Oncothermia is a method of hyperthermia in oncology, controlling the locally applied deep heat by selectively targeting the cellular membrane of the malignant cells. The selection of the method is based on various biophysical and biochemical achievements. There are various differences between the malignant and healthy cells, which could be used for their selection by heat targeting. The primary selection factor is a different metabolic activity which creates distinguishable environments of the malignant cells. The other factor is the clear difference of dielectric properties of the membrane and near-membrane extracellular electrolytes, marking off the malignancies. There is also a structural factor, which is clear in the different pathological patterns of the malignancy from their healthy counterparts. This last is described by fractal pattern evaluation technique, in which dynamic time-fractal transformation is used for further discernment of the malignancy. My objective is to show a new heating method, which makes oncological hyperthermia controllable and effective.
Oncological hyperthermia is the overheating of the malignant tissues locally or systemically. The method is deduced from the ancient medical practices, where the heat therapies had a central role in medicine. The local hyperthermia by the radiation of red-hot iron was the first known oncological treatment applied by Hypocrites, who described the method [
Treatments with coils (magnetic and inductive) are relatively rarely used due to the negligible magnetic permeability of living systems [
A method for electromagnetic energy delivery that has been widely used recently is the antenna-array coupling [
This rapidly emerging period was shadowed by skeptic opponents, which emphasized the increased dissemination of the malignant cells and so supported metastases by hyperthermia [
Many researchers had been doubtful and unsettled questioning the future of hyperthermia accepting the impressive biological effects but blaming the physical realization of the heat delivery [
What is the problem [
The same problems arise by typical capacitive coupling hyperthermia solutions. It pumps enormous energy also (1200 W) into the target, and rise of temperature was 4.8°C after 45 min. The selection by temperature between the malignant target and the nontargeted healthy tissue was approximately 1°C [
All of these problems are caused by the massive heating of the target, which has a physiological reaction to cool it down and to reestablish the homeostatic equilibrium. The complex physiological effects badly modify the desired effects [ Not only do the temperature equalizing process but also the natural, technically nonfollowable movements of the patients (i.e., due to the breathing) modify the focus. The heat flow to the surroundings can damage the healthy neighborhood. The enlargement of the sphere having certain temperature gradients increases the area of the injury current, and this supports the cell proliferation.
Compensating these effects, the acceleration of the heating with high energy has to be applied, when the incident energy might burn the skin. In consequence, certain surface cooling is necessary. The heat sink of the surface decreases the incident power, but its quantity has no measurable parameters. This way we lose the control of the treatment process by the incident energy, because the missing part by cooling is uncontrolled. It has serious consequences in the vigilance of the process: temperature measurement
The physiological feedback of the large volume temperature equalizing is the increased blood flow. The high blood flow promotes the glucose influx (delivery) and supports the malignant proliferation by this supply. The increased temperature anyway gains the metabolic rate and the proliferation even by the cells in dormant (G0) phase. The higher blood flow creates other malignant danger too: the risk of the forced disseminations and metastases, decreasing the prognostic factors of survival of the patient.
The well-focused local hyperthermia treatment creates a competitive pair of effects: killing the tumor cells by heat and supporting them by nutrients together with the risk of dissemination. The result of this competition is unpredictable and depends on the patient and on the applied techniques as well. The explanation of the controversial results of local hyperthermia in oncology may be simple: a reference point was missing [
The present main stream thinking of oncological hyperthermia is a typical loss of aims by illusions, believing the overall control of temperature. The temperature however is only a condition for the treatment and not its aim. The question “Tool or goal?” has become relevant to study the temperature alone. Take a simple example of mixing the tool and the goal in our everyday life: the graduation is a tool for our professional life; however when somebody regards the certificate of studies as a goal, its application, the aim of the study is lost. Mixing the tool with the action creates false goal in hyperthermia application: increase the temperature alone. This “autosuggestion” creates such a situation in which magnetic resonant imaging (MRI) is applied to control the temperature during the treatment instead of using this capable imaginary method to see what is happening in the tumor indeed.
