Tumor immunology

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The tumor immunology and cancer immunology is a branch of Immunology . She deals with the immunological processes that are involved in the development, course and defense, as well as the fight against tumors . The basis for tumor immunology is the theory of immune monitoring of tumors postulated by Paul Ehrlich , Lewis Thomas and Macfarlane Burnet . It assumes that changes in a cell in the course of the development of a tumor can be recognized as foreign by the immune system and attacked.

history

Tumor immunology began with studies by the New York surgeon William Coley . Coley treated a 17-year-old sarcoma patient who died quickly of the disease and then researched sarcoma patients with a positive outcome. It was noticeable that the tumor often regressed in such patients after a febrile illness. Coley then developed a mixture of bacteria, the so-called Coley toxin, and was able to observe successful courses among it. His daughter Helen Coley Nauts researched the patients treated by her father and published the cases with impressive numbers on remissions and long-term survival. The experiments of Coley and his successors are considered to be the beginning of tumor immunology and cancer immunotherapy .

Tumor repopulation

If tumor cells are irradiated with X-rays , some of the cells are so damaged that they are no longer able to divide and either die immediately or after a short time. Another part is only slightly damaged or not at all and is thus able to reproduce without restriction. The proportion of the respective fractions depends on various parameters such as the radiation dose , the type of radiation, the duration of the radiation and the individual properties of the cells.

Molecularly little is known about the influence that the dead cells have on the growth of the surviving cells. There are various possible mechanisms by which the dead cells stimulate the growth of the surviving ones. There is also the possibility that the dead cells inhibit the growth of the survivors through toxins or local inflammation (see also Abscopal effect ).

As early as 1956, two different types of tumors were examined. On the one hand, tumors caused by carcinogens and spontaneous, and on the other hand Ehrlich's ascites tumors. The solid tumors were each removed and brought into culture. Some of the cells were irradiated with X-rays in a dose well above the LD 50 . The first group of mice received only fatally damaged cells; no tumor development was observed here. The second group was injected with live cells only, the third group with a mixture of both. If one compares the second and third groups with one another, one finds that the lethally damaged cells exert a great stimulating influence on the living cells. This effect was most pronounced when the number of living cells was small compared to the number of dead cells. Here the latency period of tumorigenesis and the survival time of the animals were shortened.

The results of Ehrlich's ascites tumor varied. When the same mixture was injected as described above, the same growth stimulation was obtained. However, if only a very small number (100) of living cells were injected with the same amount of lethally damaged cells, a pronounced inhibition of cell growth was observed. 100 living cells alone led to progressive tumor growth in all cases, while the simultaneous presence of the damaged cells completely prevented their development. One could speak of an active immunization against the immunologically and genetically foreign (allogeneic) tumor. This leads to an unexpected result in the case of non-specific tumors in the genetically foreign recipient: treatment that destroys only part of the tumor cells can lead to regression through the support of the body's own immune system.

However, the situation is different with syngeneic (genetically identical) tumors. Here a partial destruction of the tumor cells stimulates the growth of the surviving cells. This can also prevent the violent local inflammation with which the host does not react.

literature

  • P. Ehrlich: About the current status of carcinoma research . In: Contributions to experimental pathology and chemotherapy , 1909, pp. 117–164, pei.de (PDF)
  • M. Burnet: Cancer; a biological approach . In: British Medical Journal . tape 1 , no. 5022 , April 6, 1957, p. 779-786 , PMID 13404306 , PMC 1973174 (free full text).
  • Gavin P. Dunn, Allen T. Bruce, Hiroaki Ikeda, Lloyd J. Old, Robert D. Schreiber: Cancer immunoediting: from immunosurveillance to tumor escape . In: Nature Immunology . tape 3 , no. 11 , 2002, p. 991-998 , doi : 10.1038 / ni1102-991 .

Individual evidence

  1. ↑ HC Nauts, WE Swift, BL Coley: The treatment of malignant tumors by bacterial toxins as developed by the late William B. Coley, MD, reviewed in the light of modern research . In: Cancer Research . tape 6 , April 1, 1946, p. 205-216 , PMID 21018724 .
  2. ↑ Gunver S. Kienle: Fever in Cancer Treatment: Coley's Therapy and Epidemiologic Observations . In: Global Advances in Health and Medicine: Improving Healthcare Outcomes Worldwide . tape 1 , no. 1 , March 1, 2012, p. 92-100 , doi : 10.7453 / gahmj.2012.1.1.016 , PMID 24278806 , PMC 3833486 (free full text).
  3. ↑ Bernadette Wiemann, Charlie O. Starnes: Coley's toxins, tumor necrosis factor and cancer research: A historical perspective . In: Pharmacology & Therapeutics . tape 64 , no. 3 , January 1, 1994, pp. 529-564 , doi : 10.1016 / 0163-7258 (94) 90023-X .
  4. ^ L. Révész: Effect of Tumor Cells killed by X-rays upon the Growth of Admixed Viable Cells . In: Nature . tape 178 , no. 4547 , December 22, 1956, p. 1391-1392 , doi : 10.1038 / 1781391a0 ( document.li ).