Interaction between the Organism and the Neoplasm
Despite the fact that the probability of malignant transformation is potentially 100% (since an oncogene is present in the genome of any cell), the body strictly controls this process. Normally, antiblastomatous resistance functions—the ability to prevent carcinogens from reaching the nucleus, suppress oncogenes, and destroy mutant cells.
The body affects the tumor through three main pathways:
- Alteration of blood supply. Growth can be halted by surgical ligation of arteries or by drugs that suppress angiogenesis (e.g., avastin).
- Action of biologically active substances. Hormones, cytokines, and mediators influence cell division (this is utilized in hormone therapy for prostate and breast cancer).
- Immunobiological surveillance (IBS). Lymphocytes, antibodies, and macrophages constantly attack foreign elements.
As a result of this confrontation, three outcomes are possible: the death of blastomatous cells (the most frequent option), transition to a latent state without invasion (cancer in situ), or progressive growth with increasing atypia.
Local effects of tumor growth
A progressive tumor aggressively affects surrounding tissues, causing a number of local pathological phenomena:
- Compression and destruction. Invasion of tumor cells destroys neighboring structures, disrupts blood and lymph microcirculation, which leads to organ functional insufficiency.
- Toxic effect of metabolites. The neoplasm releases its own hormones, enzymes, growth factors, and immunosuppressants into the intercellular fluid.
- Suppression of local defense. In the growth zone, the activity of phagocytes and lymphocytes drops sharply, and the production of interferon and lysozyme decreases, which only accelerates the progression of the disease.
Systemic influence: paraneoplastic syndromes
General nonspecific reactions of the body to a tumor are called paraneoplastic syndromes. They affect regulatory systems, metabolism, and immunity. Patients complain of weakness, low-grade fever, sweating, loss of appetite, dermatitis, and anemia.
The most frequent manifestation is cachexia (significant weight loss and wasting). Its development is triggered by:
- Tumor necrosis factor alpha (TNF-α). Excessively secreted by macrophages and monocytes, sharply enhancing lipid catabolism. Previously, this factor was referred to precisely as "cachectin".
- Competition for substrates. The tumor takes away nutrients for its own growth.
- Intoxication. The body is poisoned by tissue breakdown products.
- Anorexia and pain. Decreased appetite against the background of endotoxemia, depression, and pronounced pain syndrome.
- Loss of resources. Chronic bleeding from disintegrating vessels and impaired absorption in the gastrointestinal tract (malabsorption).
Immunopathological conditions
Tumor growth is often accompanied by the development of a specific non-infectious acquired immunodeficiency syndrome (unrelated to HIV). Clinically, this manifests as frequent infections or the appearance of second tumors.
Causes of immunosuppression:
- Antigenic overload. The immune system is depleted due to the huge amount of proteins formed during the breakdown of the neoplasm.
- Action of glucocorticoids. Chronic stress leads to an excess of adrenal cortex hormones, which suppress immunity.
- Activation of T-suppressors. Some tumors (e.g., hepatomas) purposefully increase the activity of cells that inhibit the immune response.
- Deficiency of plastic substances. Immunocytes simply lack substrates for division and differentiation.
In addition to immunodeficiency, concomitant pathologies may develop: allergies, autoimmune diseases, and pathological tolerance to antigens.
Briefly: answers to topical questions
What mechanisms comprise the body's antiblastomatous resistance?
Antiblastomatous resistance consists of mechanisms protecting the genome from carcinogens and destroying already transformed cells. This ability of the body includes the following processes:
- Protection against carcinogens — the ability to prevent carcinogens from penetrating the cell or nucleus, as well as to block their effect on the genome.
- Control of oncogenes — the ability to detect and eliminate oncogenes or suppress their expression.
- Destruction of tumor cells — the ability of the body to detect and destroy already emerged blastomatous cells, as well as to inhibit their growth.
What specific hormones and growth factors is a tumor capable of secreting into the intercellular environment?
Tumor cells are capable of ectopically secreting a number of specific hormones and producing growth factors.
Hormones produced by tumors:
- Antidiuretic hormone (ADH) — synthesized by non-endocrine tissues, often by lung tumor cells.
- Corticotropin (ACTH), Insulin, and Glucagon — may be produced by bronchogenic carcinoma.
- Parathyroid hormone-related protein (PTHRP) — secreted by breast cancer cells and bronchogenic carcinoma.
Growth factors produced by the tumor:
- Vascular endothelial growth factor (VEGF) — ensures stroma development and improves trophism.
- Epidermal, platelet-derived, and fibroblast growth factors.
Three variants of tumor development are easy to remember using the traffic light principle: Red (stop) — cell death under the action of immunity; Yellow (wait) — latent state or cancer in situ; Green (go) — progressive growth and atypia.
Class and exam questions
Is tumor growth a completely autonomous process?
No. The body constantly controls cell transformation using the immunobiological surveillance system, hormones, and blood supply regulation.
What is cancer in situ?
This is a latent state of the neoplasm in which cells form a small clone without their own stroma and feed solely through diffusion from the intercellular fluid.
Why do cancer patients experience rapid weight loss?
Cachexia develops. Its main factor is an excess of tumor necrosis factor alpha (cachectin), which enhances lipid breakdown. Also, the tumor competes for nutrients and causes intoxication.
Why do severe infections often occur in tumors?
Tumor growth causes acquired immunodeficiency syndrome. This occurs due to antigenic overload, stress-induced release of glucocorticoids, and a lack of resources for immunocyte division.
What else to study on this topic
- Mechanisms of antiblastomatous resistance at the cellular level
- The role of tumor necrosis factor alpha (TNF-α) in lipid metabolism
- Pathogenesis of thrombohemorrhagic syndromes in oncology
- Influence of hormone-active tumors on the endocrine system
- Pharmacological suppression of angiogenesis (using avastin as an example)
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