Our tasks are the correct heating and control of the hyperthermia process. For this we have to precisely select the malignant cells and not heat up all the materials in the targeted tumor only the membrane of the cancerous cells. This selected nanoscope energy absorption liberates not as much heat energy which heats up all the mass equally, so its efficacy could be significantly higher. The main advantage is that it does not stimulate the blood-flow as physiologic feedback, consequently no contra-action starts to compensate the applied nanoscopic effect. Furthermore, the membrane excitation could excite special cellular signal-transduction pathways, which are connected with the natural apoptotic cell death, and so the negative feedback loop of the complex living system is supported. (The conventional hyperthermia by its overall heating excites negative feedback mechanisms to act against the temperature growth, so the system starts “fighting” against the healing process.)
The temperature as the average of kinetic energy in the system has a double role in the control of the heat absorption. It characterizes the heat absorption, when the heating is homogeneous (see before), and its gradients (nonhomogeneities) are the driving forces of the dynamic processes in case of microscopic (nonhomogeneous) heating. The average temperature does not inform us about the distribution of the real energy absorption (see Figure
The average temperature is not able to characterize the thermodynamic situation. The internal temperature differences could serve as driving forces of various processes on the same average temperature of the system.
Smaller targets with precise selection could get propositionally higher temperature keeping the average constant. The nanorange heating is the basic of oncothermia, allowing extreme heating at the membranes of the malignant cells while the average temperature does not increase as high as the physiological feedback starts to support the malignancy by higher blood flow reactions.
The efficacy of the energy depletion intended to be pumped into the tumor is limited by the energy loss outside the malignant target. The main factors of the useless energy absorptions are the following. The absorbed energy by the tissues transfers the effect to the deep-seated tumor. The heat exchange by the blood flow. The heat exchange by the heat conduction from the tumor to the surroundings.
These heat sinks modify the overall performance of the treatment and make the full heating process for the malignancy uncontrolled. The real effect, which is used for the intended treatment, is less than the losses, and the efficacy is usually less than 25%, which is very low. The problem of this is that not only a large part of energy is wasted, but also the useless energy part could be dangerous by overheating the healthy tissues as well as increasing the metabolic rate and also having a physiology reaction to this effect which tries to break the homeostasis. The massively heated tumor volume intensifies the control of physiology and weakens the expected effect.
The adequate corrective actions for these challenges would be the more precise targeting, decreasing the losses in the surrounding and avoiding the physiological corrections to suppress the desired effect. To construct the solution some new effects have been used to increase the efficacy. Apply the electric field as carrier of the energy, and that field cannot be compensated by homeostatic control. Apply a correct microscopic targeting, using the cell-by-cell energy absorption efficiently. Apply such mechanisms, which initialize natural effects to kill the malignant cells. Apply a mechanism, which carries the information that disseminated cells are to be blocked.
Oncothermia changes the paradigm of local hyperthermia in oncology to solve the above problems [
The general idea of microscopic heating is simple: the heating energy is not liberated in a sudden single step but regulated, and multiple small energy liberation does the same job (Figure
The difference of macro- and microliberation of energy. The efficacy of the last one is much better.
The precisely targeted power and its efficacy are usually not connected. The microscopic effects, instead of the large energy liberation, is one of the most update thinking in energy source developments. The relatively low efficacy combusting engines are intended to be replaced by the fuel-cell energy sources and electric motors, which are based on the membrane regulated microscopic reactions of gases. (Mostly hydrogen and oxygen gases are in use.)
Good examples are the standard incandescent bulb and the energy saving fluorescent ones, using a fraction of the power for the same light. The incandescent bulb creates light by high-temperature filament, which heats up the environment, having only 10% efficacy, while the fluorescent has more than 40%. It could be developed further by the more nanoscopic energy liberation, when not the molecules but the electrons are directly involved in the light production. These are the LED bulbs, having more than 90% efficacy in producing light.
Oncothermia [
Oncothermia setup. The cell culture/animal/human is a part of the electric circuit. Energy is carried by 13.56 MHz RF current (fractal modulated): (a) EHY2000 local/regional treatment, (b) EHY3000 multilocal treatment.
The radiofrequency current (RF current) flows through the body and delivers energy to the malignant cells. The frequency is low (13.56 MHz) chosen to satisfy multiple requests. It is a free frequency for medical applications in hospitals and clinics, as well as in general use, for example, RF identification. It is in the range of the beta dispersion which is one of the selection factors of oncothermia. It is low enough to have long wavelength for near-field use with high penetration into the body when the impedance matching [ It is high enough to be modulated by time-fractal fluctuations.
The discussion of all these behaviors are seen below.
