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'''Experimental cancer treatments''' are |
'''Experimental cancer treatments''' are medical therapies intended or claimed to treat [[cancer]] (see also ''[[tumor]]'') by improving on, supplementing or replacing conventional methods ([[surgery]], [[chemotherapy]], [[Radiation therapy|radiation]], and [[immunotherapy]]). |
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The entries listed below vary between theoretical therapies to unproven controversial therapies. Many of these treatments are alleged to only help against specific forms of cancer. It is not a list of treatments widely available at hospitals. |
The entries listed below vary between theoretical therapies to unproven controversial therapies. Many of these treatments are alleged to only help against specific forms of cancer. It is not a list of treatments widely available at hospitals. |
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==Bacterial treatments== |
==Bacterial treatments== |
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[[Chemotherapy|Chemotherapeutic]] [[medication|drugs]] have a hard time penetrating tumors to kill them at their core because these cells may lack a good |
[[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. 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 tumour's oxygenated sides, meaning they would be harmless to the rest of the body. A major problem has been that bacteria don't consume all parts of the malignant tissue. However combining the therapy with chemotheraputic treatments can help to solve this problem. |
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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 tumour the enzyme is expressed solely in the tumour. Thus a systemically applied prodrug is metabolised to the toxic drug only in the tumour. This has been demonstrated to be effective with the non pathogenic anaerobe ''[[Clostridium sporogenes]]''.<ref name="Mengesha">{{cite book |author= Mengesha et al.|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> |
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 tumour the enzyme is expressed solely in the tumour. Thus a systemically applied prodrug is metabolised to the toxic drug only in the tumour. This has been demonstrated to be effective with the non pathogenic anaerobe ''[[Clostridium sporogenes]]''.<ref name="Mengesha">{{cite book |author= Mengesha et al.|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> |
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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. HAMLET causes apoptosis and tumor cell death in tumor cells. HAMLET has broad antitumor activity in vitro, and its therapeutic effect has been confirmed in vivo in a human glioblastoma rat xenograft model, in patients with skin papillomas and in patients with bladder cancer.<ref name=Hallgren> |
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. HAMLET causes apoptosis and tumor cell death in tumor cells. HAMLET has broad antitumor activity in vitro, and its therapeutic effect has been confirmed in vivo in a human glioblastoma rat xenograft model, in patients with skin papillomas and in patients with bladder cancer.<ref name=Hallgren> |
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{{cite journal |
{{cite journal |
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| author=Hallgren O, Aits S, Brest P, Gustafsson L, Mossberg AK, Wullt B, Svanborg C.| title=Apoptosis and tumor cell death in response to HAMLET (human alpha-lactalbumin made lethal to tumor cells).| journal=Advances in Experimental Medicine and Biology. | year=2008 | pages=217–240 | pmid=18183931 |
| author=Hallgren O, Aits S, Brest P, Gustafsson L, Mossberg AK, Wullt B, Svanborg C.| title=Apoptosis and tumor cell death in response to HAMLET (human alpha-lactalbumin made lethal to tumor cells).| journal=Advances in Experimental Medicine and Biology. | year=2008 | pages=217–240 | pmid=18183931 |
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| doi=10.1007/978-0-387-74087-4_8 |
| doi=10.1007/978-0-387-74087-4_8 |
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| volume=606 |
| volume=606 |
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}}</ref> |
}}</ref> |
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{{see|oncolytic virus}} |
{{see|oncolytic virus}} |
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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 which cannot reproduce, or reproduce only to a limited extent, within the patient to ensure safety via the avoidance of [[lytic cycle|cytolytic |
