This article is about cancer therapy.

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Biotherapy of advanced cancer using fever, viruses and autologous immune cells (dendritic cells and natural killer cells)

Fever, viruses and autologous (i.e., the patient’s own) immune cells are natural healing processes in the very special sense that Nature itself has designed them without human intervention and successfully implements them millions if not billions of times each day – if we also include the animal kingdom. The following inverse correlations have been found:

  • Patients with more fever have a lower incidence of cancer [1]
  • and Patients with more viral infections have a lower incidence of cancer. [2]

Fever and viruses are apparently proven strategies that have evolved to confer protection against cancer. That the immune system with its key elements – dendritic cells and natural killer cells – should play an important role here is self-evident.Then why does it fail so often? For several reasons: the ineffectiveness of most immunotherapies in advanced cancer is due to the inexorable rate of tumour growth. The cancer cells form factors with which they stimulate their own growth, as reflected in the following rule:

The larger the tumour, the faster it grows.

Added to this, the cancer cell can turn the knife back on to its assailants: while the cancer cell itself is partially invulnerable due to inadequate formation of the death receptor (FAS receptor, CD95) and is often immortal because the regulator gene p53 is defective, it is perfectly able to transmit the death signal (FAS ligand, CD95L) and kill its pursuers, rather like “a criminal murdering a policeman”. The following observation is therefore also true:

The larger the tumour, the weaker the immune system.

Given these tumour cell dynamics, it will be clear that the immune cell is no longer able to keep pace in advanced cancer. In this dire situation the Hiroshima-like destruction caused by chemotherapy was more an act of desperation than a scientifically based therapy. Aside from rare testicular tumours and forms of leukaemia, it has no claim to being curative. If the patient’s life is extended at all, this is often achieved at a fearsome cost of suffering, to say nothing of the financial aspects.Inhibition of blood vessel formation is an attempt to biologically control the inexorable rate of tumour growth. As to its usefulness, the jury is still out.[3] This cell biology background means that most immunotherapies only have any point in the stage of minimal tumour load: to eradicate residual cancer cells that cannot be seen with imaging techniques such as ultrasound, X-rays, computed tomography, magnetic resonance imaging and scintigraphy, and even before the conventional tumour markers indicate the presence of danger.[4]

Hyperthermia, viruses and autologous immune cells are exceptions to the rule that immunotherapy offers prospects for success only in the stage of minimal tumour load. Scientific documentation is available on each of these three treatment facets:


This covers all therapies that are associated with an increase in body temperature. We distinguish between active hyperthermia, i.e., true fever therapy, and passive hyperthermia of the whole body (whole-body hyperthermia) or of individual body parts (locoregional hyperthermia) by infrared radiation (superficial hyperthermia) or alternating electrical fields (deep hyperthermia). At or above an increase in temperature to 43°C, we tend to use the term “thermotherapy”.

1.1. Fever therapy:

Killed bacteria are used to produce fever. The uncontested standard is Coley’s toxin, a mixture of Gram-positive and Gram-negative bacteria, namely Streptococcus pyogenes and Serratia marcescens. The body of experience with this pyrogen extends back for more than a century and covers millions of applications![5]Other mixtures or substitutes, such as a-interferon, have proved less effective. Three comparative studies[6] as well as a pilot study from a German university[7]have been published, providing unequivocal statistical evidence of efficacy in advanced cancer. According to Prof. Abel, a statistician at the German Cancer Research Centre in Heidelberg, the fundamental efficacy of fever therapy in cancer is beyond doubt.[8]

1.2. Locoregional deep thermotherapy:

Fever stimulates the immune system more comprehensively and with greater success than many other immunostimulants. However, the temperatures achieved are not sufficient for oncolysis. At the same time, passive whole-body hyperthermia procedures up to 42° and 42.5°C, such as are attempted today in many hyperthermia centres, damage not only the cancer cells but also the immune system, giving the same contradictory results as chemotherapy.Hence the strategy of combining fever therapy with locoregional deep thermotherapy[9]when the fever reaches its peak. This offers two decisive advantages:

1.2.1. The temperatures are additive. With currently available hyperthermia devices, it is possible to achieve temperature increases in the tumour of 4° - 8°C above the ambient temperature. Therefore at a fever temperature of 39° - 40°C, temperatures of 43° - 48°C can be achieved in the tumour. It is currently believed that this is sufficient to achieve the necessary heat build-up for oncolysis; in contrast, because heat is distributed unevenly, locoregional deep thermotherapy alone does not attain oncolytic temperatures in places and therefore concomitant chemotherapy is often necessary.