The current which flows through the chosen part of the body starts from one electrode and ends on the other one, periodically changing its direction according to the carrier frequency. The current is directed by the impedances inside the targeted volume; the current automatically flows to the “easiest” direction, where the conductance and dielectric conditions are optimal. Oncothermia uses three factors to direct the current to select malignant cells, that is, those current paths are favored which include malignant cells are favoured. Certainly, the biophysical behaviors have to be studied to fix the optimum.
The first selection factor is the well-known metabolic differences between the malignant and healthy cells. Due to the high energy demand of the malignant proliferation, the malignant cells metabolize more to supply their needs. Furthermore, the process to produce ATP differs in malignant cells from normal. While the dominance of the mitochondrial ATP production in the healthy tissue produces 36 ATP from one glucose molecule during the complete cycle, the fermentative ATP production, which dominates the metabolism of malignant cells, results only two ATPs from one glucose molecule [
The radiofrequency current is focused on the tumor lesion and microscopically flows in the extracellular electrolytes around the malignant cells.
This gives us a possibility to distinguish the malignant cells automatically and individually (Figure
The microscopic heating of the extracellular electrolyte around the malignant cells excites the membrane and makes temperature gradient in a few nanometer distance.
The above selection is based on the conductive component of tissue impedance. The permittivity component is also selective. Malignant cells not only differ from their healthy counterpart by their metabolic processes, but also their collective behavior sharply identifies them. The malignant cells are autonomic; they are individual “fighters,” having no collective driving of their activity, while the healthy cells have social signals [
The difference of the healthy and malignant tissues is well observable by their organization structure.
This dielectric differences are well completed by the specialties of the cell membrane of the malignant cells. The efficacy of the ATP production in cancerous cell is low. The large ATP demand for the proliferative energy consumption allows less ATP for active membrane stabilization by K+ and Na+ transport, so the membrane potentiating weakens [ The cellular membrane of cancerous cells differs electrochemically also from the normal, and its charge distribution also deviates [ The membrane of the cancerous cell differs in its lipid and sterol content from its healthy counterpart [
The membrane permeability is changed by the above differences. In consequence of these the efflux of the K+, Mg++, and Ca++ ions increases, while the efflux of Na+ decreases together with the water transport from the cell. Consequently, the cell swallows, and its membrane potential decreases further [
There is further selection based on complex impedance, the
Oncothermia selects by the above electromagnetic differences and heats up the membrane of the malignant cells. The RF-current, which flows through the cancerous lesion, is automatically focused by its lower complex impedance [
Oncothermia delivers its energy mainly into the extracellular electrolyte, creating a temperature gradient through the cellular membrane (a). The thermal gradient action due to the nonhomogenous heating is active until the thermal equilibrium equalizes the temperature (b).
The cell killing needs energy, and afterwards the overall energy of the system would be decreased from a well-ordered (bounded) state (which was in the case of the living cell) to a disordered chemical state with some broken chemical bonds. The transition from the ordered (chemically higher energy) state to the disordered (chemically lower state) arrangement of the well-known gap energy must be pumped. This gap energy has different components. For hyperthermia, the heat energy gives the full energy consumption; however, in oncothermia, a significant field effect takes part in the distortion mechanism [
Oncothermia needs less thermal energy to make the same distortion than the classical hyperthermia does.
The missing connections (adherent bonds, junctions) not only are selected by the dielectric properties of the cells but also affect the energy absorption and the cellular protections against the energy overload. The absorbed energy by a healthy cell can easily be shared by the connections with the neighboring cells, damping the effect of the energy overload. The malignant cells have no such possibility, the no network distribution could protect them from the energy overload.
The large extracellular SAR makes not only thermal but also the electric inhomogeneity in the tissue; the extracellular matrix has higher current density than the other electrolytes. The current density gradient is accompanied with the gradient of the electric field, which could reorient the high-dielectric constant proteins in the extracellular liquid. The orientation of these protein molecules would be constrained perpendicular on the membrane surface. By this effect, the lost adherent connections could be rebuilt between the malignant cells, which were indeed shown experimentally [
An important and unique specialty of oncothermia is the modulation of the carrier frequency. This time-fractal pattern carried by the basic frequency distinguishes on similar way as the pathological evaluation does. The famous Adey window was the first proof of the special modulation effects [
The fractals in patterns are accompanied by fractal dynamics. This new discipline is the “Fractal Physiology,” ([
The fractal modulation which is applied by oncothermia selects and reestablishes the apoptotic pathway functions. A day after oncothermia, a definite difference can be detected between the anyway identical oncothermia treatments which are different only in the application of the modulation. Both treatments cause the same effect immediately after the application; however a day later definite differences appear. The treated lesion by nonmodulated signal started regrowth; the ratio of dead volume in the tumor decreases. At the same time the modulated treatment caused the opposite: the dead volume increases, and in two days the complete tumor was almost destroyed after a single shot treatment reaching 42°C in average in both the modulated and nonmodulated cases.
