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pmid: 793552
The difference between the chemotherapeutic response in patients with acute myelocytic leukemia (AML) and in those with acute lymphocytic leukemia (ALL) would appear to be more a problem of lack of regeneration of normal myeloid tissues than a lack of susceptibility of the neoplastic cell to chemotherapy. The lymphoblasts of ALL are more readily damaged by treatments used in induction than are the leukemic cells in AML. It is easily possible, however, to produce marrow aplasia in patients with AML with the multitude of myelosuppressive drugs available. The therapeutic dilemma is that treatments that are active in this regard also damage the normal myeloid tissue. This damage is often not repaired during the period available prior to death from infection or bleeding. The fact that differentiation between neoplastic and normal cells can be accomplished at all on chemotherapeutic grounds in such a critical organ as the marrow is remarkable. That
Mercaptopurine, Daunorubicin, Cytarabine, Neuraminidase, Mycobacterium bovis, Mice, Leukemia, Myeloid, BCG Vaccine, Animals, Humans, Drug Therapy, Combination, Immunotherapy, Leukemia L1210, Thioguanine
Mercaptopurine, Daunorubicin, Cytarabine, Neuraminidase, Mycobacterium bovis, Mice, Leukemia, Myeloid, BCG Vaccine, Animals, Humans, Drug Therapy, Combination, Immunotherapy, Leukemia L1210, Thioguanine
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 98 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Average | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 1% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 1% |