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BURKITT ON BURKITT'S LYMPHOMA
229
approach to the aaiology of localised congenital defects. Improper embryonic-tissue growth patterns during the development of the cleft defects might lead to localised chromosomal anomalies; and vice versa, at least in a small proportion of the sporadic cases of cleft-palate defects, the presence of chromosome mosaicism might cause asynchromous development of the growth centres with failure of coalescence and fusion. In our laboratory, we are now beginning to study human tissues from the sites of other localised malformations, such as cardiac anomalies, in an attempt to evaluate the significance of localised autosomal chromosomal mosaicism. This study was supported by a University of Louisville General Research Support grant from the National Institute of Health. Genetic Counselling Unit, Department of Pediatrics, University of Louisville JOHN W. MURPHY School of Medicine, LEONARD E. REISMAN. Louisville, Kentucky.
BURKITT ON BURKITT’S LYMPHOMA SIR,-In your annotation (April 9), you state that this lymphoma has not been detected in Zanzibar, but I have jointly described it in a 6-year-old Arab boy from Zanzibar, who also had acute lymphoblastic leukaemia.1 Neither the boy nor his relatives had left the island before the development of the
lymphoma. Burkitt’s statement, which you cite, that the incidence of the disease is similar in children of all races within the endemic areas is, as far as Kenya is concerned, incorrect. The European and Asian population (including Arabs) of Kenya is at present 230,000, many of whom live in areas where Burkitt’s lymphoma is endemic (e.g., Mombasa and Kisumu). Commenting further on the report by Khan,2Iwish to point out that this disease has not been recorded in Kenya in a nonAfrican child over the past 8 years. The statement that the British type of leukaemia appears " in Kenya with roughly the " same frequency as in Britain is correct if applied only to the relatively small European and Asian community. Leukxmia is rare in Kenya African children. Dalldorf et al.,3 comparing the incidence of leukaemia and lymphoma in African children in Kenya, have suggested that lymphatic malignancies of young children which are usually leukxmia in North America are characteristically tumorous in East Africa. Department of Head and Neck Surgery, Kenyatta National Hospital, PETER CLIFFORD. P.O. Box 30024, Nairobi.
THE GEOGRAPHY OF MULTIPLE SCLEROSIS SIR,-As the tempo quickens in the effort to solve the strange geography of multiple sclerosis4 about which you have written (July 9), epidemiologists should not overlook the considered belief of several observers 5-8 that multiple sclerosis is either a psychosomatic disorder, or has a predominant psychosomatic component; after twenty years of study I have no doubt on this point. This does not exclude the relevance of autoimmunity for which there is accumulating evidence, or of increased platelet stickiness-the first of these is strongly influenced by the emotional state (what could be more " psychosomatic than autoclasis ?), while the second falls into Cannon’s theory of " flight and fight". Assessment of cultural patterns of social behaviour, of attitudes within the family to marriage, to children, and to parents, 1 Cft, R. A., Wright, D. H., Clifford, P. Blood, 1963, 20, 243. "
2 Khan, A. G. J. Lar. Otol. 1964, 78, 480. 3 Dadorf, G., Linsell, C. A., Barnhart, F. E., Martyn,
R.
Perspect. Biol.
Med. 1964, 7, 435.
4 McAlpine, D., Lumsden,
C. E., Acheson, E. D. A Reappraisal. Edinburgh, 1965. 5 Inman, W. S. Br. J. med. Psychol. 1948, 21, 135. 6 Groen, J. J. Mt Sinai Hosp. 1951, 18, 71. 7 Jonez, H. D. Ann. Allergy, 1951, 9, 653. 8 lley, J. W. Lancet, 1952 i, 1305.