Oncothermia selects the malignant cells and acts differently from the physiological homeostatic reactions (heat flow on the membrane supported by the electric field effects). It is natural, it is not against the homeostasis, and physiology does not work against the action [
Using the modern achievements of the physiology, oncothermia answers positively on the doubts about the conventional hyperthermia. The experimental and preclinical results are described in other papers presented in this conference [
62 studies were performed with altogether 3790 patients, from six countries (Hungary, Germany, Korea, China, Italy, and Austria) [
Collection of the studies (phase II) made by oncothermia in combination with various conventional oncotherapies. (Data are weighted averages of the study results.)
Study | Number of studies | Number of patients ( |
1st year survival (%) | Median overall survival (m) | Responding patients/ratio (%) | Median overall survival of responding patients (m) | Median overall survival of nonresponding patients (m) |
---|---|---|---|---|---|---|---|
Brain studies | 10 | 521 | 73.99 | 22.19 | 44.09 | 51.31 | 15.88 |
Pancreas studies | 6 | 184 | 47.04 | 11.02 | 53.05 | 28.09 | 7.58 |
Lung studies | 5 | 636 | 64.76 | 15.79 | 25.73 | ||
Bone | 3 | 79 | 40.10 | 90.90 | |||
Liver metastasis | 7 | 267 | 86.00 | 18.06 | 80.00 | ||
Colorectal | 7 | 447 | 63.18 | 109.80 | 23.20 | ||
Gynecology (pelvic) | 5 | 100 | 93.22 | 33.25 | 44.82 | 89.36 | 21.70 |
Breast | 1 | 103 | 97.10 | 52.10 | 45.00 | 274.80 | 10.90 |
Esophagus | 2 | 19 | 41.70 | 55.64 | 35.00 | 29.40 | 8.50 |
Stomach study | 1 | 68 | 58.90 | 14.40 | |||
Kidney cancer | 1 | 39 | 84.60 | 35.90 | 48.00 | 78.40 | 33.70 |
Urinary bladder cancer | 1 | 18 | 85.00 | 36.50 | 73.00 | 42.00 | 22.60 |
Head and neck | 1 | 64 | 92.20 | 26.10 | |||
Soft tissue sarcoma | 1 | 16 | 100.00 | 35.90 | 31.00 | 115.30 | 31.30 |
Prostate | 3 | 135 | 88.90 | 38.80 | 72.00 | 53.40 | 7.60 |
| |||||||
SUM | 54 | 2796 | 51.63 |
Collection of the miscellaneous studies made by oncothermia in combination with various other therapies.
Miscellaneous study | Number of patients ( |
---|---|
Borreliosis | 12 |
General oncology | 277 |
TCM general oncology | 306 |
Abdominal effusion | 49 |
Peyronie’s disease | 25 |
Chronic pelvic inflammation | 283 |
Asthma | 7 |
Chronic bronchitis | 35 |
| |
SUM patients | 994 |
Summary of the studies made by oncothermia treatment (end points are survival connected).
