136 It does not follow that female hormones should be given males for the same purpose. However since (a) restradiol is the strongest known natural stimulant of the reticuloendothelial system (R.E.S.).10 (b) cestrogens are produced in the male in small quantities by secretion and metabolic transformation of testosterone, and (c) testosterone strongly potentiates the stimulant action of estradiol on Rjs.s," the combination of free testosterone (method of Christian Hamburger) and a:stradiol in a 40,’l(or smaller) ratio should be investigated for its possibly equivalent prophylactic action against cancer in males. Judged by the overall proportion of long-term successes, the record of cancer therapy is dismal. It is strongly urged that cancer funds be directed towards the study in humans of cancer pre°berrtion, which is part of the whole problem of
to
biological ageing.* Division of Mathematical
Anthropo-biology, University of Leyden,
JAMES G. DEFARES.
Netherlands.
POSSIBLE EFFECT OF MEASLES ON LEUKÆMIA SIR,-In relation to the article by Webb and Gordon Smith on viruses in the treatment of cancer,ll I should like to report two observations suggesting that measles contracted during treatment of lymphoblastic leukaemia may have beneficial effects. Among the cases of lymphoblastic leukaemia treated in our department, four began treatment in 1965, and two of these died in 1967. The other two had measles during treatment; and both are still alive and well. The first patient is a girl who began treatment in May, 1965, at the age of 3. Remission was obtained with cortisone and hypoxanthine, and she was maintained on alternate methotrexate, hypoxanthine, and cyclophosphamide. In August, 1967, and January, 1968, she had meningeal relapses which were treated with intrathecal methotrexate. In March, 1967, she had a moderately severe attack of measles. In November, 1967, and February, 1968, she had two more meningeal relapses. In March, 1968, she contracted rubella from her mother, with fever and rash, The following despite gamma-globulin prophylaxis. month all chemotherapy was stopped because her fathera good Neapolitan-thought that St. Gennaro might help. The second patient is a boy who began treatment, at the age of 5, in November, 1965. Remission was obtained with cortisone and hypoxanthine. At the end of January, 1966, while in remission, he had a severe attack of measles complicated by bronchopneumonia. Since then he has had no serious relapses; he has continued on maintenance methotrexate and hypoxanthine, and was given courses of vincristine and daunorubicin in 1968 and 1969. The factors responsible for long-term remissions in some It cases of lymphoblastic leukaemia are still unknown. therefore seems justifiable to consider the possibility that measles virus ’or live or dead measles vaccine) might be useful in the immunotherapy of lymphoblastic leukxmia. The virus is one of the most powerful stimulators of both humoral and cell-mediated imm unity.12 (wit would, of course, be necessary to suspend chemotherapy before giving live Some thought might also be given to the measles virus. rubella virus, which is in many respects similar to measles virus. Our first patient has had no further chemotherapy since she had rubella 3 years ago. Pædiatric Cliniz, Primario Pediatra Ospedale di Viareggio,
Civile
G. PASQUINUCCI. Italy. 10. Nicol, T., Vernon-Roberts, B., Quantock, D. C. J. Endocr, 1965,
33, 365. 11. Webb. H. E., Gordon Smith, C. E. Lancet, 1970, i, 1206. 12. Burnett, F. M. ibid. 1968, ii. 610.
CELL SURFACE AND GROWTH CONTROL SIR,—Apropos your editorial,1 could it be that epithelial cells are more liable than mesenchymal ones to lose their contact inhibition or to suffer exposure of the agglutinin receptor
reason-at least in partthan sarcomas ??
layer, and that for this
carcinomas
are more common
Ipswich.
S. L. BARLEY. BARLEY,
EXTERNAL PRESSURE AND FEMORAL-VEIN FLOW SiR,-Professor Calnan and his colleagueshave drawn attention to the application of intermittent external pressure as a means of producing rhythmic variations in femoral-vein blood-flow. A detailed investigation into the effects of external pressure on femoral-vein blood-flow has lately been reported by our department,3 and Professor Calnan’s article prompted me to re-examine the flow recordings obtained during this investigation. The general pattern of the flow recordings is shown in fig. 1. External pressure is applied to the limb by means of
Fig. 1-Clianges in blood flow caused by inflation of pneumatic splint. a pneumatic splint at time t1. The flow in the femoral vein rises transiently and then falls to a new stable level at
This final flow will be greater or less than the on the magnitude of the external pressure. The volume of blood ejected from the compressed venous system can be determined by measuring the shaded portion of the flow-curve. This was done for each of the recordings obtained during our original investigation, and the results are shown in fig. 2. These curves reveal that for splint-pressures less than 10 mm. Hg the mean volume of blood ejected is identical for both the below-knee and the full-length splints. With the below-knee splint (which is similar to the device used by Professor Calnan and his colleagues) the volume ejected tends to be maximal at 20 mm. Hg splint-pressure, higher pressures only leading to small increases in the ejected volume. These results agree very closely with those reported in an earlier investigation into the effects of compression stockings.4 In this it was reported that when an external pressure of 15 mm. Hg was applied to the leg, the venous volume was reduced from 3-0 to 0-6 ml. per 100 ml. of leg. If we assume a calf-foot volume of 3000 ml., this gives an ejected volume of 72 ml., which agrees with the results presented here. These results prompt two observations. Firstly, if the
time t2.
original flow, depending
1. Lancet, 1970, ii, 1294. 2. Calnan, J. S., Pflug, J. J., Mills, C. J. Lancet, 1970, ii, 502. 3. Spiro, M., Roberts, V. C., Richards, J. B. Br. med. J. 1970, i, 719 4. Wilkins, R. W., Mixter, G., Stanton, J. R., Litter, J. Nem Engl. J Med. 1952, 246, 360.