Abbreviated as ALL, Acute Lymphoblastic Leukemia is a malignant clonal disease of the bone marrow that results in the proliferation of lymphoid precursors which replace the hematopoietic cells. Usually, numerous cooperative genetic mutations in a single B- or T-lymphoid generator lead to changed blast cell proliferation, survival, and mutation, and eventually results in lethal accumulation of leukemic cells. Cases of ALL can be classified depending on stages of either B or T-cell maturation. Theoretically, however, they are only useful in the recognition of B-cell, B-cell precursor, T-cell, and early precursor stage. ALL is the most common type of cancer and Leukemia among children in the U.S. While most children can be cured, prognosis among infants and children is poor. Recent genome-profiling has identified the epidemiology including risk factors, signs and symptoms, and treatment of ALL.
Epidemiology
Just like cancer in general, the causation of ALL is considered to be a number of factors including chance, genetic susceptibility, and both exogenous and endogenous exposure. These factors account for approximately 4000 new cases on Acute Lymphoblastic Leukemia in the U.S. on an annual basis. The predominant population of ALL is children, 60% of those diagnosed being less than 20 years of age. Notably, ALL has a peak incidence in patients of 2 to 5 years (Ribera, 2016). The role of exposures in ALL has remained contentious with recent studies revealing that there are numerous of them that contribute to childhood ALL. These range from exposure to radiation to infections. Radiation is an established cause of ALL as evidenced by the atomic bombs of Hiroshima and Nagasaki in Japan and pelvic X-rays done during pregnancy (Peres-Saldivar, Rangel-Lopez, Fajardo-Gutierrez, & Mejia-Arangure, 2016).
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Based on recent studies, infections are postulated as the number one causative agents of leukemia. The study reveals that abnormal response to common infections among children results in ALL. Influenza viruses are the number one infection candidates that cause ALL (Inaba, Greaves & Mullighan, 2013). Susceptible children have exposure to infections which then persist depending on the response of the immunes system to them.
Another risk factor for Acute Lymphoblastic Leukemia is inherited genetic syndromes. However, there is little evidence of inherited predisposition to ALL through genetic mutations in either children or adults except for identical twins whose explanation is still not genetic related. Infants born with genetic syndromes such as Down syndrome, Klinefelter syndrome, Fanconi anemia, and Bloom syndrome stand a higher risk of ALL, especially between 0 to 4 years. Studies reveal that various genes impinge directly on regulators that impact cell development, proliferation, and differentiation (Inaba, Greaves & Mullighan, 2013). Furthermore in most cases of ALL somatic mutants of certain genes have been detected. The conclusion drawn from the study reveals that inherited gene variants contribute to vulnerability of precursor blood cell transformation and subsequently clonal evolution.
Signs and Symptoms
Most signs and symptoms of ALL are associated with shortages of normal blood cells which result from the accumulation of leukemic cells in the bone marrow. Common signs and symptoms of ALL include feeling tired, weak, and dizzy, shortness of breath, infections that are persistent, pale skin, infections that do not go away and bruises on the skin (Ribera, 2016). ALL is also associated with loss of weight, fever, night sweats, and a loss of appetite.
Treatment
Improvement in treatment has abolished the prognosis of clinical variables that were previously associated with very poor outcomes. Today, ALL has a cure rate of up to 90% with contemporary treatments. Typically, the treatment of ALL spans between two to 2.5 years. Usually, there are three phases involved; remission-induction, intensification, and continuation (Inaba, Greaves & Mullighan, 2013). The first phase involves chemotherapy with agents such as vincristine or asparagine. Four to six weeks of induction treatment eradicate leukemic cells and restores hematopoiesis. The next phase, intensification, is administered after remission to eradicate residual leukemic cells. High doses of methotrexate are administered for uninterrupted 20-30 weeks. Also, hematopoietic stem cell transportation is done if children stand a high risk of ALL. After which continuation therapy is done for and lasts two years. In the final phase of treatment, mercaptopurine and methotrexate are administered daily and weekly respectively.
In conclusion, recent genome-profiling has identified the epidemiology including risk factors, signs and symptoms, and treatment of ALL. At its core, Acute Lymphoblastic Leukemia is a cancer of the bone marrow that is highly prevalent in children. Causative agents are mainly radiation and infections in infants. There has been improved treatment in recent years with survival rates up to 90%. Future research on ALL should focus on identifying patients at risk of relapse and give more evidence on genetic susceptibility.
References
Inaba, H., Greaves, M., & Mullighan, C. G. (2013). Acute lymphoblastic leukemia. The Lancet , 381 (9881), 1943-1955.
Pérez-Saldivar, M. L., Rangel-Lopez, A., Fajardo-Gutiérrez, A., & Mejía-Aranguré, J. M. (2016). Environmental factors and exposure time windows related to the etiology of acute lymphoblastic leukemia in children. In Etiology of Acute Leukemia in Children (pp. 207-290). Springer, Cham.
Ribera, J. M. (2016). Acute lymphoblastic leukemia. In HIV-associated Hematological Malignancies (pp. 145-151). Springer, Cham.
