Host-Tumor Interactions
Although the theoretical probability of malignant transformation is high (since oncogenes exist within the genome of any cell), the body tightly regulates this process. Normally, anti-tumor resistance operates—the ability to prevent carcinogens from reaching the nucleus, suppress oncogenes, and destroy mutant cells.
The body influences the tumor through three main pathways:
- Modification of blood supply. Growth can be halted by surgical ligation of feeding arteries or by anti-angiogenic drugs (e.g., bevacizumab).
- Action of biologically active substances. Hormones, cytokines, and mediators affect cell division (this principle is utilized in hormone therapy for prostate and breast cancer).
- Immune surveillance. Lymphocytes, antibodies, and macrophages constantly attack foreign elements.
As a result of this interplay, three outcomes are possible: the destruction of neoplastic cells (the most frequent outcome), a transition to a dormant state without invasion (cancer in situ), or progressive growth with increasing cellular atypia.
Local Effects of Tumor Growth
A growing tumor aggressively affects surrounding tissues, triggering several local pathological phenomena:
- Compression and destruction. The invasion of tumor cells destroys neighboring structures, disrupts microcirculation of blood and lymph, and leads to organ functional failure.
- Toxic effects of metabolites. The neoplasm releases its own hormones, enzymes, growth factors, and immunosuppressive agents into the intercellular fluid.
- Suppression of local defenses. Phagocyte and lymphocyte activity drops sharply in the growth zone, accompanied by decreased production of interferon and lysozyme, which further accelerates disease progression.
Systemic Effects: Paraneoplastic Syndromes
General nonspecific systemic reactions of the body to a tumor are termed paraneoplastic syndromes. They affect regulatory systems, metabolism, and immunity. Patients report fatigue, low-grade fever, sweating, loss of appetite, dermatitis, and anemia.
The most common manifestation is cachexia (significant weight loss and wasting). Its development is driven by:
- Tumor necrosis factor-alpha (TNF-α). Excessively released by macrophages and monocytes, it sharply enhances lipid catabolism. Historically, this factor was known as "cachectin."
- Competition for substrates. The tumor consumes nutrients required for normal host homeostasis.
- Intoxication. The body is poisoned by tissue breakdown products.
- Anorexia and pain. Loss of appetite driven by endotoxemia, depression, and severe pain syndromes.
- Depletion of resources. Chronic bleeding from eroded blood vessels and impaired gastrointestinal absorption (malabsorption).
Immunopathological Conditions
Tumor growth is frequently accompanied by a secondary, non-HIV-related acquired immunodeficiency state. Clinically, this manifests as frequent infections or the development of secondary malignancies.
Causes of immunosuppression:
- Antigenic overload. The immune system becomes exhausted by the massive load of proteins generated by tumor breakdown.
- Glucocorticoid action. Chronic stress leads to excess adrenal cortical hormones, which suppress immunity.
- Activation of T-suppressor cells. Certain tumors (e.g., hepatomas) actively upregulate cells that dampen the immune response.
- Deficiency of plastic substrates. Immunocytes literally lack the building blocks required for division and differentiation.
In addition to immunodeficiency, secondary pathologies may develop, including allergies, autoimmune phenomena, and pathological tolerance to antigens.