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 which 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 which 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 |author=Rein DT, Breidenbach M, Curiel DT |title=Current developments in adenovirus-based cancer gene therapy |journal=Future Oncol |volume=2 |issue=1 |pages=137–43 |year=2006 |month=February |pmid=16556080 |pmc=1781528 |doi=10.2217/14796694.2.1.137 |url=http://www.futuremedicine.com/doi/abs/10.2217/14796694.2.1.137?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov}}</ref><ref>{{cite journal |author=Kanerva A, Lavilla-Alonso S, Raki M, ''et al.'' |title=Systemic therapy for cervical cancer with potentially regulatable oncolytic adenoviruses |journal=PLoS ONE |volume=3 |issue=8 |pages=e2917 |year=2008 |pmid=18698374 |pmc=2500220 |doi=10.1371/journal.pone.0002917 |url=http://dx.plos.org/10.1371/journal.pone.0002917}}</ref> |
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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. |
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. |
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More prolonged moderate heating to temperatures just a few degrees above normal 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 in cell, including slowed cell division and increased sensitivity to ionizing [[radiation therapy]]. |
More prolonged moderate heating to temperatures just a few degrees above normal 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 in cell, including slowed cell division and increased sensitivity to ionizing [[radiation therapy]]. |
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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]] or direct application of heat through the use of heated saline pumped through catheters. Experiments have been done with carbon nanotubes that selectively bind to cancer cells. 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 which 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 |
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]] or direct application of heat through the use of heated saline pumped through catheters. Experiments have been done with carbon nanotubes that selectively bind to cancer cells. 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 which 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. |
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[[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> |
[[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> |
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==Controversial therapies== |
==Controversial therapies== |
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{{Main|Alternative cancer treatments}} |
{{Main|Alternative cancer treatments}} |
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=== Diet therapy === |
=== Diet therapy === |
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Johanna Budwig proposed a diet therapy claimed to treat cancer. Most oncologists have a belief that a diet alone cannot treat cancer. Reports of dramatic remissions as a result of the Budwig diet are anecdotal, and not supported by [[peer-review]]ed research. (On the other hand, her diet is good from a nutritional point of view to counteract some side-effects of other treatments.) Some basic research on flax oil (preferred by Budwig) is available.<ref>{{cite journal |author=Li D, Yee JA, Thompson LU, Yan L |title=Dietary supplementation with secoisolariciresinol diglycoside (SDG) reduces experimental metastasis of melanoma cells in mice |journal=Cancer Lett. |volume=142 |issue=1 |pages=91–6 |year=1999 |month=July |pmid=10424786 |url=http://linkinghub.elsevier.com/retrieve/pii/S0304-3835(99)00158-5 |doi=10.1016/S0304-3835(99)00158-5}}</ref><ref>{{cite journal |author=Wang L, Chen J, Thompson LU |title=The inhibitory effect of flaxseed on the growth and metastasis of estrogen receptor negative human breast cancer xenograftsis attributed to both its lignan and oil components |journal=Int. J. Cancer |volume=116 |issue=5 |pages=793–8 |year=2005 |month=September |pmid=15849746 |doi=10.1002/ijc.21067 }}</ref><ref>{{cite journal |author=Chen J, Stavro PM, Thompson LU |title=Dietary flaxseed inhibits human breast cancer growth and metastasis and downregulates expression of insulin-like growth factor and epidermal growth factor receptor |journal=Nutr Cancer |volume=43 |issue=2 |pages=187–92 |year=2002 |pmid=12588699 |doi=10.1207/S15327914NC432_9 }}</ref><ref>{{cite journal |author=Thompson LU, Chen JM, Li T, Strasser-Weippl K, Goss PE |title=Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer |journal=Clin. Cancer Res. |volume=11 |issue=10 |pages=3828–35 |year=2005 |month=May |pmid=15897583 |doi=10.1158/1078-0432.CCR-04-2326 |url=http://clincancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=15897583}}</ref><ref>{{cite journal |author=Dabrosin C, Chen J, Wang L, Thompson LU |title=Flaxseed inhibits metastasis and decreases extracellular vascular endothelial growth factor in human breast cancer xenografts |journal=Cancer Lett. |volume=185 |issue=1 |pages=31–7 |year=2002 |month=November |pmid=12142076 |url=http://linkinghub.elsevier.com/retrieve/pii/S0304383502002392 |doi=10.1016/S0304-3835(02)00239-2}}</ref> |
