Current status of cytogenetic research in childhood acute lymphoblastic leukemia.
نویسنده
چکیده
LIMITED understanding of leukemogenesis and the A neoplastic phenotype of transformed lymphoid progenitors has been a major obstacle to the development of safe, uniformly effective therapy for children with acute lymphoblastic leukemia (ALL). Studies of isoenzymes, immunologic markers, and other expressions of cell phenotype provide valuable clues to ALL etiology, but ultimately they fail to divulge mechanisms for leukemic transformation or maintenance of the malignant state. A more fruitful approach has been to classify ALL by its cytogenetic features, both numeric and structural.' Admittedly, a proportion of the chromosomal changes reported to date have proved to be little more than genetic epiphenomena with vague links to pathogenesis and treatment outcome. This fact notwithstanding, the presence of specific cytogenetic abnormalities in leukemic cells has stimulated molecular study of genes near the chromosomal breakpoints and characterization of their protein products.' The picture emerging from these investigations is varied but has a consistent theme: genes disrupted by recurrent translocations or other chromosomal alterations tend to participate in cell regulatory pathways that control cell growth and de~elopment.~-~ Thus, cytogenetic classification of childhood ALL has the potential to suggest causative mechanisms and thereby to provide consistent guidelines for treatment. This review updates progress in the cytogenetic study of ALL and attempts to relate new findings to prognosis.
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ورودعنوان ژورنال:
- Blood
دوره 81 9 شماره
صفحات -
تاریخ انتشار 1993