1.2.2. Fever therapy provides optimal immunostimulation. Effective tumour destruction is achieved by locoregional deep thermotherapy when the fever reaches its peak.The contradictory goals of optimal immune stimulation and effective tumour destruction can only be achieved by combining fever therapy with locoregional deep thermotherapy.

2. Therapy with oncolytic viruses:

In this field there is even a multicentre, placebo-controlled study in very advanced cancer showing an impressive outcome in favour of the virus group, with the result that this particular treatment facet is better evaluated than most cytostatics.[10]In an ongoing observational study, 14 patients with glioblastoma multiforme are currently being treated exclusively with Newcastle disease virus.[11]Survival for longer than 1 year – despite surgery, radiation and chemotherapy – is so unusual with this brain tumour that doubts can arise as to the accuracy of the diagnosis. Therefore all 14 patients in this study have had their diagnosis verified histologically. Seven patients are still alive and have hardly any disease-related handicap. In 4 of these patients between 5 and 9 years have now elapsed since the initial diagnosis. It is tempting to think that almost one-third of the patients with this unfavourable prognosis are perhaps really cured! No other treatment option comes even close in terms of success.

Whereas typical fowl plague (avian influenza) is caused by an influenza virus, which is also perfectly capable of infecting humans, the causative organism of atypical fowl plague is the Newcastle disease virus, which is unknown in human medicine. This virus therefore gives grounds for optimism that it might be an ideal cytostatic: all cancer cells are affected,[12] whereas healthy human cells are spared. The cancer cells disintegrate or are at least “labelled” by the virus in such a way that they can be identified and attacked by the immune system. This therefore increases the immunogenicity of the tumour as well as the prospects of success for immunotherapy even in cancers, such as breast and colon cancer, which are normally minimally responsive or unresponsive to immunotherapy.Over and above this the viruses also act directly on the immune cells and stimulate them to secrete messenger substances that activate the entire immune system. It is only a question of the dose, and then body temperature increases after just a few hours, long before the tumour cells disintegrate. In this way they stimulate the specific and the non-specific immune system and also lead to a reduction in the tumour load and hence lighten the burden on the immune defences.These many varied effects mean that viruses occupy a unique place among immunostimulants, thus lending fuel to the conviction that in future no cancer therapy will be successful without enlisting help from viruses.

From the patient’s standpoint, however, theory counts for nothing, and the results achieved appear far more sobering. The obverse conclusion from the promising brain tumour study is that, despite the use of effective viruses, the likelihood of dying from the disease is greater than that of recovering. Two small details were needed before therapy with oncolytic viruses could make the real breakthrough:

2.1. The efficacy of the viruses had to be improved. In order for this to happen,

2.1.1. A test method had to be developed, a “virogram” (similar to the “antibiogram” for bacteria to determine resistance to various antibiotics), in order to identify the most effective cancer-killing virus from a wide range of oncotropic viruses, i.e., viruses that are capable of infecting a tumour cell. There are two key criteria: lysis time, i.e., the time to destruction of the cell culture, and the capacity for syncytia formation, i.e., the capacity of the virus to spread into neighbouring cells even before the destruction of the tumour cell. The cell walls are permeated, resulting in “giant cells” with several cell nuclei (syncytia), before these giants are destroyed. The virus should spread as rapidly as possible into neighbouring cells before the immune system and the tumour are able to defend themselves against the virus by forming interferon and antibodies.