Johanna Budwig proposed a diet therapy claimed to treat cancer. Most oncologists have a belief that a diet alone cannot treat cancer. Reports of dramatic remissions as a result of the Budwig diet are anecdotal, and not supported by [[peer-review]]ed research. (On the other hand, her diet is good from a nutritional point of view to counteract some side-effects of other treatments.) Some basic research on flax oil (preferred by Budwig) is available.<ref>{{cite journal |author=Li D, Yee JA, Thompson LU, Yan L |title=Dietary supplementation with secoisolariciresinol diglycoside (SDG) reduces experimental metastasis of melanoma cells in mice |journal=Cancer Lett. |volume=142 |issue=1 |pages=91–6 |year=1999 |month=July |pmid=10424786 |url=http://linkinghub.elsevier.com/retrieve/pii/S0304-3835(99)00158-5 |doi=10.1016/S0304-3835(99)00158-5}}</ref><ref>{{cite journal |author=Wang L, Chen J, Thompson LU |title=The inhibitory effect of flaxseed on the growth and metastasis of estrogen receptor negative human breast cancer xenograftsis attributed to both its lignan and oil components |journal=Int. J. Cancer |volume=116 |issue=5 |pages=793–8 |year=2005 |month=September |pmid=15849746 |doi=10.1002/ijc.21067 }}</ref><ref>{{cite journal |author=Chen J, Stavro PM, Thompson LU |title=Dietary flaxseed inhibits human breast cancer growth and metastasis and downregulates expression of insulin-like growth factor and epidermal growth factor receptor |journal=Nutr Cancer |volume=43 |issue=2 |pages=187–92 |year=2002 |pmid=12588699 |doi=10.1207/S15327914NC432_9 }}</ref><ref>{{cite journal |author=Thompson LU, Chen JM, Li T, Strasser-Weippl K, Goss PE |title=Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer |journal=Clin. Cancer Res. |volume=11 |issue=10 |pages=3828–35 |year=2005 |month=May |pmid=15897583 |doi=10.1158/1078-0432.CCR-04-2326 |url=http://clincancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=15897583}}</ref><ref>{{cite journal |author=Dabrosin C, Chen J, Wang L, Thompson LU |title=Flaxseed inhibits metastasis and decreases extracellular vascular endothelial growth factor in human breast cancer xenografts |journal=Cancer Lett. |volume=185 |issue=1 |pages=31–7 |year=2002 |month=November |pmid=12142076 |url=http://linkinghub.elsevier.com/retrieve/pii/S0304383502002392 |doi=10.1016/S0304-3835(02)00239-2}}</ref> |
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In [[insulin potentiation therapy]] (IPT), [[insulin]] is given in conjunction with low-dose chemotherapy. Its proponents claim insulin therapy increases the uptake of chemotherapeutic drugs by malignant cells, permitting the use of lower total drug doses and reducing side effects. |
In [[insulin potentiation therapy]] (IPT), [[insulin]] is given in conjunction with low-dose chemotherapy. Its proponents claim insulin therapy increases the uptake of chemotherapeutic drugs by malignant cells, permitting the use of lower total drug doses and reducing side effects. |
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Some ''In vitro'' studies have demonstrated the principle of IPT.<ref>{{cite journal |author=Alabaster O, Vonderhaar BK, Shafie SM |title=Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer cells |journal=Eur J Cancer Clin Oncol |volume=17 |issue=11 |pages=1223–8 |year=1981 |month=November |pmid=7037424 |doi=10.1016/S0277-5379(81)80027-2 }}</ref><ref>{{cite journal |author=Witt KA, Huber JD, Egleton RD, Davis TP |title=Insulin enhancement of opioid peptide transport across the blood-brain barrier and assessment of analgesic effect |journal=J. Pharmacol. Exp. Ther. |volume=295 |issue=3 |pages=972–8 |year=2000 |month=December |pmid=11082431 |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=11082431}}</ref> |
Some ''In vitro'' studies have demonstrated the principle of IPT.<ref>{{cite journal |author=Alabaster O, Vonderhaar BK, Shafie SM |title=Metabolic modification by insulin enhances methotrexate cytotoxicity in MCF-7 human breast cancer cells |journal=Eur J Cancer Clin Oncol |volume=17 |issue=11 |pages=1223–8 |year=1981 |month=November |pmid=7037424 |doi=10.1016/S0277-5379(81)80027-2 }}</ref><ref>{{cite journal |author=Witt KA, Huber JD, Egleton RD, Davis TP |title=Insulin enhancement of opioid peptide transport across the blood-brain barrier and assessment of analgesic effect |journal=J. Pharmacol. Exp. Ther. |volume=295 |issue=3 |pages=972–8 |year=2000 |month=December |pmid=11082431 |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=11082431}}</ref> |
