Unraveling the causes of acute Leukemia: A Comprehensive Review of Genetic and Environmental Factors

Background: One of the most prevalent cancers afflicting people worldwide is leukemia. Leukemia was the eleventh leading cause of death from malignant illnesses worldwide in 2018, accounting for 437,033 cases and 309,006 fatalities, making it the fifteenth most prevalent diagnosed malignancy. Acute leukemias are malignant clonal illnesses of blood-forming organs that affect one or more hematopoietic system cell lines. These conditions are characterized by a broad substitution of aberrant immature and undifferentiated hematopoietic cells for bone arrow, which lowers the quantity of erythrocytes and platelets in the peripheral circulation. These illnesses are categorized according to the hematopoietic cells affected, such as lymphoid, myeloid, mixed, or undifferentiated. On the other hand, a wide range of illnesses known as chronic leukemias are distinguished by the unchecked growth and division of adult, differentiated hematopoietic system cells. Therefore, the type of hemopoietic cells involved determines the classification of chronic leukemias. Environmental factors that increase the risk of developing acute myeloid leukemia (AML) include smoking, benzene exposure, chemotherapy, and radiation treatment. AML is the most common acute leukemia in adults and accounts for 15–20% of cases in children. Acute myeloid leukemia (AML) is a genetically heterogeneous disease that is characterized by malignant clonal proliferation of immature myeloid cells in the bone marrow, peripheral blood, and occasionally other body tissues. AML can potentially originate from myeloproliferative neoplasm (MPN) or myelodysplastic syndrome (MDS). With an overall 5-year survival rate of about 25%, the prognosis for the majority of AML subtypes remains bleak despite their extreme variability. The risk of relapse and the possibility of remission are influenced by the genetic and epigenetic makeup of the cancerous cells. Gaining more knowledge about the underlying genetic and epigenetic mechanisms could help identify novel treatment targets, prognostic factors, and the mechanism of leukemogenesis in AML. Many molecular mutations in AML have well-documented prognostic effects. Less is known about the function of mutations in genes with epigenetic function, though.