Epidemiology of acute lymphoblastic leukemia.
Although the etiology of acute leukemia is largely unknown, some facets of the puzzle are becoming clarified. Recognition of important patterns in age-specific mortality rates has suggested that events early in life, perhaps even prenatally, may have an influence on developing leukemia in childhood. The racial differences evident in mortality, incidence, and immunologic subtype of ALL suggest either differences in exposures to certain "factors" or differences in responses to those "factors" by white children. Hereditary factors appear to play a role. Familial and hereditary conditions exist that have high incidences of acute leukemia. Chromosomal anomalies are common in these conditions. Viral infections may play a role by contributing to alteration in genetic material through incorporation of the viral genome. How that virus is dealt with after primary infection seems important. The presence of immunodeficiency may allow wider dissemination or enhanced replication of such viruses, thereby increasing the likelihood of cellular transformation to an abnormal cell. Proliferation of that malignant cell to a clone may depend on other cofactors. Perhaps prolonged exposure to substances like benzene or alkylating agents may enhance these interactions between virus and genetic material. Does this change DNA repair mechanisms? Are viral infections handled differently? Is viral genomic information more easily integrated into host cells? Ionizing radiation has multiple effects. Alteration in genetic material occurs both at the molecular and chromosomal levels. DNA may be altered, lost, or added in the cell's attempt to recover from the injury. These changes may lead to altered susceptibility to other environmental agents, and host response may be altered. The past 40 years have seen dramatic progress in the treatment of ALL. We have just begun to unravel the complex interactions of genetic makeup, immune response, and the environment on the development of ALL. Whether factors can be identified that may allow prevention of acute leukemia remains to be seen.
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000352:Africa, Northern; D000368:Aged; D002273:Carcinogens; D002648:Child; D002675:Child, Preschool; D004781:Environmental Exposure; D005260:Female; D006801:Humans; D007945:Leukemia, Lymphoid / Q000453:epidemiology* / Q000235:genetics / Q000401:mortality / Q000473:pathology; D008297:Male; D008875:Middle Aged; D008877:Middle East; D009381:Neoplasms, Radiation-Induced; D010290:Parents; D044469:Racial Groups; D012306:Risk; D012737:Sex Factors; D014481:United States; D018406:Virus Physiological Phenomena
D002273:Carcinogens