Poor vascularization in tumors will also result in necrosis and tissue damage. Most of the surrounding tissue will inhibit the uncontrolled growth. Until organs, bones, periost, tendons and tendon vaginal may temporarily inhibit tumor expansion.
More general circumstances that affect the growth, perhaps even influence the occurrence of tumors, is the status of individual hormonal and immunological defenses. Surely not just those factors that play a role in this regard. These factors will be discussed separately, since it is the starting point of a particular therapy.
It is known that some malignant tumors such as prostate carcinoma, breast carcinoma and endometrial carcinoma may also, showed a susceptibility to hormonal and growth can be affected by changing the hormonal status of the individual concerned.
Sometimes prostate carcinoma showed good reaction to castration or estrogen administration. Breast carcinoma can sometimes be improved by administering hormones, castration and adrenalectomy. Pda pregnancy sometimes we find the opposite, namely an existing breast carcinoma sometimes grow faster.
Hormonal status and hormonal therapy will be discussed separately in the relevant chapters in the special part of this book. Until recent time the possibility that the organism can affect tumor growth in immunologik not be taken seriously.
Because tumor cells occurs in the host organism itself otochton, so they would be recognized as 'self' alone because the cells were not there '' determinants-determinants '' antigens that are not tolerated by the organism.
So different from the organisms-microorganisms that have entered '' determinants-determinants '' this will be recognized as foreign by the organism on tumor growth is not expected that the reaction of the organism immunologik.
But the transplant experiments led to the discovery of the laws of tissue transplantation and familiar immunogenetik 'genes' dominant undergoing segregation according to Mendel's laws and then are called '' histocompatibility genes '' or '' H-H-gene-gene ''.
Antigens present in tumor cells that induce immunity reaction, called 'Tumor Specific Transplantation Antigens'' (TSTA) or '' Tumor Associated Transplantation Antigenecity '' (TATA). As demonstrated by the transplantation experiments showed antigen-entigen transplantation is associated with tumors in a purely tribal.
So healthy recipients suddenly confronted with tumor cells. With this it is clear that tumor antigens are located in the host ctochton be bound to a tumor that occurs in the organism, and induces immunity reaction is not really a transplant antigens earnest but to simply so called.
In tumors experimentally dituymbuhkan emergence is dependent antigens than the agent that causes the growth of the tumor. Experimental tumors as a result of viral infection have surface antigens specified in the code by the viral genome.
The vaccines are made from such tumor cells can sometimes protect other animals against oncogene activity of the virus. Tumors induced by chemical carcinogens and different physical reactions. Tumor cells resulting from stimulation of the carcinogen, showed only weak antigenicity together.
If in this case the specific antigenicity increases, then this may indicate that large differences within the population of tumor cells. Tumors induced by a non-carcinogen in an animal virus antigenicity can show large differences.
There are two kinds of immunity reactions. There humoral response means no '' antibodies '' made directed against TSTA, and no cellular reaction, meaning that the tumor cells can be destroyed by specific lymphoid cells. Perhaps the destruction of tumor cells is a very complex process with a synergistic role of T cells-lymphocytes, B-lymphocytes and macrophages-magrofag.
Immunity against tumors solide based mainly on the activity of T-lymphocytes, T-lymphocytes. 'Antibodies' made by B-lymphocytes, B-lymphocytes may have the ability to destroy tumor cells in circulation. Despite the proven existence of immunologic rejection power against tumors that grow in an organism, but the tumor cells can also escape from this reaction.
Way of escape that can be demonstrated experimentally, which is certainly a bit much also found in humans may be three kinds. They can occur at the level of tumor cell host interaction at the level of the tumor cells, and at the host level.
At the level of the host tumor experiments destroy tumor cells by immunologic reactions show that this mechanism can only be the tumor cells are limited in number, and the level of immune reaction that occurs is dependent on the strength of excitatory antigenetik the tumor cells.
This is in contrast to tumors with one another. Can be described that the tumor is growing quickly and is a bona fide antigenistas, can easily penetrate the immunologic barrier. At the level of the tumor cells, we are dealing with some theoretical possibilities:
1 tumor cells while having no antigenic akspresi, which is specific for the tumor. This we call modulation.
2 There antigenitas loss, because the loss of genetic determinants, or due to epigenetic changes.
3 Sometimes it looks interactions between lymphocytes that disensibilisasi specifically by antigen, and tumor cells is inhibited. This effect may be due to blockade of the antibodies or antigen-antibody complexes that exist.
At the host level decreased immunological surveillance role. With immunologic surveillance is the ability of higher organisms to protect themselves by immunologic mechanisms against tumor cells of the organism itself can take place as a result of cell transformation.
Certain drugs and corticosteroids among sitostatica and ionizing rays, reducing the activity of immunologic apparatus. Also the aging process, this activity is reduced and this leads to a lack of immunological surveillance. Because the tumor cell population is usually not homogeneous, then the existence of such surveillance a certain portion of the population can be eliminated earlier, so that the others would get a better chance and also can infiltrate or form metastases.
How important immunologic apparatus in humans in preventing and inhibiting tumor growth is still not clear. Things are pointing in this direction is more often found malignant tumors in people who use drugs that inhibit the immunologic apparatus, in people with congenital immunologic deficiency and in advanced age. Therapy based on immunologic rejection will be discussed in a separate chapter.
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