Etiology of acute leukemia

Etiology of acute leukemia

In most cases, the etiology of the disease is impossible to establish. In connection with the frequent detection of various chromosomal changes in tumor blast cells, various carcinogens are assumed to be the causes of acute leukemia.

Ionizing radiation as a cause of acute leukemia. Persons who survived the atomic bombing of Hiroshima and Nagasaki had a 30–50-fold increase in the frequency of secondary acute leukemia (almost always AML), with the largest number of diseases occurring 4–8 years after exposure to ionizing radiation.

An increased risk of developing acute myeloblastic leukemia (AML) is promoted by radiation therapy and, especially, combined chemoradiotherapy. Leykozogenny effect of small doses of ionizing radiation (diagnostic x-ray or radionuclide studies) and electromagnetic fields has not been proven.

Cigarette smoke contains many different carcinogens and therefore is a risk factor for the development of acute leukemia (OL). In smoking patients over 60, specific chromosomal abnormalities that are typical for exposure to chemical mutagens are often detected. It is estimated that at least 20% of AML cases are associated with smoking.

Chemical compounds with strictly proven leukemic properties are benzene and cytotoxic drugs. Benzene contributes to the development of secondary acute leukemia with prolonged production contact.

Secondary leukemias are acute myeloblastic leukemias (AML) that occur at different times (more often 5-6 years) after the completion of chemotherapy and / or radiation therapy for tumor or non-tumor diseases. Among cytostatic drugs, alkylating agents and podophyllotoxins have the greatest leukemic potential. The likelihood of developing secondary AML is increased in patients with breast and ovarian cancer who received alkylating agents.

Among the alkylating agents, cyclophosphamide has the lowest leukemic potential. The use of podophyllotoxins (etoposide and teniposide) and alkylating agents in children with acute lymphoblastic leukemia increases the incidence of secondary acute myeloblastic leukemia (AML).

Treatment of podophyllotoxins in adults and children is accompanied by an increased frequency of secondary acute monoblastic leukemia with a chromosomal abnormality llq23. The use of etoposide, doxorubicin increases the risk of developing acute promyelocytic leukemia (APL) with t (15; 17).

Genetic diseases as a cause of acute leukemia. Some genetic defects (Down syndrome, Fanconi anemia, Blum syndrome, ataxia-telangiectasia) are accompanied by an increased risk of developing OL. In Down syndrome, there is a 20-fold increase in the frequency of OL (in children under 3 years of age – megakaryoblastic leukemia, older than 3 years – pre-B-ALL). In patients with Fanconi anemia, AML is significantly more likely to develop, with ataxia-telangiectasia, ALL and non-Hodgkin lymphomas.

Viruses as a cause of acute leukemia. Human T-lymphotropic retrovirus (HTLV-1) has been found to be relevant in the occurrence of adult T-cell leukemia / lymphoma. The role of oncogenic retroviruses in the development of human NL has not been proven. Epstein-Barr virus (EBV) is important in oncogenesis in B-ALL, endemic Burkitt lymphomas and lymphomas associated with the human immunodeficiency virus.

The immunological susceptibility to the development of acute leukemia has not been proven, however, analysis of various cytogenetic variants of acute myeloid leukemia (AML) revealed an association between certain HLA loci and karyotype disorders.

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