2.1.2. To improve efficacy further, this best natural virus is adapted to the tumour in cell cultures, even before it is used. The lysis time can be markedly reduced by continuous passages in autologous or homologous cultures. The result is a “tumour-adapted oncolytic virus strain”, a “TAO virus”, obtained by persistent training of “natural talents” on tumour cultures.

2.2. The viruses need to be administered regionally.

Oncological virologists are unanimous: the viruses work best if they are administered close to the tumour.[13]After many years of experience I am able to say that intratumoral injection always leads to a reduction in tumour size or at least to marked softening of the tumour due to the accompanying immune response. However, this gratifying development had no visible effect on neighbouring foci. The true breakthrough was achieved only with regional administration, i.e., we inject the TAO viruses into the blood vessel supplying the tumour. For lung tumours a conventional Port-a-Cath into the right atrium is sufficient, as is currently common practice for systemic chemotherapy. For all other tumours, however, the viruses have to be injected into the supplying artery, e.g., into the hepatic artery in the case of liver metastases, or into the aortic arch where there is extensive metastatic spread.

Currently, it has long been the practice for skilled interventional radiologists to insert similar port systems under local anaesthesia also for regional chemotherapy. My modest contribution was to administer the viruses precisely in the way that modern oncology is increasingly administering chemotherapeutic agents, namely regionally. However, this tiny modification was apparently the emphasis that was lacking in this context. Whereas classic oncology still has some difficulty in documenting the superiority of regional over systemic (intravenous) chemotherapy, the superiority of regional therapy with oncolytic viruses over systemic and over local administration is so evident that a comparative study would be impossible to justify on ethical grounds.

With the previously usual practice of injection into a peripheral vein, the long inflow pathway and the capillary network of the lung reduced the proportion of viruses finally reaching the tumour to one thousandth or even less. The situation was similar with inhalation. In this case the mucous membranes were the critical obstacle. While the Newcastle disease viruses do not infect any healthy human cells, they are absorbed by all possible cells, i.e., they are bound and thus taken out of circulation. Put plainly, this means that the viruses have minimal tumour targeting. This is why it is so important to manoeuvre the virus cannon right up to the gates of the tumour.

The situation has changed dramatically since we have been administering the viruses in this way: the exception has become the rule! Now for the first time the viruses are able to unfold their full potential. Aside from terminal cases, we now almost always see a clinical response as reflected in the typical development of parameters in the course of immunotherapy: tumour cells are eliminated by “inflammation” because the more elegant “apoptosis pathway” is usually defective. Inflammation leads firstly to softening and swelling of the tumour. Only in the later course of events does it become smaller. Tumour markers behave similarly. As a result of tumour disintegration, they show an initial rapid rise and then decline over the course of a few weeks, and in rare cases over a period of months. A similar picture is seen with well-being. The disintegrating tumour masses may sap vitality in a major way. The patients are tired, worn out, something is going on in the tumour and in the body as a whole – it’s a revolution! The patients only feel better after this “reaction phase”. These are the laws of “stimulation therapy”. These “labour pangs of healing” are similar to the process of giving birth: simply knowing the purpose behind this discomfort reduces it to a level that can be easily tolerated.If a patient is unresponsive (or inadequately or no longer responsive) to regional virus administration, then there is every reason to doubt the proper functioning of the port system. Further vascular visualisation with contrast medium is indicated in order to ensure that the viruses have “access” to their target.

3. Therapy with autologous immune cells:

We distinguish between specific (acquired) and non-specific (innate) immunity. These fulfil different tasks and are equally important.[14]

“Specific” means that each cell in this system has a single objective, e.g., to destroy a breast cancer cell. Presumably, an immune cell of this type would have little idea how to handle a leukaemia cell because this looks totally different, and it would not be at all appropriate for dealing with bacteria and viruses. It is highly specialised and has all the good and bad points of an “expert”. This category includes T and B lymphocytes. The B lymphocytes are transformed into plasma cells and form antibodies that label the cancer cells for the complement system and for the cytotoxic T lymphocytes. These are able to kill the cancer cells either by triggering programmed cell death (apoptosis) or by means of a cylindrical protein (perforin) which acts rather like an arrow.

