Leukemia Research VoL 17, No. 9, p. 821, 1993. Printed in Great Britain.
0145-2126/93 $6.00 + .00 Pergamon Press Ltd
BOOK REVIEW
Leukemia, 2nd Edn (Whittaker J. A., Ed.). Blackwell, London (1962) 682 pp.
leukemia, and the prognostically favorable inv. (16) in myelomonocytic leukemia, but without a really clear picture of the prognostic significance of cytogenetics in AML, e.g. ( - 5 ; - 7 ) , trisomy 8, 5q- or 7q-. Campana and Behm mention, but do not emphasize, the uncertain fidelity of antigen expression and lineage commitment in leukemic cells. The detection of 'leukemic' marker combinations could precede relapses by 1-6 months, and could be used as an indication for transplantation. Since Holmes's chapter on drug resistance was written, other papers have appeared, suggesting a limited number of second remissions when verapamil is added to the combination to which the patients became resistant. Napier has relatively liberal indications for platelet transfusions, and does not mention the residual non-A, non-B hepatitis transmission risk. Yin describes by now well known principles to treat infection. Whittaker has an interesting table (with some mean remission durations as low as 4-8 months?) regarding maintenance treatment, which probably benefits very little. Immunotherapy is not mentioned, but some remissions are seen after IL-2 alone, some autologous transplants may do better with IL-2, and Winfields chapter mentions the interesting finding of a doubled risk for secondary leukemia in splenectomized Hodgkin patients as compared to those with spleens. Whittaker also has an excellent discussion of why survival rates in some chemotherapy trials approximate to those for allogeneic transplants, apparently only slightly better than the autotogous ones. In Franklin's transplant chapter, on the other hand, this comparison is very brief, but indications rather wide. It is true, however, that 3/4 prospective, randomized trials do show an advantage for allo-transplants. For autotransplants, Burnett is careful to point out that 'a straightforward study in first remission will require impossibly large n u m b e r s . . . ' . To take it all in all, this is really more or less a must for the hematologist, because of its good fundamental and clinical chapters and very good review of the literature.
Five years after the first edition, the second one appears, with 28 chapters by 43 very well known and experienced contributors. The literature is well followed up to at least 1990. Cartwright reviews the epidemiology of the no less than 30 different subforms of leukemia in the ICD 9 classification, with good descriptions both of the high dose rate radiation-induced leukemias in Japan, and those after low dose rates after the 'Smoky' tests or around Sellafield. Jarrett and Onions write interestingly about the viruses, including the changes in the EBV antibody pattern preceding Hodgkins disease. Taylor finds little genetic susceptibility for leukemia (a little in contrast to what was recently shown by Seed after radiation). Cooper confirms the findings of prolonged intermitotic times and reduced BrdU-labelling indices in AML, and Padua reviews the molecular biology. Testa and Dexter review growth factors and in oitro growth, but without very much discussion of findings in various leukemias, MDS, etc. This is mentioned, however, in Jacobs and Culligan's excellent MDS chapter, which contains a fascinating review of MDS pathogenesis. In animals, high doses of carcinogen lead to leukemia, low ones to a repopulation of the marrow via growth factor sensitization, increased mutation risk during proliferation and perhaps malignant transformation. It is possible that the development is similar, irrespective of the carcinogen (radiation, chemical or Friend virus). Winfield and Lilleyman, in one of the most complete chapters, review the relative risk, between 6.6 and 130.0 and increasing with dose, both of radiation and of cytostatics, of AML after chemotherapy, suggesting that up to 17% of the patients could get AML. Actually, the oldest myeloma studies by Videbaek, not mentioned showed even higher risks. In man, lymphomas still in complete remission may show RAS and FMS mutations in marrow cells. Nguyen and Imbert review morphology, and Thompson and White, i.a., the t(15;17) (q22;q21) in promyelocytic
PETER REIZENSTEIN Stockholm, Sweden
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