Lymphoma

Intensive remission chemotherapy followed by post-remission consolidation and maintenance therapies has achieved complete remission rates of 75% to 90% and 3-year survival rates of 25% to 50% in adults with acute lymphoblastic leukemia (ALL). These results, although promising, are still less favorable than those achieved in childhood ALL. However, various novel experimental and clinical approaches show promise for improving cure rates. Also, specific therapies directed at high-risk subgroups with ALL are beginning to emerge. Detection of specific chromosomal abnormalities at diagnosis identifies patients who are at risk of failing to achieve remission, as well as those who are likely to have short, intermediate, or prolonged disease-free intervals after successful remission induction. Such prognostic information may, ultimately, be used to assign risk categories and to individualize post-remission therapy. [ONCOLOGY 9(5):433-450, 1995]

Acute lymphoblastic leukemia (ALL) in adults is clearly a "different disease" than ALL in children-a fact that is well documented in the article by Ong and Larson. As they indicate, more than half of adult patients relapse despite modern therapy, most within the first 2 years. It should be pointed out, however, as is mentioned at the beginning of the article, that "modern" induction was defined by Cancer and Leukemia Group B study 7612--a study begun in 1976 [1]. Thus, induction therapy has not changed substantially in 20 years. The addition of consolidation therapy and prolonged maintenance therapy has resulted in modest increases in response duration, but despite many variations on current regimens, there has been little change in outcome during the past decade.

Today, we can cure a significant portion of people with aggressive non-Hodgkin's lymphomas. The cure rate at 5 years for all patients with advanced diffuse large-cell lymphoma is approximately 35%.

Acute lymphocytic leukemia (ALL) is a malignant disorder resulting from the clonal proliferation of lymphoid precursors with arrested maturation [1]. The disease can originate in lymphoid cells of different lineages, thus giving rise to B- or T-cell leukemias or sometimes mixed-lineage leukemia.