Paradoxically, a certain antagonism exists between antibody-mediated (humoral) and cell-mediated immunity. Whereas the cytotoxic T lymphocytes (TH1 response) increase the aggressiveness of the immune system, the humoral (TH2) response not infrequently leads to tumour tolerance. We seek to steer the immune system in the proper direction by using suitable drugs, e.g., COX-2 inhibitors, which are also employed in rheumatology.

The non-specific immune system includes the granulocytes, macrophages and natural killer (NK) cells. Basically, these cells are “jacks of all trades” although they do have certain key emphases. The natural killer cells exist chiefly to eliminate cancer cells and virus-infected cells. The lion’s share of immunological work is accomplished by the non-specific immune system.

The non-specific immune system also includes cells that are beneficial to the tumour. It is claimed that macrophages clean the tumour and hence contribute to its well-being. We therefore try to inhibit macrophages by using suitable drugs such as H2-blockers (cimetidine), a medicine otherwise in common use as a gastroprotective agent.Most immunotherapies such as phytotherapy (e.g., mistletoe, echinacea, taiga root), organ therapy (e.g., thymus preparations) and orthomolecular therapy (e.g., selenium, vitamin A, C and E) stimulate the non-specific immune system in particular. Fever and natural killer cells also number among the non-specific immunostimulants. Viruses act on both systems: after just a few hours they stimulate the non-specific immune system This is reflected in a slight increase in body temperature. Then when the tumour cells disintegrate due to virus infection, this also leads to a specific immune response that is potentiated by the presence of the viruses.

3.1. Specific immunity is stimulated most powerfully by the dendritic cells.

These are the cells that set the immune response in motion. They form the bridge between the innate and the acquired immune systems. They identify the cancer cell, devour and dismantle it, migrate into the lymph nodes (or more likely, according to more recent findings from Prof. Schirrmacher, into the bone marrow) and “present” appropriate fragments to those lymphocytes, which Nature has already prepared with wise foresight. These are simply waiting for this signal to transform themselves into activated cytotoxic T-lymphocytes, i.e., immune cells that mature in the thymus and kill the tumour cells in a duel.Dendritic cells have demonstrated extraordinary efficacy in renal cell carcinoma.[15]Success has not been as convincing in other cancer types. Renal cell carcinoma is one of the easily identifiable cancers. It is highly “immunogenic”. If the same wonderful effect is also to occur in other cancer types, these first have to be made identifiable.This can be done most simply with our viruses. They thus belong to the most effective co-stimulants of dendritic cells. This is one of the reasons why the individual components in our treatment strategy are not merely additive but actually potentiate each other.


Treatment with dendritic cells alone confers definite clinical benefit in 30 – 50% of patients at best. This means that immunotherapy has gone through the sound barrier and gives every reason for celebration. In everyday clinical practice, however, failure is still encountered more frequently than success if hope is invested in dendritic cells alone. This is why we attack cancer using several strategies at once.One entirely novel attempt to improve therapy with immunocompetent cells is to combine dendritic cells with natural killer cells.The drawback of dendritic cells and their effector cells, the T lymphocytes, is that they can only attack if the cancer cell has formed transplantation antigens (MHC epitopes) on its surface. If the cancer cell does not have this “personal ID”, which distinguishes my kidney cell from every other human kidney cell, then the T lymphocytes do not move into action.This limits their usefulness in tumour defence because the cancer cell is often characterised by a complete “loss of identity”. It has lost these antigens, its “ID”, and has become “anonymous”: either it no longer forms these markers on its surface at all because it has become so “primitive” in the course of dedifferentiation or, having got into distress, it sheds these identity characteristics – in a similar way to tumour markers.These faceless cells therefore suddenly become invisible for the specific, acquired immune system. Thankfully, however, they can still be identified by the innate immune system, part of which is composed of natural killer cells. These are a very important pillar in the defence against tumours, and they mark the true dawn of the era of “immunotherapy with defined immunocompetent cells”. With them Rosenberg has brought some cancers into remission.[16]When implemented as monotherapy, this approach has largely remained unsuccessful. However, in combination with dendritic cells, these “good old” killer cells will presumably experience a renaissance in future. Cancers that have been unresponsive or inadequately responsive to dendritic cells alone have disappeared completely in response to killer cells.I am delighted that in my practice I am able to offer the highest standard of immunotherapy in cooperation with several German universities.

