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Prevention and Treatment of Tumors

For medical students2 min readUpdated 2026-10-10

Neoplasm prevention is based on protecting the cellular genome from mutagens and early elimination of preneoplastic pathologies. Cancer therapy relies on a comprehensive approach, ranging from carcinogen elimination to targeted disruption of tumor growth mechanisms.

Primary GoalProtection of the cellular genome from carcinogen exposure
SanogenesisActivation of the body's anti-blastomogenic mechanisms
Radical ApproachComplete eradication of the tumor to achieve remission
PathogenesisDisruption of the key links of carcinogenesis

Strategy for Neoplasm Prevention

To prevent tumor development, it is necessary to minimize contact with carcinogens and increase overall bodily resistance.

Main directions of prevention:

Four Principles of Antitumor Therapy

Medical care for patients with neoplasms relies on four fundamental principles:

  1. Etiotropic. Aims at inactivating and eliminating carcinogens from the body.
  2. Pathogenetic. Aims to disrupt key links of carcinogenesis and physically destroy or remove the tumor.
  3. Sanogenetic. Focuses on activating the tissue's own anti-blastomogenic mechanisms using adaptogens, immunomodulators, and immunostimulants.
  4. Symptomatic. Designed to alleviate distressing symptoms (e.g., pain syndrome) that worsen the patient's condition, using analgesics and tranquilizers.

Modern Pathogenetic Methods

Pathogenetic treatment is the basis of oncology, aiming to destroy the neoplasm. In addition to classical non-pharmacological methods (surgical, radiation, thermal) and standard polychemotherapy, modern targeted and immunologic agents are actively used:

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, the presence of metastases, as well as the patient's sex, age, and comorbidities.

Globally, two approaches to differentiated treatment are distinguished:

Mnemonic

EPSS — Four principles of treatment: Etiotropic (cause), Pathogenetic (mechanism), Sanogenetic (defense), Symptomatic (symptoms).

Frequently asked questions

What classes of chemical carcinogens exist based on their mechanism of action?

Based on the provided sources, chemical substances belong to genotropic (mutagenic) carcinogens.

According to directness of action, carcinogens are divided into:

  • Direct-acting carcinogens.
  • Indirect-acting carcinogens — metabolized in the body, such as nitro compounds.

Chemical carcinogens exert their effect by damaging cellular genomic 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 — loss of classical MHC-I molecules while retaining 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.
  • Impaired 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 proinflammatory cytokines and exerts suppressive effects via IL-10 and vascular endothelial growth factor.
  • Masking of antigenic determinants — shielding of foreign cells with antibodies, preventing their recognition and destruction by T killers.
  • Insufficient T lymphocyte costimulation — the absence of a second activation signal leads to anergy instead of an immune response.
Why remove teratomas in the first months of life?

Early removal (before 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 they are then returned to destroy the tumor.

How do immune checkpoint inhibitors work?

They block inhibitory signals (such as via PD1 or B7-CTLA-4 receptors), preventing the tumor from evading the immune response and increasing T lymphocyte activity.

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