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The first clinical trial of IPT for treating breast cancer was done in Uruguay and published in 2003/2004. Insulin combined with low-dose methotrexate (a chemotherapy drug) resulted in greatly increased stable disease, and much reduced progressive disease, compared with insulin or low-dose methotrexate alone. Although the study was very small (30 women, 10 per group), the results appear to be very promising.<ref>{{cite journal |author=Lasalvia-Prisco E, Cucchi S, Vázquez J, Lasalvia-Galante E, Golomar W, Gordon W |title=Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients |journal=Cancer Chemother. Pharmacol. |volume=53 |issue=3 |pages=220–4 |year=2004 |month=March |pmid=14655024 |doi=10.1007/s00280-003-0716-7 }}</ref> |
The first clinical trial of IPT for treating breast cancer was done in Uruguay and published in 2003/2004. Insulin combined with low-dose methotrexate (a chemotherapy drug) resulted in greatly increased stable disease, and much reduced progressive disease, compared with insulin or low-dose methotrexate alone. Although the study was very small (30 women, 10 per group), the results appear to be very promising.<ref>{{cite journal |author=Lasalvia-Prisco E, Cucchi S, Vázquez J, Lasalvia-Galante E, Golomar W, Gordon W |title=Insulin-induced enhancement of antitumoral response to methotrexate in breast cancer patients |journal=Cancer Chemother. Pharmacol. |volume=53 |issue=3 |pages=220–4 |year=2004 |month=March |pmid=14655024 |doi=10.1007/s00280-003-0716-7 }}</ref> |
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{{Tumors}} |
{{Tumors}} |
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{{Use dmy dates|date={{subst:currentmonthname}} {{subst:currentyear}}}} |
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{{DEFAULTSORT:Experimental Cancer Treatment}} |
{{DEFAULTSORT:Experimental Cancer Treatment}} |
Revision as of 11:54, 22 December 2010
Experimental cancer treatments are medical therapies intended or claimed to treat cancer (see also tumor) by improving on, supplementing or replacing conventional methods (surgery, chemotherapy, radiation, and immunotherapy).
The entries listed below vary between theoretical therapies to unproven controversial therapies. Many of these treatments are alleged to only help against specific forms of cancer. It is not a list of treatments widely available at hospitals.
Bacterial treatments
Chemotherapeutic drugs have a hard time penetrating tumors to kill them at their core because these cells may lack a good blood supply. 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 tumour's oxygenated sides, meaning they would be harmless to the rest of the body. A major problem has been that bacteria don't consume all parts of the malignant tissue. However combining the therapy with chemotheraputic 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 tumour the enzyme is expressed solely in the tumour. Thus a systemically applied prodrug is metabolised to the toxic drug only in the tumour. This has been demonstrated to be effective with the non pathogenic anaerobe Clostridium sporogenes.[1]
Photodynamic therapy
Photodynamic therapy is generally a non-invasive treatment using a combination of light and a photosensitive drug. Photodynamic Therapy, also known as PDT, uses photosensitive drugs (such as 5-ALA, Foscan, Metvix, Tookad, WST09, WST11, Photofrin and Visudyne) which are triggered by light of a specific wavelength.
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. HAMLET causes apoptosis and tumor cell death in tumor cells. HAMLET has broad antitumor activity in vitro, and its therapeutic effect has been confirmed in vivo in a human glioblastoma rat xenograft model, in patients with skin papillomas and in patients with bladder cancer.[2]
Gene therapy
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 which 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 which 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.[3][4] 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.
Telomerase therapy
Because most malignant cells rely on the activity of the protein telomerase for their immortality, it has been proposed that a drug which 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.[5]
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 drug (GRN163L).
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 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 in cell, including slowed cell division and increased sensitivity to ionizing radiation therapy.
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 or direct application of heat through the use of heated saline pumped through catheters. Experiments have been done with carbon nanotubes that selectively bind to cancer cells. 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 which 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.[6]
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.
