023.
  19. ^ Nyquist MD, Ang LS, Corella A, Coleman IM, Meers MP, Christiani AJ, Pierce C, Janssens DH, Meade HE, Bose A, Brady L, Howard T, De Sarkar N, Frank SB, Dumpit RF, Dalton JT, Corey E, Plymate SR, Haffner MC, Mostaghel EA, Nelson PS (2021). "Selective androgen receptor modulators activate the canonical prostate cancer androgen receptor program and repress cancer growth". The Journal of Clinical Investigation. 131 (10): e146777. doi:10.1172/JCI146777. ISSN 0021-9738. PMC 8121509. PMID 33998604.
  20. ^ Rein DT, Breidenbach M, Curiel DT (February 2006). "Current developments in adenovirus-based cancer gene therapy". Future Oncology. 2 (1): 137–43. doi:10.2217/14796694.2.1.137. PMC 1781528. PMID 16556080.
  21. ^ Kanerva A, Lavilla-Alonso S, Raki M, Kangasniemi L, Bauerschmitz GJ, Takayama K, Ristimäki A, Desmond RA, Hemminki A (August 2008). "Systemic therapy for cervical cancer with potentially regulatable oncolytic adenoviruses". PLOS ONE. 3 (8): e2917. Bibcode:2008PLoSO...3.2917K. doi:10.1371/journal.pone.0002917. PMC 2500220. PMID 18698374.
  22. ^ Wang LG, Chiao JW (September 2010). "Prostate cancer chemopreventive activity of phenethyl isothiocyanate through epigenetic regulation (review)". International Journal of Oncology. 37 (3): 533–9. doi:10.3892/ijo_00000702. PMID 20664922.
  23. ^ Iglesias-Linares A, Yañez-Vico RM, González-Moles MA (May 2010). "Potential role of HDAC inhibitors in cancer therapy: insights into oral squamous cell carcinoma". Oral Oncology. 46 (5): 323–9. doi:10.1016/j.oraloncology.2010.01.009. PMID 20207580.
  24. ^ Li LC, Carroll PR, Dahiya R (January 2005). "Epigenetic changes in prostate cancer: implication for diagnosis and treatment". Journal of the National Cancer Institute. 97 (2): 103–15. doi:10.1093/jnci/dji010. PMID 15657340.
  25. ^ Beil L (Winter 2008). "Medicine's New Epicenter? Epigenetics: New field of epigenetics may hold the secret to flipping cancer's "off" switch". CURE (Cancer Updates, Research and Education). Archived from the original on 29 May 2009. Retrieved 20 January 2014.
  26. ^ Jagadeesh S, Banerjee PP (November 2006). "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". Biochemical and Biophysical Research Communications. 349 (4): 1361–7. doi:10.1016/j.bbrc.2006.09.002. PMID 16979586.
  27. ^ Dr med Peter Wolf, 2008, Innovations in biological cancer therapy, a guide for patients and their relatives, p 31-32
  28. ^ Hyperthermia - Cancer therapy hots up on physics.org
  29. ^ Javidi M, Heydari M, Attar MM, Haghpanahi M, Karimi A, Navidbakhsh M, Amanpour S (February 2015). "Cylindrical agar gel with fluid flow subjected to an alternating magnetic field during hyperthermia". International Journal of Hyperthermia. 31 (1): 33–9. doi:10.3109/02656736.2014.988661. PMID 25523967. S2CID 881157.
  30. ^ Javidi M, Heydari M, Karimi A, Haghpanahi M, Navidbakhsh M, Razmkon A (December 2014). "Evaluation of the effects of injection velocity and different gel concentrations on nanoparticles in hyperthermia therapy". Journal of Biomedical Physics & Engineering. 4 (4): 151–62. PMC 4289522. PMID 25599061.
  31. ^ Heydari M, Javidi M, Attar MM, Karimi A, Navidbakhsh M, Haghpanahi M, Amanpour S (2015). "Magnetic Fluid Hyperthermia in a Cylindrical Gel Contains Water Flow". Journal of Mechanics in Medicine and Biology. 15 (5): 1550088. doi:10.1142/S0219519415500888.