I am delighted that in my practice I am able to offer the highest standard of immunotherapy in cooperation with several German universities.

Immunotherapy is performed in cycles. The first cycle lasts for 3 weeks, with subsequent cycles each lasting 2 weeks. The cycles are separated by an interval of about 3 weeks, during which only viruses continue to be administered. A basic course of immunisation comprises 4 cycles, i.e., it takes about 6 months.

In advanced cancers the various components of our treatment strategy are as follows:

1. At initial presentation a biographical history is taken on mainstream medical and homeopathic principles. The social context and the patient’s inner attitude to his/her illness are also very important. The initial diagnosis and therapeutic measures with documentary evidence of success provide a first estimate of the current tumour load.

2. The general examination serves two purposes:

2.1. To assess the patient’s ability to cope with fever. The greatest risk is posed by heart disease. An exercise ECG and a spirogram are indispensable for the careful assessment of the benefits and risks of fever therapy.

2.2. To provide a definitive assessment of the current tumour load. Laboratory investigations and imaging techniques (ultrasound, CT, MRI, scintigraphy) are essential for this.

2.3. Focal diagnosis based on Nogier’s ear acupuncture is used to reveal important causes of the immunodeficiency “cancer”. Patients frequently have chronic inflammation of the tonsils and paranasal sinuses as well as dental foci (purulent infection and metal intolerance). The abdominal cavity may also accommodate important foci: chronic inflammation of the Fallopian tubes, prostate, appendix and gallbladder.

On the basis of history-taking and focal diagnosis, ahomeopathic prescription is prepared with the aim of achieving detoxification. We differentiate between:

2.4.1. Non-specific detoxification, e.g., resulting from increased metabolism in the context of fever therapy or from pharmacological and physical stimulation of the organs of excretion (liver, kidneys, intestine), and

2.4.2. Specific detoxification, e.g., DDT in breast cancer. Homeopathic prescriptions can promote both processes – organ function as well as counter-signal interruption of pathological signal transduction by the carcinogen leading to transformation, i.e., we need the corresponding isopathic agents for the most important cancer-producing substances. In post-chemotherapy states, the administration of homeopathised chemotherapeutic agents is also indispensable for the restoration of immunocompetence.

3. On the basis of all important reports and findings, a detailed treatment plan is prepared.

4. Instruction in simple qigong exercises to prevent and eliminate influenza symptoms related to fever and to improve patients’ inner attitude to illness and to their own life (psycho-oncology), because their will to live has often been broken. Patients often travel long distances for treatment – not so as to become well, but in order to try everything so that they don’t have to “reproach” themselves.

5. Installation of port systems for the injection of oncolytic viruses in the immediate vicinity of the tumour, daily or every other day.

6. Blood collection
to obtain dendritic cells and natural killer cells. UVB therapy or ozone therapy with approx. 800 µg O3/100 ml blood should be performed shortly before blood collection. This stimulates the natural killer cells to proliferate vigorously.

7. Combined hyperthermia (fever therapy + locoregional deep thermotherapy) is performed in two-week cycles daily from Monday to Friday.

One week after blood collection the dendritic cells are mature. They are injected either unloaded into the tumour, or loaded (with autologous or foreign tumour material) into the skin or into a lymph node.

9. Two weeks after blood collection the natural killer cells are injected into the tumour or into the artery.

10. After a two- to three-week treatment pause (during which only the viruses are administered), these two-week treatment cycles are initially repeated 4 times. Success is monitored (ultrasound, CT, MRI, tumour markers) once a month. As soon as the tumour starts to regress, the intervals between treatments can be extended.

