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Physical Carcinogens

Carcinogena physica

For medical students2 min readUpdated 2026-10-10

Physical carcinogens are environmental agents capable of inducing malignant cell transformation. They include various types of ionizing radiation and ultraviolet rays.

Main TypesIonizing radiation (X-rays, neutrons, isotopes) and ultraviolet (UV) radiation.

Radiation RiskIncreased incidence of leukemias and thyroid cancer following exposure.

CT DiagnosticsRisk of brain tumors and leukemias in individuals under 22 increases by 3- to 9-fold.

Core MechanismDamage to the genetic apparatus and disruption of DNA repair mechanisms.

Classification and Nature of Impact

Physical carcinogens include high-energy factors capable of damaging cellular structures:

Ionizing radiation: includes X-rays, neutron beams, 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 high radiation (e.g., from nuclear power plant accidents) show a significant increase in leukemia and thyroid cancer cases.
Medical radiation exposure: repeated head CT scans in individuals under 22 have been shown to increase the risk of brain neoplasms and leukemias. With 2–3 procedures, the risk increases 3-fold; with 5–10, it increases 9-fold.

Mechanism of Malignant Transformation

Tumor transformation is based on the accumulation of non-lethal mutations in key gene groups:

Proto-oncogenes: upon activation, they convert into oncogenes, stimulating uncontrolled growth.
Tumor suppressor genes: their inactivation deprives the cell of growth "brakes."
Apoptosis genes: blocking the death of damaged cells.
Repair genes: impaired DNA structural restoration, which locks in mutations.

Mnemonic

"RADIO-UV": X-rays (R), Alpha/Beta/Gamma, DNA damage, Isotopes, Tumors, Ultra-Violet.

Frequently asked questions

What is the molecular mechanism of the damaging effect of ultraviolet radiation?

The molecular mechanism of UV radiation damage involves altering the DNA structure through the formation of abnormal bonds. This physical factor produces the following defects:

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, 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 end result of physical carcinogens, just like chemical or biological ones, is tumor transformation. Therefore, the stages of the tumor process for physical carcinogenesis include:

Initiation — tumor transformation.
Promotion — activation.
Progression.
Outcome.

Which types of tumors are specific to prolonged exposure to ultraviolet radiation?

Ultraviolet rays are classified as physical carcinogens, and avoiding sunburns and artificial UV exposure is recommended to reduce skin cancer risk. Based on sources, these include:

Cutaneous melanoma.
Non-melanoma skin cancers, including squamous cell carcinoma of the skin.
Skin cancer in general.

Why is a head CT scan particularly dangerous at a young age?

In individuals under 22, tissues are more sensitive to ionizing radiation, and the cumulative radiation dose significantly increases the risk of mutations in actively dividing cells.

How do physical carcinogens convert a normal cell into a tumor cell?

They cause DNA damage that, when DNA repair genes are impaired, leads to the activation of proto-oncogenes and the loss of tumor suppressor gene functions.

What is the monoclonal origin of a tumor?

It is the development of a neoplasm from a single transformed cell that, during the process of progression, gives rise to heterogeneous clones.

Go deeper

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.