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Regular Review 960 BRITISH MEDICAL JOURNAL VOLUME 281 11 OCTOBER 1980 produced by a simple horizontal infection. These viruses can be C-type or similar viruses play at least some part in some transmitted vertically (that is, inherited) after they have been cases of childhood but their leukaemia, role does not appear Br Med J: first published as 10.1136/bmj.281.6246.960 on 11 October 1980. Downloaded from incorporated into the host genome, and the infections they simple and may prove similar to an explosive charge which cause tend to have very long latent periods. Though leukaemia requires an unusual set of circumstances for detonation. is rare in childhood, C-type viruses are probably widely dis- tributed; so other infrequent host factors would have to come Wang A, Till M, Soothill JF. Antiglobulin antibody in the sera of contacts into play to allow the viruses to escape from being repressed. of children with leukaemia. Arch Dis Child 1980;55:384-8. 2 Kaplan HS. Etiology of lymphomas and leukaemias: role of C-type RNA Such factors probably include heredity,8 exposure to physical viruses. Leukaemia Research 1978 ;2 :253-71. or chemical agents (such as radiation9 or cytotoxic drugs3), and 3Anonymous. Who will get leukaemia? Lancet 1980;i:1007-8. of as occur 4 Epstein MA. Epstein-Barr virus as the cause of a human cancer. Nature temporary alteration immunity might after infection 1978 ;274 :740. with a non-oncogenic virus. In lymphoblastic leukaemia, such 5 Kellett CE. Acute myeloid leukaemia in one of identical twins. Arch Dis a factor might mediate its effect through the loss ofa functional Child 1973;12:239-52. 6Heath CW, Hasterlik RJ. Leukemia among children in a suburban lymphocyte suppressor cell population, which theoretically community. Am J Med 1963;34:796-812. might either fail to control aberrant malignant lympho- 7 Gunz FW, Spears GFS. Distribution of acute leukaemia in time and proliferation or alternatively, lead to increased autoimmune space. Studies in New Zealand. Br MedJ 1968;iv:604-8. 8 Snyder AL, Frederick PLi, Henderson ES, Todaro GJ. Possible inherited disease.10 Both are frequently observed in New Zealand mice, leukaemogenic factors in familial acute myelogenous leukaemia. Lancet which lose such suppressor functions for both B and T cell 1970;i :586-9. activities spontaneously early in life. Interestingly, the first- 9 Mole RH. Ionizing radiation as a carcinogen: practical questions and academic pursuits. BrJ Radiol 1975;48:157-69. degree relatives of children with lymphoblastic leukaemia have 10 Gershwin ME, Steinberg AD. Loss of suppressor function as a cause of an increased incidence of autoimmune disease.'1 lymphoid malignancy. Lancet 1973 ;ii: 1 174-6. in the title of this article cannot be 11 Till M, Rapson N, Smith PG. Family studies in acute leukaemia in The question posed childhood: a possible association with autoimmune disease. Br J Cancer answered. Information is slowly accumulating to indicate that 1979;40:62-71. Regular Review Advances in the management of adult acute myelogenous leukaemia http://www.bmj.com/ J A WHITTAKER For many years now the results of treatment for adults with monocytic leukaemia (M4). The less frequently seen but more acute myelogenous leukaemia have made dismal reading, easily recognisable monocytic leukaemia is M5, and erythro- particularly when compared with the advances achieved in leukaemia is M6. Immunological methods are particularly on 26 September 2021 by guest. Protected copyright. the past decade or so in the treatment of childhood acute useful in characterising acute lymphoblastic leukaemia, but lymphoblastic leukaemia. Nevertheless, some recent substantial their application to acute myelogenous leukaemia has not yet improvements in chemotherapy and supportive care, coupled proved of practical value, and cytochemical markers give only with impressive preliminary results of bone marrow trans- very approximate confirmation ofthe French-American-British plantation, suggest a more encouraging future. classification.3 Acute myelogenous leukaemia represents a wide range of Induction chemotherapy-The first stage of treatment is to diseases lumped together under a heading of convenience, and induce a complete remission-to reduce blood and bone current attempts to separate these diseases using new marrow blast cells to morphologically undetectable levels, to classification schemes, chromosomal changes, cell-growth re-establish normal bone marrow function, to return the patterns, cytochemical, and other differences may have granulocyte and platelet counts to normal, and, most important, prognostic significance and are aimed eventually at more to restore normal health without physical signs or symptoms. individual treatment for the patient with acute myelogenous