Where the tumour load is small, i.e., after curative mainstream medical treatment, to prevent recurrence and to prevent metastases
, dendritic cells(Immuntherapie.net) are omitted, unless tumour material is available, and natural killer cells are also omitted. However, if tumour material has been properly stored, then therapy with dendritic cells constitutes an outstanding enrichment of the therapeutic arsenal particularly in the stage of minimal tumour load. The risk of recurrence can be reduced considerably by this measure alone. Depending on the aggressiveness of the tumour, we also recommend 1 - 2 series annually, each consisting of 6 fever therapies.

Aggressiveness is determined by the tumour load and the histological findings. Where the prognosis is poor, e.g., in “black” skin cancer (malignant melanoma) above a layer thickness of 1.5 mm, it is advisable also to add in one or other facet of the treatment strategy for advanced cancer, in particular, dendritic cells and lymphokine-activated killer (LAK) cells. In the absence of autologous tumour material (i.e., from the patient in question), the dendritic cells are primed in the laboratory using foreign cancer cells that are known to carry most of the cancer-specific surface antigens, i.e., identifying markers. With the help of these “photofit images”, the “commanders” of the immune defence system are well prepared for their battle with the enemy.

In this favourable stage of clinical tumour freedom, it is wise to attack the focal diseases with firm determination, i.e., to free the patient from suppurative foci, e.g., in the paranasal sinuses by Luffa cleansing, and from the junk of various metals in the mouth – including the destructive agent mercury.

It remains a vital task to resolve the question: “Why have I become ill?” This should be neither forced nor forgotten. The illness could be a good reason for the patient to make radical changes to his or her life.[17]

Tuesday, January 29, 2008
Nick West

On the Right Track!

Good news from the oncologist today. My bone scan from a couple of weeks ago came back, and most of the bone metastases have retreated considerably! My normally reserved oncologist broke into a rare use of positive phrases: "it's remarkable -- we almost never see the metastases diminish."

Also, at the end of December my PSA had declined again, to 1.6 ("almost" normal!)

Apparently most of the time, the "standard" treatment I'm on (the hormone blockage therapy that zeroes out my testosterone) merely slows the metastases down. (Or in the best case, brings it to a halt). The bone scan instead shows that the spots have almost disappeared -- the doctor says that some of what's left is evidence of arthritis rather than cancer (I'll take that choice any day!)

This confirms what the technician said a couple of weeks ago when she printed out the film of my scan and exclaimed -- 'wow, we never see that happen!"

Apparently all the effort (and expense) that we went to to get to Germany for the treatments by Dr. Thaller have paid off handsomely -- what he did had an amazing effect! Thanks to all of you who contributed for making this possible!

Now comes the hard part, which is keeping these gains intact, and continuing to work on the cancer that remains. Today is the start of my enzyme therapy treatment, which is a lot more labor-intensive, but reportedly very effective! (More on that in a later post.)

Nick West, USA

[1] Hager, E.D., Abel, U.: Biomodulation und Biotherapie des Krebses [Biomodulation and biotherapy of cancer], Heidelberg 1987, p. 26.

[2] Kölmel, K.F.: Infections and melanoma risk: results of a multicentre EORTC case-control study. Melanoma Research 1999; 9: 11-519.

[3] Brewer, G., Dick, R., Grover, D., LeClaire, V., Tseng, M., Wicha, M., Pienta, K., Redman, B., Jahan, T., Sondak, V., Strawderman, M., LeCarpentier, G., Merajver, S.: Treatment of metastatic cancer with tetrathiomolybdate, an anticopper, antiangiogenic agent: Phase I study. Clinical Cancer Research 2000; 6: 1-10.