  32. ^ David Templeton (18 January 2007). "Research on local man's cancer treatment idea shows it has promise". Pittsburgh Post-Gazette. Retrieved 4 November 2007.
  33. ^ Gannon CJ, Cherukuri P, Yakobson BI, Cognet L, Kanzius JS, Kittrell C, Weisman RB, Pasquali M, Schmidt HK, Smalley RE, Curley SA (December 2007). "Carbon nanotube-enhanced thermal destruction of cancer cells in a noninvasive radiofrequency field". Cancer. 110 (12): 2654–65. doi:10.1002/cncr.23155. PMID 17960610. S2CID 15680068.
  34. ^ "The cure to cancer could be in your radio!". Winknews.com. 2007. Archived from the original on 2 November 2007. Retrieved 1 November 2007.
  35. ^ Pless M, Weinberg U (August 2011). "Tumor treating fields: concept, evidence and future". Expert Opinion on Investigational Drugs. 20 (8): 1099–106. doi:10.1517/13543784.2011.583236. PMID 21548832. S2CID 903933.
  36. ^ "Tumour Treating Fields explained". ted.com. 2012. Retrieved 31 January 2012.
  37. ^ Mo S, Coussios CC, Seymour L, Carlisle R (December 2012). "Ultrasound-enhanced drug delivery for cancer". Expert Opinion on Drug Delivery. 9 (12): 1525–38. doi:10.1517/17425247.2012.739603. PMID 23121385. S2CID 31178343.
  38. ^ Mo S, Carlisle R, Laga R, Myers R, Graham S, Cawood R, Ulbrich K, Seymour L, Coussios CC (July 2015). "Increasing the density of nanomedicines improves their ultrasound-mediated delivery to tumours". Journal of Controlled Release. 210 (10): 10–8. doi:10.1016/j.jconrel.2015.05.265. PMID 25975831.
  39. ^ Babington P, Rajjoub K, Canady J, Siu A, Keidar M, Sherman JH (June 2015). "Use of cold atmospheric plasma in the treatment of cancer". Biointerphases. 10 (2): 029403. doi:10.1116/1.4915264. PMID 25791295.
  40. ^ Weiss M, Gümbel D, Hanschmann EM, Mandelkow R, Gelbrich N, Zimmermann U, Walther R, Ekkernkamp A, Sckell A, Kramer A, Burchardt M, Lillig CH, Stope MB (1 July 2015). "Cold Atmospheric Plasma Treatment Induces Anti-Proliferative Effects in Prostate Cancer Cells by Redox and Apoptotic Signaling Pathways". PLOS ONE. 10 (7): e0130350. Bibcode:2015PLoSO..1030350W. doi:10.1371/journal.pone.0130350. PMC 4488447. PMID 26132846.
  41. ^ Davies AM, Weinberg U, Palti Y (July 2013). "Tumor treating fields: a new frontier in cancer therapy". Annals of the New York Academy of Sciences. 1291 (1): 86–95. Bibcode:2013NYASA1291...86D. doi:10.1111/nyas.12112. PMID 23659608. S2CID 33153055.
  42. ^ Cassileth BR, Deng G (2004). "Complementary and alternative therapies for cancer". The Oncologist. 9 (1): 80–9. doi:10.1634/theoncologist.9-1-80. PMID 14755017.
  43. ^ What Is CAM? National Center for Complementary and Integrative Health. retrieved 3 February 2008.
  44. ^ Richardson MA, Sanders T, Palmer JL, Greisinger A, Singletary SE (July 2000). "Complementary/alternative medicine use in a comprehensive cancer center and the implications for oncology". Journal of Clinical Oncology. 18 (13): 2505–14. doi:10.1200/JCO.2000.18.13.2505. PMID 10893280.
  45. ^ Vickers A (2004). "Alternative cancer cures: "unproven" or "disproven"?". CA: A Cancer Journal for Clinicians. 54 (2): 110–8. CiteSeerX 10.1.1.521.2180. doi:10.3322/canjclin.54.2.110. PMID 15061600. S2CID 35124492.
edit
Retrieved from "https://en.wikipedia.org/w/index.php?title=Experimental_cancer_treatment&oldid=1215198767"