Classification and nature of exposure
Physical carcinogens include high-energy factors capable of damaging cellular structures:
- Ionizing radiation: includes X-rays, neutron flux, and radioactive isotopes (e.g., $^{32}P$, $^{131}I$, $^{90}Sr$).
- Corpuscular radiation: exposure to $\alpha$-, $\beta$-, and $\gamma$-particles.
- Ultraviolet radiation: a spectrum of electromagnetic waves causing damage at the DNA molecular level.
Clinical significance and risks
Exposure to physical agents has a proven link to cancer incidence:
- Radiation accidents: populations exposed to radiation (e.g., during the Chernobyl disaster) show a significant increase in cases of leukemia and thyroid cancer.
- Medical radiation exposure: it has been proven that multiple head CT scans under the age of 22 increase the risk of developing brain neoplasms and leukemia. With 2–3 procedures, the risk increases 3-fold; with 5–10 procedures, 9-fold.
Mechanism of malignant transformation
Tumor transformation is based on the accumulation of non-lethal mutations in key gene groups:
- Proto-oncogenes: when activated, they turn into oncogenes, stimulating uncontrolled growth.
- Suppressor genes: their inactivation deprives the cell of growth "brakes".
- Apoptosis genes: blocking the death of damaged cells.
- Repair genes: disruption of DNA structure restoration, which fixes mutations.
Briefly: answers to topical questions
What is the molecular mechanism of the damaging effect of ultraviolet radiation?
The molecular mechanism of the damaging effect of ultraviolet radiation consists in altering the DNA structure through the formation of anomalous bonds. Under the influence of this physical factor, the following defects are formed:
- Thymine dimers — cross-links between thymine residues.
- Cytosine dimers — bonds between cytosine molecules.
- Thymine-cytosine dimers — pathological connections between thymine and cytosine.
Normally, to restore the DNA structure, the process of photoreactivation is activated, during which the photolyase enzyme cleaves the bonds formed between adjacent pyrimidine bases.
What stages are distinguished in the process of physical carcinogenesis?
The process of carcinogenesis at the cellular level is universal: the final result of the action of physical carcinogens, as well as chemical or biological ones, is tumor transformation. Therefore, the stages of the tumor process can be indicated for physical carcinogenesis:
- Initiation — tumor transformation.
- Promotion — activation.
- Progression.
- Outcome.
What types of tumors are specific to prolonged exposure to ultraviolet radiation?
Sources classify ultraviolet rays as physical carcinogens, and avoiding sunburn and exposure to artificial UV light is indicated as a measure to reduce the risk of skin tumors. Based on the sources, one can name:
- Cutaneous melanoma.
- Non-melanoma skin malignancies, including squamous cell skin carcinoma.
- Skin cancer in general.
"RADIO-UV": X-rays, Alpha/Beta/Gamma, DNA damage, Isotopes, Tumors, Ultra-Violet.
Class and exam questions
Why is a head CT dangerous specifically at a young age?
In individuals under 22 years of age, tissues are more sensitive to ionizing radiation, and the accumulated radiation dose significantly increases the risk of mutations in actively dividing cells.
How do physical carcinogens turn a normal cell into a tumor cell?
They cause DNA damage which, when repair genes malfunction, leads to the activation of proto-oncogenes and the loss of suppressor gene functions.
What is the monoclonal origin of a tumor?
This is the development of a neoplasm from a single transformed cell, which gives rise to heterogeneous clones during progression.
What else to study on this topic
- Tumor progression and clonal selection mechanisms.
- Genetic heterogeneity of tumor tissue.
- The role of oncogenic viruses (DNA- and RNA-containing) in carcinogenesis.
- Functions of proto-oncogenes and their activation (using N-myc as an example).
- Epigenetic mechanisms of malignant transformation.
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