Acute Lymphoblastic Leukemia Essay

1185 words - 5 pages

Acute lymphoblastic leukaemia is the most common childhood cancer accounting for around 20-30% of all childhood neoplasms. Annual incidence rates vary worldwide between one and four cases per 100,000, primarily in children ages two - six years old (1). The disease is less common in adults, with only around 1,000 cases being diagnosed annually and with a significantly lower cure rate, rarely exceeding 40%. In turn, infants diagnosed under the age of one have an even poorer survival rate of 30%. Several studies in monozygotic twins and neonatal blood smears have indicated a clear prenatal origin for childhood cases, detecting specific genetic abnormalities in prenatal samples, which may act as initiating events although clearly further postnatal events are required for transformation (2; 3; 4). TEL-AML fusion genes, for example, were found in 1% of newborn samples, which is significantly greater than the number of ALL cases, clearly demonstrating that there may often be a prenatal origin for initial genetic aberrations and that further genetic alterations are necessary to develop ALL (3; 4). A small study further supports a prenatal origin in a pair of monozygotic twins with childhood B cell precursor (BCP) ALL with identical cytogenetic abnormalities, signifying a prenatal foundation, as well various contrasting genetic lesions illustrating that further genetic events are required to generate a malignant phenotype (2). A few inherited syndromes such as Down’s syndrome, Bloom’s syndrome and other genetic syndromes have also been associated with a risk. Environmental factors may also play a role in the development of ALL such as exposure to radiation, chemotherapy and possibly infections. Two infection based theories based on observations that there can be an occasional clustering of cases, along with the modern industrializations of societies and the peak age groups affected may provide some explanation in the mechanism for the development of ALL (4). Kinlen’s hypothesis speculates that it may be fueled by exposure of common pathogens to susceptible individuals after population mixing, while Greave hypothesizes that it may be as the result of a late exposure to a pathogen which may aggregate or push a prenatally derived hematologic cell with predisposed genetics lesions into a transformed leukaemia cell, although no causative infectious agents have been identified to fully support these theories for ALL (4; 5). Lymphocytes committed to differentiate into a B or T cell are transformed at an early stage in development, often as a consequence of chromosomal translocations, a hallmark of leukaemias (4).

Symptoms and Diagnosis
Symptoms are the consequence of the aggressive over proliferation of lymphocytes in the bone marrow overcrowding other hematopoietic cells, resulting in symptoms of bone marrow failure, such as anemia, thrombocytopenia and recurrent infections from a lack of leukocytes. Initial symptoms may include fever, fatigue, malaise...

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