[4]Nous avons fondé une société pour le diagnostic précoce et le traitement du cancer.
“Gesellschaft für Krebs-Frühdiagnostik und -Therapie e.V.”, Arno Thaller, President, Benzing 6, 91801 Markt Berolzheim, tel.: 09146-9429714, fax: 09146-224, e-mail: Krebsfruehdiagnostik@no_Spam.t-online.de

[5] Helen Coley Nauts, in: Bibliographie von Berichten zur klinischen oder experimentellen Anwendung von Coley-Toxinen.(Streptococcus pyogenes und Serratia marcescens) 1893 – 1986 [Bibliography of reports on the clinical or experimental administration of Coley’s toxins; (Streptococcus pyogenes and Serratia marcescens) 1893 – 1986] in: Hager, E.D., Abel, U.: Biomodulation und Biotherapie des Krebses. Endogene Fiebertherapie und exogene Hyperthermie in der Onkologie [Biomodulation and biotherapy of cancer.  Endogenous fever therapy and exogenous hyperthermia in oncology], Heidelberg 1987, pp. 168 - 188.     

[6]Kempin, S., Cirrincone, C., Myers, J., Lee III, B., Straus, D., Koziner, B., Arlin, Z., Gee, T., Mertelsmann, R., Pinsky, C., Comacho, E., Nisce, L., Old, L.,  Clarkson, B., Oettgen, H.: Combined modality therapy of advanced nodular  lymphomas (NL): the role of non-specific immunotherapy (MBV) as an important determinant of response and survival. Memorial Sloan-Kettering Cancer Center, New York, N. Y. 10021, in: Proceedings of ASCO (American Society of Clinical Oncology) 2=19, 56 (1983), C218.

Oettgen, H.F., Old, L.J., Hoffmann, M.K. and Moore, M.A.S.: Antitumor effects of endotoxin: possible mechanism of action, in: Homma, Y., Kanegasaki, S., Lüderitz, O., Shiba, T., Westphal, O., Bacterial Endotoxin, Weinheim, 1984, pp. 205 -21.

Zhao You Tang, Hai Yan Zhou, Gang Zhao, Li Mian Chai, Ming Zhou, Ji Zhen Lu, Kang Da Liu, H. Francis Havas, Helen Coley Nauts: Preliminary result of mixed bacterial vaccine as adjuvant treatment of hepatocellular carcinoma. Med. Oncol & Tumor Pharmacother. 1990; 8 (1): 23-28.

Johnston, B.J.: Clinical effect of Coley’s toxin - I.: a controlled study, in: Cancer Chemother. Rep. no. 21, 19-41 (1962).

Johnston, B.J., and Novales, E.T.: Clinical effect of Coley’s toxin - II.: a seven-year study, in: Cancer Chemother. Rep. no. 21, 43-68 (1962).

[7]   Kölmel, K.F., Abel, U., Kuhn, B., Vehmeyer, K., Wieding, J. U.: Behandlung      des metastasierenden malignen Melanoms mit einem Endotoxin enthaltenden      Bakterienlysat. Ergebnisse einer Pilotstudie [Treatment of metastasising malignant melanoma with a bacterial lysate containing endotoxin.  Results from a pilot study], in: Waclawizel, H. W., Gebhart, W., Manfreda, D., Schlag, P. (eds.): Das maligne Melanom [Malignant melanoma], Berlin, Heidelberg, New York 1991, pp. 238 – 241.

[8]Abel, U.: Die Wirksamkeit der aktiven Fiebertherapie des      Krebses mit Bakterientoxinen [The efficacy of active fever therapy of cancer      with bacterial toxins]. Zeitschrift für Onkologie 1999; 31 (2): 47-55.

Hager, E.D., Abel, U.: Biomodulation und Biotherapie des Krebses. Endogene Fiebertherapieund exogene Hyperthermie in der Onkologie [Biomodulation and biotherapy of cancer.  Endogenous fever therapy and exogenous hyperthermia in oncology], Heidelberg 1987, 168 - 188.