Dichloroacetate (DCA)
Dichloroacetate has been found to shrink tumors in vitro in rats.[7] These studies received attention in the media,[8] and some doctors began controversially using the chemical off-label.[9] A small clinical trial (enrollment- up to 50 patients) has been planned with patients originating from the Edmonton area.[10][11]
Quercetin
In vitro, quercetin shows some antitumor activity. Cultured skin and prostate cancer cells showed significant mortality (compared to nonmalignant cells) when treated with a combination of quercetin and ultrasound[12] Note that ultrasound also promotes topical absorption by up to 1,000 times, making the use of topical quercetin and ultrasound wands an interesting proposition.[citation needed]
High dietary intake of fruits and vegetables is associated with reduction in cancer, and some scientists[who?] suspect quercetin may be partly responsible. Research shows that quercetin influences cellular mechanisms in vitro and in animal studies, and there is limited evidence from human population studies that quercetin may reduce the risk of lung cancer.[13][14]
Non-invasive RF cancer treatment
This preclinical treatment involves using radio waves to heat up tiny metals which are implanted in cancerous tissue. Gold nanoparticles or carbon nanotubes are the most likely candidate. Promising preclinical trials have been conducted,[15][16] although clinical trials may not be held for another few years.[17]
Complementary and alternative
Complementary and alternative medicine (CAM) treatments are the diverse group of medical and health care systems, practices, and products that are not part of conventional medicine and have not been shown to be effective.[18] "Complementary medicine" refers to methods and substances used along with conventional medicine, while "alternative medicine" refers to compounds used instead of conventional medicine.[19] CAM use is common among people with cancer; a 2000 study found that 69% of cancer patients had used at least one CAM therapy as part of their cancer treatment.[20] Most complementary and alternative medicines for cancer have not been rigorously studied or tested. Some alternative treatments which have been investigated and shown to be ineffective continue to be marketed and promoted.[21]
Controversial therapies
Diet therapy
Johanna Budwig proposed a diet therapy claimed to treat cancer. Most oncologists have a belief that a diet alone cannot treat cancer. Reports of dramatic remissions as a result of the Budwig diet are anecdotal, and not supported by peer-reviewed research. (On the other hand, her diet is good from a nutritional point of view to counteract some side-effects of other treatments.) Some basic research on flax oil (preferred by Budwig) is available.[22][23][24][25][26]
Unfortunately, the proponents of this approach have been consistently unable to produce a single surviving patient who meets all of these criteria:
- was diagnosed by an independent oncologist instead of by a proponent,
- actually appears to have been cured, and
- did not undergo conventional cancer therapies which could reasonably explain the successful treatment.
Insulin potentiation therapy
In insulin potentiation therapy (IPT), insulin is given in conjunction with low-dose chemotherapy. Its proponents claim insulin therapy increases the uptake of chemotherapeutic drugs by malignant cells, permitting the use of lower total drug doses and reducing side effects.
Some In vitro studies have demonstrated the principle of IPT.[27][28]
The first clinical trial of IPT for treating breast cancer was done in Uruguay and published in 2003/2004. Insulin combined with low-dose methotrexate (a chemotherapy drug) resulted in greatly increased stable disease, and much reduced progressive disease, compared with insulin or low-dose methotrexate alone. Although the study was very small (30 women, 10 per group), the results appear to be very promising.[29]
References
- ^ Mengesha; et al. (2009). "Clostridia in Anti-tumor Therapy". Clostridia: Molecular Biology in the Post-genomic Era. Caister Academic Press. ISBN 978-1-904455-38-7.
{{cite book}}
: Explicit use of et al. in:|author=
(help) - ^
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 alpha-lactalbumin made lethal to tumor cells)". Advances in Experimental Medicine and Biology. 606: 217–240. doi:10.1007/978-0-387-74087-4_8. PMID 18183931.
{{cite journal}}
: CS1 maint: multiple names: authors list (link) - ^ Rein DT, Breidenbach M, Curiel DT (2006). "Current developments in adenovirus-based cancer gene therapy". Future Oncol. 2 (1): 137–43. doi:10.2217/14796694.2.1.137. PMC 1781528. PMID 16556080.
{{cite journal}}
: Unknown parameter|month=
ignored (help)CS1 maint: multiple names: authors list (link) - ^ Kanerva A, Lavilla-Alonso S, Raki M; et al. (2008). "Systemic therapy for cervical cancer with potentially regulatable oncolytic adenoviruses". PLoS ONE. 3 (8): e2917. doi:10.1371/journal.pone.0002917. PMC 2500220. PMID 18698374.
{{cite journal}}
: Explicit use of et al. in:|author=
(help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - ^ http://www.ncbi.nlm.nih.gov/pubmed/16979586?log$=activity
- ^ Hyperthermia - Cancer therapy hots up on physics.org
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External links
- American Cancer Society
- National Cancer Institute
- Dichloroacetate (DCA) Research
- Nature Reviews Cancer website
- Audio-video Physician Interviews on Cancer Treatment Breakthroughs
- "Questionable Cancer Therapies"
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