Study | Number of patients | 1st year survival (%) | Median overall survival (m) | Responding patients/ratio (%) | Median overall survival of responding patients (m) | Median overall survival of nonresponding patients (m) | Reference |
---|---|---|---|---|---|---|---|
Brain gliomas | 27 | 86.2 | 23.6 | 43 | 66.2 | 18.2 | [ |
Brain lioma study, phase II | 140 | 71.7 | |||||
Astrocytoma | 40 | 25.8 | 80 | 40.2 | 20.2 | [ | |
Glioblastoma | 92 | 16 | 73 | 21.*9 | 13.1 | ||
Diffuse astrocytoma | 8 | 52.9 | |||||
Glioma (WHO IV) study, phase II, prospective, two arms | 45 | 15 | |||||
Passive arm | 36 | 40 | 11 | [ | |||
Active arm | 9 | 65 | 14.5 | 43 | 66.2 | 18.2 | |
Recurrent glioblastoma study, phase II | 19 | 68.0 | 21.8 | 59 | 32.6 | 12.4 | [ |
Glioma study, phase II | 36 | 60.0 | |||||
Astrocytoma | 9 | 106 | [ | ||||
Glioblastoma | 27 | 20 | |||||
Glioma study, phase II | 179 | ||||||
Astrocytoma | 53 | 100 | 103 | [ | |||
Glioblastoma | 126 | 76 | 16 | ||||
Advanced, relapsed brain gliomas, phase II | 12 | 10 | 25 | [ | |||
Advanced, relapsed brain gliomas, phase II | 24 | 55 | 12 | 25 | [ | ||
Brain glioma WHO III-IV, phase I, safety prospective | 24 | [ | |||||
Metastatic brain tumors study, phase II | 15 | 90.0 | 46.2 | 73 | 48.2 | 16.1 | [ |
Head and neck study, phase II | 64 | 92.2 | 26.1 | [ | |||
Bone-metastases, monotherapy, phase II | 6 | 100 | 40.1 | [ | |||
Refractory bone-metastases study, phase II | 11 | 90.9 | [ | ||||
Kidney cancer study, phase II | 39 | 84.6 | 35.9 | 48 | 78.4 | 33.7 | [ |
Urinary bladder cancer study, phase II | 18 | 85.0 | 36.5 | 73 | 42.0 | 22.6 | [ |
Nonsmall cell lung cancer meta-analysis | 311 | ||||||
Passive arm | 53 | 26.5 | 14 | ||||
Active arm | 258 | 67.0 | 15.8 | 21 | 53.4 | 18.1 | [ |
Nonadvanced (WHO < III) | 77 | 11 | 17 | ||||
Advanced (WHO ≥ III) | 140 | 14.7 | 88 | ||||
Small-cell lung cancer | 28 | ||||||
Passive arm | 9 | 29 | [ | ||||
Active arm | 19 | 58 | |||||
Lung carcinoma study, phase II | 61 | 67.2 | 16.4 | [ | |||
Breast cancers | 103 | 97.1 | 52.1 | 45 | 274.8 | 10.9 | [ |
Soft tissue sarcoma study, phase II | 16 | 100 | 35.9 | 31 | 115.3 | 31.3 | [ |
Esophagus study, phase II | 12 | 41.7 | 28.5 | 35 | 29.4 | 8.5 | [ |
Esophagus study, phase II | 7 | 6.8 | 100 | [ | |||
Liver metastases from various origin, phase II | 25 | 20.5 | [ | ||||
Liver metastases from various origin, comparative study, phase II | 28 | ||||||
With radiotherapy | 16 | 81 | [ | ||||
With chemotherapy | 8 | 38 | |||||
Monotherapy | 4 | 25 | |||||
Liver metastasis form colorectal origin, phase II | 80 | 86.0 | 24.1 | ||||
Passive arm | 53 | 11 | |||||
Active arm | 80 | 91 | 24.1 | [ | |||
With chemotherapy | 30 | 80 | 21.5 | ||||
Monotherapy | 50 | 92 | 24.4 | ||||
Liver metastasis form colorectal origin, phase II | 15 | 23 | 80 | [ | |||
Liver metastasis form colorectal origin, phase II | 22 | 28 | [ | ||||
Liver metastasis | 29 | 86 | |||||
Liver metastasis form colorectal origin, phase II | 30 | 22 | [ | ||||
Pancreas tumor study, phase II | 26 | 46.2 | 11.6 | [ | |||
Pancreas tumor study, phase II | 107 | ||||||
Passive arm | 34 | 6.5 | [ | ||||
Active arm | 73 | 52.1 | 9.93 | 58 | 25.5 | 8.4 | |
