Abstract:
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.
Keywords: Acute Disease Adolescence Adult Africa, Northern Aged Carcinogens Child Child, Preschool Environmental Exposure Female Human Leukemia, Lymphocytic/*EPIDEMIOLOGY/GENETICS/MORTALITY/PATHOLOGY Male Middle Age Middle East Neoplasms, Radiation-Induced Parents Racial Stocks Risk Sex Factors United States Viruses/PHYSIOLOGY JOURNAL ARTICLE
AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Bristol-Myers Squibb Company, Elton John AIDS Foundation, Gill Foundation, the National Library of Medicine, Quest Diagnostics, Roche and Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 1985. This material is designed to support, not replace, the relationship that exists between you and your doctor.
AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.
Important note: Information in this article was accurate in 1985. The state of the art may have changed since the publication date.
