Strategy for tumor prevention
To prevent tumor development, it is necessary to minimize contact with carcinogens and increase the body's overall resistance.
Main directions of prevention:
- Prevention of carcinogen action. The main task is to protect the cell genome from mutations.
- Reduction of the carcinogenic burden. Includes the modernization of technologies in industry, agriculture, and everyday life. In hazardous industries, personal protection is mandatory (special clothing, respirators, remote manipulators). Special attention is paid to protecting women during pregnancy and lactation to exclude any blastmogenic effect on the unborn child.
- Enhancement of antiblastoma resistance. Achieved through a healthy lifestyle: complete cessation of smoking and alcohol, regular physical exercise and sports, and a regulated diet.
- Elimination of preneoplastic conditions. Maximum early detection of potentially dangerous pathologies is extremely vital. For example, timely treatment of cryptorchidism in boys prevents the development of germ cell testicular tumors, and removal of teratomas under the age of three months prevents their transformation into malignant teratoblastomas.
Four principles of antitumor therapy
Medical care for patients with neoplasms relies on four fundamental principles:
- Etiotropic. Aimed at the inactivation and elimination (removal) of carcinogens from the body.
- Pathogenetic. Aims to disrupt key links of carcinogenesis and physically destroy or remove the tumor.
- Sanogenetic. Focuses on activating the tissue's own antiblastoma mechanisms using adaptogens, immunomodulators, and immunostimulants.
- Symptomatic. Designed to alleviate distressing symptoms (e.g., pain syndrome) that worsen the patient's condition. Analgesics and tranquilizers are used for this purpose.
Modern pathogenetic methods
Pathogenetic treatment is the basis of oncology. Its goal is the destruction of the neoplasm. In addition to classical non-pharmacological (surgical, radiation, thermal) methods and standard polychemotherapy, modern targeted and immunologic drugs are actively used:
- Telomerase inhibitors (primarily for the treatment of leukemias) and apoptosis modulators.
- Cadherin expression regulators, which help limit the metastasis process.
- Cytokines (using IL-2 as an example). They stimulate the proliferation of NK cells, enhance the synthesis of cytotoxic molecules that trigger the apoptosis of target cells, increase the number of receptors on the cell surface, and accelerate the migration potential of immunocompetent cells.
- Cellular adoptive therapy. The patient's immune cells (macrophages, T lymphocytes, NK cells) are isolated, their killer activity is enhanced ex vivo using leukokines or tumor cells, and they are then reintroduced into the body. This produces a significant cancerolytic effect. Examples: LAK cells (NK cells activated by IL-2), TIL cells (a mixture of NK cells and tumor tissue cells), and CIK cells.
- Inhibitors of negative immunogenic checkpoints. Monoclonal antibody-based drugs block inhibitory signals (B7-CTLA-4 interaction or PD1 receptors). This removes the "brakes" from the immune system and dramatically increases the killer effect of T lymphocytes and NK cells.
Approaches to patient management tactics
The choice of specific tactics is always strictly individualized. The physician considers the type and histological structure of the tumor, the stage of development of the process, the presence of metastases, as well as the patient's sex, age, and comorbidities.
Globally, two approaches to differentiated treatment are distinguished:
- Radical intervention. Aimed at the complete elimination of the tumor. The expected result is a complete recovery of the patient or the achievement of long-term remission.
- Palliative treatment. Used under strict indications when radical therapy is impossible (e.g., in late stages of the tumor process).
The best results are shown by combination therapy, which implies a combination of various treatment modalities: surgery, radiation therapy, chemotherapy methods, immunotherapy, and the use of genetically engineered selective antitumor agents.
Briefly: answers to topical questions
What are the classes of chemical carcinogens according to their mechanism of action?
According to the cited sources, chemical substances belong to genotropic (mutagenic) carcinogens.
According to the directness of action, carcinogens are distinguished into:
- Direct-acting carcinogens.
- Indirect-acting carcinogens — metabolized in the body, such as nitro compounds.
Chemical carcinogens exert their effect through damage to the cellular genome DNA.
What are the main mechanisms of tumor "escape" from immune surveillance?
Mechanisms of immunological tolerance and tumor escape from immune surveillance include:
- Alteration of MHC molecule expression — the loss of classical MHC-I while preserving non-classical molecules makes the cell inaccessible to NK cells and CD8+ T cells.
- Mutation or modulation of tumor antigens — the tumor antigen may disappear from the cell surface.
- Impairment of antigen processing and presentation by antigen-presenting cells to CD4+ and CD8+ lymphocytes.
- Role of the tumor microenvironment — it does not promote APC activation due to extremely low levels of pro-inflammatory cytokines and exerts a suppressive effect via IL-10 and endothelial growth factor.
- Masking of antigenic determinants — shielding of foreign cells by antibodies, interfering with their recognition and destruction by T-killers.
- Insufficiency of T-lymphocyte costimulation — the absence of a second activation signal leads to anergy instead of an immune response.
EPSS — four principles of treatment: Etiotropic (cause), Pathogenetic (mechanism), Sanogenetic (defense), Symptomatic (symptoms).
Class and exam questions
Why is it necessary to remove teratomas in the first months of life?
Early removal (under 3 months) prevents their malignant transformation into teratoblastomas.
What is the essence of cellular adoptive therapy?
The patient's immune cells are isolated, their killer activity is enhanced outside the body (ex vivo), and then they are returned back to destroy the tumor.
How do immune checkpoint inhibitors work?
They block inhibitory signals (e.g., via PD1 receptors or B7-CTLA-4), preventing the tumor from "escaping" the immune response and increasing the activity of T lymphocytes.
What else to study on this topic
- Mechanisms of action of telomerase inhibitors in leukemias.
- The role of cytokines (using IL-2 as an example) in NK cell activation.
- Types of cells for adoptive therapy: LAK, TIL, and CIK.
- Regulation of cadherin expression to limit metastasis.
- Factors determining the choice of an individualized treatment regimen.
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