Hager, E.D.: Mikrobielle Immunmodulatoren: Aktive Fiebertherapie mit Bakterientoxinen [Microbial immunomodulators: active fever therapy with bacterial toxins], in: Naturheilverfahren und unkonventionelle medizinische Richtungen.Grundlagen, Methoden, Nachweissituationen [Natural healing and unconventional medical trends, principles, methods, detection situations], eds. M. Bühring and F.H. Kemper. Berlin, Heidelberg, New York, 1992ff: Chapter 10.05, pp. 1-39.

[9] Øvergaard, J., The Design of Clinical Trials in Hyperthermic Oncology, Danish Cancer Society, Department of Experimental Clinical Oncology, Radiumstationen, D-8000 Aarhus C, Denmark, in: Physics and Technology of Hyperthermia, ed. by Fields, S.B. and Franconi C., 1987.

Sugahara, T., Yamamoto, I.: Clinical response of hyperthermia. Biomedical Engineering Application Basis Communication 1994; 6: 340-362.

van der Zee, J. et al.: Comparison of radiotherapy alone with radiotherapy plus hyperthermia in locally advanced pelvic tumors: a prospective, randomised, multicentre trial. Dutch Deep Hyperthermia Group, Lancet 2000; 355(9210): 1119-1125.

Szasz, A., Szasz, O., Szasz, N., Electro-hyperthermia. a new paradigm in cancer therapy, Deutsche Zeitschrift für Onkologie, 2001; 33: 91-99

Hager, E.D, Dziambor, H. et al.: Deep hyperthermia with radiofrequency in patients with liver metastases of colorectal cancer.  Anticancer Research 1999; 19: 3403-8.

Sahinbas, H., Grönemeyer, D.H.W., Böcher, E.R., Lange, S.: Hyperthermia treatment of advanced relapsed gliomas and astrocytomas. University Witten/Herdecke, Bochum, Hyperthermia Symposium, Cologne 26. -27.10.2003.

Hager, E.D.: The treatment of patients with high-grade glioma with deep RF-hyperthermia, ASCO Meeting 2003.

[10] Csatary, L.K., Eckhardt, S., Bukosza, I., Czegledi, F., Fenyvesi, C., Gergely, P., Bodey, B., and  Csatary, C.M.: Attenuated veterinary virus vaccine for the treatment of cancer, in: Cancer Detection and Prevention 1993; 17(6): 619-627.

Driever, P. H., Rabkin, S. D.: Replication-competent viruses for cancer therapy. Basel, 2001, Monographs in Virology Vol. 22, ed. Doerr, H.

[11] Csatary, L.K., Gosztonyi, G., Szeberenyi, J., Fabian, Z., Liszka, V., Bodey, B., Csatary, C.M.: MTH-68/H oncolytic viral treatment in human high-grade gliomas. Journal of Neuro-Oncology 2004; 67: 83-93.

[12] Le professeur Schirrmacher du centre allemand de recherche contre le cancer(DKFZ) à Heidelberg a étudié “des centaines de cultures cellulaires de tumeurs humaines” et n’a pas pu découvrir un seul clone résistant (communication personnelle). Cela représente un avantage majeur de plus par rapport aux cytostatiques.

Comparé aux autres virus, le virus de la maladie de Newcastle se distingue par la stabilité de son code génétique et par le fait qu’il n’est pas incorporé au génome humain. Dans ce contexte, les craintes que ce virus bénéfique puisse un jour changer d’apparence par une mutation et produire ainsi des tumeurs semble totalement irréalisable.

[13] Schirrmacher, V., Griesbach, A. and Ahlert, T.: Antitumor      effects of Newcastle Disease Virus in vivo: local versus systemic effects.     International Journal of Oncology 2001; 18: 945-952.

[14] Thaller, A.: Tumortherapie mit Fieber, Viren und Visualisierung, ein Konzept, das alte Erfahrung, moderne Wissenschaft und die Kraft des Glaubens in sich vereint [Tumour therapy with fever, viruses and visualisation: a strategy that combines ancient experience, modern science and the power of faith].In: Leben mit Krebs, Perspektiven in das 21. Jahrhundert [Living with cancer – a look ahead into the 21st century], ed. Heiss, G., Mainz 2001. This article is based on :

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