Pancreas tumor study, phase II | 30 | 31.0 | 41 | 34.4 | 5.6 | [ | |
Pancreas tumor study, phase II | 42 | 52.4 | 12.3 | [ | |||
Pancreas tumor study, phase II | 13 | 40.0 | 11.9 | [ | |||
Stomach cancer study, phase II | 68 | 58.9 | 14.4 | [ | |||
Colorectal cancer () | 218 | 84.9 | 28.5 | ||||
Sigma | 12 | 34.1 | [ | ||||
Rectum | 92 | 57.1 | 58 | 21 | |||
Colon | 114 | 44.2 | 109.8 | 23.2 | |||
Colon cancer study, phase II, prospective, three arms, randomized | 154 | [ | |||||
Clifford TCM | 53 | 75 | |||||
Monotherapy | 50 | 81 | |||||
Combined therapy | 51 | 91 | |||||
Rectum cancer study, Inoperable→operable, phase II | 7 | 71 | [ | ||||
Rectal cancer, nonoperable, phase II | 65 | 96 | [ | ||||
Pelvic gynecological cancer studies, phase II | 74 | ||||||
Cervix | 38 | 86.8 | 27.6 | 25 | 63.5 | 20.9 | [ |
Ovary | 27 | 100 | 37.8 | 67 | 132.7 | 19.4 | |
Uterus | 9 | 100 | 61.5 | 62 | 68.5 | 32.0 | |
Ovary, advanced, relapsed | 26 | [ | |||||
Heavily pretreated | 13 | 14.3 | |||||
Not heavily pretreated | 13 | 27 | |||||
Prostate cancer study, phase II | 18 | 88.9 | 38.8 | 72 | 53.4 | 7.6 | [ |
The survival time connected data, response rate connected data, the quality of life connected data, and tumor-marker connected data are collected in Tables
Summary of the studies made by oncothermia treatment. (end points are response connected.)
Study | Number of patients | Complete remission (CR) [%] | Partial remission (PR) [%] | No change (NC), stable disease (SD) [%] | Overall response rate (CR + PR + SD) [%] | Reference |
---|---|---|---|---|---|---|
Colorectal inoperable, liver metastasis | 60 | |||||
CDDP | 28 | 0 | 3.57 | 3.57 | 7.14 | [ |
OXALI | 32 | 0 | 15.63 | 15.63 | 31.25 | |
Ovary (relapsed, advanced epithelial) | 26 | [ | ||||
Heavily pretreated | 13 | 0.00 | 23.08 | 38.46 | 61.54 | |
Not heavily pretreated | 13 | 30.77 | 23.08 | 38.46 | 92.31 | |
General oncology | 277 | 21.50 | 37.00 | 58.50 | [ | |
TCM general oncology | 306 | |||||
Oncothermia + TCM | 75 | 6.67 | 57.33 | 26.67 | 90.67 | [ |
Oncothermia + TCM + i.v.CTx | 65 | |||||
Passive arm | 51 | 7.84 | 60.78 | 15.69 | 84.31 | [ |
Active arm | 14 | 14.29 | 64.28 | 21.43 | 100.00 | |
Oncothermia + TCM + abdominal perfusion | 87 | 0.00 | ||||
Passive arm | 45 | 2.22 | 40 | 24.44 | 66.66 | [ |
Active arm | 42 | 7.14 | 54.76 | 26.19 | 88.09 | |
Oncothermia + TCM + bladder perfusion | 37 | |||||
Passive arm | 24 | 0 | 50 | 12.5 | 62.50 | [ |
Active arm | 13 | 7.69 | 53.85 | 30.77 | 92.31 | |
Oncothermia + TCM + RTx | 42 | |||||
Passive arm | 30 | 3.33 | 50 | 16.67 | 70.00 | [ |
Active arm | 12 | 8.33 | 66.67 | 16.67 | 91.67 | |
Abdominal effusion + oncothermia | 49 | 4.08 | 53.06 | 16.38 | 73.52 | [ |
Chronic pelvic inflammation | 283 | [ | ||||
Passive arm | 143 | |||||
Active arm | 140 | 46.10 | 29.40 | 19.60 | 95.10 | |
Chronic bronchitis, TCM + oncothermia | 35 | 30.00 | 24.30 | 25.70 | 80.00 | [ |
Colon cancer study, phase II, prospective, three arms, randomized | 154 | [ | ||||
Clifford TCM | 53 | 5.7 | 28.3 | 18.9 | 52.90 | |
Monotherapy | 50 | 10 | 26 | 26 | 62.00 | |
Combined therapy | 51 | 13.7 | 45.1 | 23.5 | 82.30 | |
Colon operability | 7 | 71 | 71.00 | [ | ||
