Here is an option that will if nothing else help you to understand you disease.
One thing that is not to often made known to cancer patients, probably because it is a little bit technical, is that malignant tumors shed antigen and that when this is in excess with antibodies , antigen-antibody complexes are formed, which block further attack and shields the tumor from the immune system both locally and system wide.
There is also not only a suppression of the immune response to the tumor by suppressor T-cells but there is also a mechanism of tolerance called T-Cells and B-cells anergy, where these important players in the immune response become unresponsive. This seems to be somewhat reversible with the removal of the antigen though (Sci. aug21 92).
Beside these problem there is also an immuno-selection process where easily targeted tumor cells are killed off and the surviving tumor cells increasingly produce new undetected lines of descendants.
In a nutshell these seem to be the main problems as to the persistence of diseased state in the face of natural defense mechanisms.
There is however a white blood cell that is capable of eating (phagocytes) antigen-antibody complexes and adcc (antibody dependant cell mediated cytotoxicity). This is where the immune cell locks on to the tail (fc) region of the antibody that is attached to the cancer cell and chemically destroys it..
This white blood cell is call the eosinophil and because of these attributes and ease of access it is functionally equipped to combat multicellular parasites (helminthes), which present similar strategy requirements to cancer (size [relatively speaking], immunological shielding, and evasion).
Other immunotherapies fail because these therapies attemp to employ via vaccines, and other modes, macrophages, neutrophils, monocytes, and cytotoxic t’s which are equipped to elimiate smaller pathogens, and although these cells are needed in the total response they are by themselves ineffective against targets that are too large and that are immunolgically shielded by antigen antibody complexes.
I believe that in the use of il-2 to treat cancer; the eosinophil is a key component in the cases that are successful. I am not sure of this though. (see1698 Year 1998 Biological Responses to Intraperitoneal Interlekin-2 (IPIL-2) Infusions In the peritoneal cavity....... R. Edwards et.al. www.asco.org/prof/me/html/98abstracts/ibt/m_1698.htm)
Because activated eosinophils are associated with the strong and persistent th-2 immune response and because eosinophils are capable of both phagocytsising antigen and antibody complexes (Clinical and Basic Immunology 1977 edition page 285), have adcc capablities and have ease of access to and into the tumor, they meet the necessary strategic requirements in reducing tumor size.
Futhermore, because helminth excretory and secretory (HES) antigens elicite such a pronounced Th2 immune response that they cause bystander (Eur. J. Immunol. 2000. 30: 1977-1987 J. Holland et. al.) antigens (tumor) responses to also be driven to a Th2 response.
This will result in the immunolgical response to the tumor as if it were a helminth.
Freeze/thaw killed helminth ova have a similar effect but not as pronounced.
It can be implemented by first inoculating the patient with helminth antigen (not HES or ova).
When the serum activated eosinophil level reaches at least 20%; the HES or freeze/thaw killed ova of the same species as the inoculation can now be injected into the tumor or tumors.
Best wishes
Ps
Circumstantial evidence:
) antigen-antibody complexes and adcc (antibody dependant cell mediated cytotoxicity). This is where the immune cell locks on to the tail (fc) region of the antibody that is attached to the cancer cell and chemically destroys it..
This white blood cell is call the eosinophil and because of these attributes and ease of access it is functionally equipped to combat multicellular parasites (helminthes), which present similar strategy requirements to cancer (size [relatively speaking], immunological shielding, and evasion).
Other immunotherapies fail because these therapies attemp to employ via vaccines, and other modes, macrophages, neutrophils, monocytes, and cytotoxic t’s which are equipped to elimiate smaller pathogens, and although these cells are needed in the total response they are by themselves ineffective against targets that are too large and that are immunolgically shielded by antigen antibody complexes.
I believe that in the use of il-2 to treat cancer; the eosinophil is a key component in the cases that are successful. I am not sure of this though. (see1698 Year 1998 Biological Responses to Intraperitoneal Interlekin-2 (IPIL-2) Infusions In the peritoneal cavity....... R. Edwards et.al. www.asco.org/prof/me/html/98abstracts/ibt/m_1698.htm)
Because activated eosinophils are associated with the strong and persistent th-2 immune response and because eosinophils are capable of both phagocytsising antigen and antibody complexes (Clinical and Basic Immunology 1977 edition page 285), have adcc capablities and have ease of access to and into the tumor, they meet the necessary strategic requirements in reducing tumor size.
Futhermore, because helminth excretory and secretory (HES) antigens elicite such a pronounced Th2 immune response that they cause bystander (Eur. J. Immunol. 2000. 30: 1977-1987 J. Holland et. al.) antigens (tumor) responses to also be driven to a Th2 response.
This will result in the immunolgical response to the tumor as if it were a helminth.
Freeze/thaw killed helminth ova have a similar effect but not as pronounced.
It can be implemented by first inoculating the patient with helminth antigen (not HES or ova).
When the serum activated eosinophil level reaches at least 20%; the HES or freeze/thaw killed ova of the same species as the inoculation can now be injected into the tumor or tumors.
Best wishes
Ps
Circumstantial evidence:
Because activated eosinophils are associated with the strong and persistent th-2 immune response and because eosinophils are capable of both phagocytsising antigen and antibody complexes (Clinical and Basic Immunology 1977 edition page 285), have adcc capablities and have ease of access to and into the tumor, they meet the necessary strategic requirements in reducing tumor size.
Futhermore, because helminth excretory and secretory (HES) antigens elicite such a pronounced Th2 immune response that they cause bystander (Eur. J. Immunol. 2000. 30: 1977-1987 J. Holland et. al.) antigens (tumor) responses to also be driven to a Th2 response.
This will result in the immunolgical response to the tumor as if it were a helminth.
Freeze/thaw killed helminth ova have a similar effect but not as pronounced.
It can be implemented by first inoculating the patient with helminth antigen (not HES or ova).
When the serum activated eosinophil level reaches at least 20%; the HES or freeze/thaw killed ova of the same species as the inoculation can now be injected into the tumor or tumors.
Best wishes
Ps
Circumstantial evidence:
1) http://jcsmr.anu.edu.au/org/imm/canc-vascbiol/cellular/resea (see bottom bullet point).
2)