From the Research
Introduction to Acute Myeloid Leukemia (AML) and Benzene Exposure
Acute Myeloid Leukemia (AML) is a type of cancer that affects the blood and bone marrow, characterized by the rapid growth of abnormal white blood cells that accumulate in the bone marrow and interfere with the production of normal blood cells. Benzene exposure has been established as a causative factor for AML, with the mechanism involving the toxicity of benzene to hematopoietic stem cells (HSC) or progenitor cells [ 1 ].
Pathophysiological Processes
The pathophysiological processes that lead to AML following benzene exposure involve several key events, including:
- Genetic, chromosomal, or epigenetic abnormalities and genomic instability in HSCs [ 2 ]
- Stromal cell dysregulation
- Apoptosis of HSCs and stromal cells
- Altered proliferation and differentiation of HSCs These effects are modulated by benzene-induced oxidative stress, aryl hydrocarbon receptor dysregulation, and reduced immunosurveillance, ultimately leading to the generation of leukemic stem cells and subsequent clonal evolution to leukemia [ 2 ].
Cell Functions and Biochemical Processes
The cell functions and biochemical processes affected by benzene exposure include:
- Hematopoietic stem cell toxicity, leading to lowered blood counts (hematotoxicity) [ 1 ]
- Induction of multiple alterations that contribute to the leukemogenic process [ 1 ]
- Operation via multiple modes of action, including genetic and epigenetic changes [ 1 ]
Treatment and Prevention
While there is no specific treatment for benzene-induced AML, the management of AML typically involves chemotherapy, radiation therapy, and bone marrow transplantation. Prevention of benzene exposure is crucial, and regulatory agencies have established permissible occupational exposure limits to minimize the risk of benzene-induced leukemia [ 3 ].
Differentials and Caveats
It is essential to note that benzene exposure is not the only cause of AML, and other established non-genetic causes, such as smoking, ionizing radiation, and cancer chemotherapy, also contribute to the incidence of AML [ 1 ]. Additionally, the majority of de novo AML cases remain unexplained, highlighting the need for further research into the causes of AML [ 1 ].
Conclusion
In conclusion, the pathophysiological processes that lead to AML following benzene exposure involve the toxicity of benzene to hematopoietic stem cells, leading to genetic, chromosomal, or epigenetic abnormalities and genomic instability. Understanding these processes is crucial for the development of effective prevention and treatment strategies for benzene-induced AML [ 2 ].