Prostatitis | 72 | [ | ||||
Passive arm | 36 | 16.70 | 27.80 | 19.40 | 63.90 | |
Active arm | 36 | 41.70 | 36.10 | 22.20 | 100.00 | |
Prostate study | 184 | 49.5 | 15.2 | 15.8 | 80.50 | [ |
Prostate cancer (Kleef) (Gleason Score 2–6) | 16 | [ | ||||
Oncothermia + hormone therapy | 8 | 50 | ||||
Oncothermia monotherapy | 8 | 37.5 | ||||
Prostate cancer (Kleef) (Gleason Score 7–9) | 17 | [ | ||||
Oncothermia + hormone therapy | 11 | 81.82 | ||||
Oncothermia monotherapy | 6 | 33.33 | ||||
Peyronie’s disease | 25 | 100 | ||||
Pancreas | 42 | 23.8 | 31 | 54.80 | [ | |
Pancreas | 30 | 3.3 | 33.3 | 40 | 76.60 | [ |
Esophagus | 8 | 50 | 42 | 100.00 | [ | |
CRC liver | 22 | 5 | 23 | 28 | [ | |
CRC liver | 15 | 20 | 60 | 80.00 | [ | |
CRC liver oxalplatin | 12 | 8.3 | [ | |||
CRC liver cisplatin | 18 | 27.8 | ||||
Advancer liver | 28 | [ | ||||
Oncothermia + RTx | 16 | 31 | 50 | 81 | ||
Oncothermia + CTx | 8 | 13 | 25 | 38 | ||
Oncothermia monotherapy | 4 | 25 | 25 | |||
Brain | 19 | 11 | 32 | 43 | [ | |
Asthma | 7 | 75 | 10 | 85 | [ | |
Small-cell lung cancer (SCLC) | 38 | 44.7 | 15.8 | 60.5 | [ | |
Benign tumors oncothermia + TCM | 35 | 54.3 | 25.7 | 80.00 | [ |
Summary of the studies made by oncothermia treatment. (end points are quality of life connected.)
Study | Number of patients | Pain reduction [%] | Increasing performances [%] | Better overall QoL [%] | Reference |
---|---|---|---|---|---|
Colorectal inoperable, liver metastasis | 60 | ||||
CDDP | 28 | 17.86 | 39.29 | 57.14 | [ |
OXALI | 32 | 46.88 | 7.86 | 100.00 | |
Borreliosis | 12 | 100.00 | 100.00 | [ | |
Abdominal effusion + oncothermia | 49 | 88.88 | 73.91 | 85.70 | [ |
Colon cancer study, phase II, prospective, three arms, randomized | 154 | [ | |||
Clifford TCM | 53 | 37.7 | 13.73 | 58.49 | |
Monotherapy | 50 | 36 | 23.53 | 60 | |
Combined therapy | 51 | 58.8 | 62.75 | 86.28 | |
Prostate study | 184 | [ | |||
Prostate study | 115 | 76.2 | 94.1 | [ | |
Colon operability | 7 | 86 | 43 | [ | |
CRC liver | 15 | [ | |||
CRC liver oxaliplatin | 12 | 66.7 | 83.3 | [ | |
CRC liver cisplatin | 18 | 11.1 | 27.8 |
Summary of the studies made by oncothermia treatment. (end points are tumor-marker connected.)
Study | Number of patients | Tumor-marker decrease [%] | References |
---|---|---|---|
Colorectal inoperable, liver metastasis | 60 | [ | |
CDDP | 28 | 14.29 | |
OXALI | 32 | 37.50 | |
CRC liver oxaliplatin | 12 | 58.30 | [ |
CRC liver cisplatin | 18 | 5.60 |
Further clinical trials are in progress on advanced ovary, esophagus, breast, and pancreas tumors.
Oncothermia is the cellular selective, highly effective nanoscopic heating of malignant cells. It is a feasible treatment for oncology in all the phases of malignant diseases. This nanothermic application solved the uncontrolled controversies of the conventional hyperthermia in oncology. Numerous new ways of research can be initialized by the presently achieved results. Further basic research and clinical studies are in progress.
The author express his gratitude for the valuable discussions with Professor A. Szasz and Drs. G. Andocs, N. Meggyeshazi, Cs. Kovago, N. Iluri, and Zs. Csih. This work is devoted to memory of Reka Sz.