When treatment was given with single-agent chemotherapy leukaemia. with drugs such as prednisone, vincristine, methotrexate, and The French-American-British classification of acute 6-mercaptopurine (which had been used with some success in leukaemias' has been widely accepted, though like any acute lymphoblastic leukaemia) the results in acute myelo- morphological classification system its reproducibility between genous leukaemia were disappointing (table I). The excellent independent observers is a major difficulty.2 Acute myelo- results of combination chemotherapy for acute lymphoblastic genous leukaemia is divided into myeloblastic leukaemia leukaemia in childhood soon led to the use of combinations of without maturation (M1) or with features of maturation (M2), two or more agents for the treatment of acute myelogenous promyelocytic leukaemia characterised by hypergranular leukaemia. Remission rates of 20-30%, were achieved, but it promyelocytes with abundant Auer rods (M3), and myelo- was not until the introduction of the pyrimidine analogue BRITISH MEDICAL JOURNAL VOLUME 281 11 OCTOBER 1980 961 TABLE I-Induction chemotherapy using single drugs Most patients subsequently relapse, presumably because their induction treatment did not completely abolish the leukaemia. Complete remission Br Med J: first published as 10.1136/bmj.281.6246.960 on 11 October 1980. Downloaded from rate Treatment Reference On the other hand, a few patients have survived for up to 5 )O Methotrexate 1-25-2-5 mg/kg daily Vogler et al (1967)5 10 years without further treatment. Clearly, however, most 1380, 6-Mercaptopurine 2-5 mg/kg daily Hayhoe (1955)6 15 ',0 Prednisone 40 mg daily Medical Research Council patients have some residual leukaemic cells, which will (1966)7 25'% Ara-C 50-100 mg/m2 (1-hr or Ellison et al (1968)8 probably begin to multiply as soon as induction chemotherapy 12-hr infusion daily to stops. In theory, hypoplasia) further treatment either with high doses of 42% Ara-C 4 mg/kg (8-hr infusion Armentrout and Burns the drugs used in induction treatment (consolidation chemo- daily i- 4-14 days) (1974)9 50,, DNR 60 mg m2 days 1-3 Wiernik and Serpick therapy) or with lower doses of these or other drugs (mainte- (1972)1u nance chemotherapy) should improve results. Unfortunately, the place of both these types of treatment is based mainly on Ara-C = Cytosine arabinoside. DNR = Daunorubicin. anecdotal, uncontrolled observations. The few controlled clinical trials of maintenance treatment reported have been on small numbers of patients and the results have been cytosine arabinoside (ara-C) that the modern era of chemo- conflicting.'6 18 Furthermore, the possible benefits of mainte- therapy for acute myelogenous leukaemia began. This drug nance chemotherapy have to be weighed against the upset it causes competitive inhibition of DNA polymerase, resulting causes. This is seen most clearly with schedules which include in inhibition of synthesis of DNA. Used alone, ara-C has the anthracycline antibiotics, because of the definite risk that achieved remission rates of about 25%, but in combination their cardiotoxicity will rule them out for second or subsequent with other drugs the remission rates have been as high as attempts to induce remission. On balance, some form of 56o.4 maintenance chemotherapy for one to two years seems A further major advance was the introduction of the reasonable, but many centres discontinue the anthracyclines anthracycline antibiotics daunorubicin and doxorubicin. once remission has been reached. Unfortunately, the median These drugs are chemically and pharmacologically closely remission duration for most patients with acute myelogenous similar and act by inhibiting replication of DNA. Complete leukaemia has been short and the reported median survivals remission rates of up to 500 ' have been seen when anthra- of between 10 and 21 months remain disappointing. Further- cyclines have been used as single agents5-10 (table I). more, the high remission rates being achieved seem to be Modern treatment logically combines the purine antagonist associated with a high proportion of unexpectedly short 6-thioguanine and ara-C, in courses of five to seven days, remissions,'415 which may reflect a more resistant disease with daily intravenous daunorubicin or doxorubicin for one to process. three days (table II). Ara-C is now often given as a continuous Immunotherapy-The discovery of tumour-specific antigens intravenous infusion, though its toxicity is probably less when in experimental tumours and the regression induced in leukaemic mice treated with irradiated leukaemic blast cells or with BCG'9 led to a number of clinical trials of immuno- TABLE iI-Induction chemotherapy schedules which include daunorubicin (or therapy. Data
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