Multiple Sclerosis:
and of the influence of taboos and religion in certain subcultures on emotional maturation and emotional release, especially of aggression, seems at first sight prohibitive. But I think an attempt on these lines should be made because it is in this area of emotional conflict that one has seen multiple sclerosis flourish. I am not at all surprised that the rate of incidence falls when Northern Europeans emigrate. They leave behind not only the northern fogs, but also the cold cramp of cloying family ties which have possibly become unhealthily prevalent in our culture, and in its place find the challenge of survival in expanding societies. This could also have some bearing on the unproven higher incidence in smaller communities or in those long-settled with traditions or rigidity. At the same time the effect of climate on social behaviour and attitudes can hardly be doubted. Crude though they are, inventories are improving, and it should be possible to design one to measure some of these things. Meanwhile more information on membership of religious sects and social class would be helpful-my current impression is of an undue incidence of multiple sclerosis in social classes n and III, which is much in accord with the findings of Miller et al.that it is hish in I and II. Ipswich and East Suffolk Hospital, J. W. PAULLEY. Ipswich, Suffolk. ’
MALIGNANT CELLULAR EVOLUTION SiR,—The hypothesis by Dr. Ravenholt 10 gives a refreshing view of malignant growth seen as a part of the total picture of cell growth, rather than as mysterious cells possessed of a devil. Certain additions to, or extensions of, Dr. Ravenholt’s theories may be in order. He defines a mutagen as " any agent which acts specifically to increase heritable change during cell division ". In a letter in the same issue of The Lancet, Dr. Reid 11 mentions the possibility that cervical cancer may be initiated by " the presence of deoxyribonucleic acid of sperm origin in the host cell acting as a mutagen ". If nuclear material from a sperm cell can enter another cell and act as a mutagen, it would seem possible that material from other adjacent cells might act likewise. In biology, the union of cells or parts of cells, which are not " sex cells, is spoken of as conjugation ". This process of conjugation is an occasional supplement to the usual asexual reproduction in many unicellular organisms. Such a process seems equally possible in multicellular organisms. It would be much more difficult to observe, but this is no argument for its non-existence. Perhaps, with excessive damage and repeated " repair, producing many generations of Dr. Ravenholt’s serial reproduction ", the cells of the body may exhaust their vitality and weaken their genetic pattern. They may then be stimulated to proliferation by a sort of conjugation with nuclear materials from adjacent body cells, thus initiating malignant growth. Williamsburg, Virginia, U.S.A.
JANET C. KIMBROUGH.
VIRUS INDUCTION OF AUTOIMMUNE DISEASE AND NEOPLASIA SIR,-Autoimmune leukxmogenesis has been rather thoroughly discussed by Professor Stanley and Dr. Walters 12 and Professor Dameshek.13 In 1961 I found lymphoid cells, deriving from the cell population of a murine lymphoma, which caused either typical runt disease or malignant lymphoma (with leukaemic generalisation) in recipient newborn mice.14 Some mice which survived chronic runt disease later developed leukaemia.15 Just how 9. Miller, H., Ridley, A., Schapira, K. Br. med. J. 10. Ravenholt, R. T. Lancet, 1966, i, 523. 11. Reid, B. L. ibid. p. 548. 12. Stanley, N. F., Walters, N. I. M. ibid. p. 962. 13. Dameshek, W. ibid. p. 1268. 14. Sinkovics, J. G. J. Infect. Dis. 1962, 110, 282. 15 Sinkovics, J. G. Arch. Virusforsch. 1962, 12, 143.
1960, ii, 243.
approach to the aaiology of localised congenital defects. Improper embryonic-tissue growth patterns during the development of the cleft defects might lead to localised chromosomal anomalies; and vice versa, at least in a small proportion of the sporadic cases of cleft-palate defects, the presence of chromosome mosaicism might cause asynchromous development of the growth centres with failure of coalescence and fusion. In our laboratory, we are now beginning to study human tissues from the sites of other localised malformations, such as cardiac anomalies, in an attempt to evaluate the significance of localised autosomal chromosomal mosaicism. This study was supported by a University of Louisville General Research Support grant from the National Institute of Health. Genetic Counselling Unit, Department of Pediatrics, University of Louisville JOHN W. MURPHY School of Medicine, LEONARD E. REISMAN. Louisville, Kentucky.
BURKITT ON BURKITT’S LYMPHOMA SIR,-In your annotation (April 9), you state that this lymphoma has not been detected in Zanzibar, but I have jointly described it in a 6-year-old Arab boy from Zanzibar, who also had acute lymphoblastic leukaemia.1 Neither the boy nor his relatives had left the island before the development of the
lymphoma. Burkitt’s statement, which you cite, that the incidence of the disease is similar in children of all races within the endemic areas is, as far as Kenya is concerned, incorrect. The European and Asian population (including Arabs) of Kenya is at present 230,000, many of whom live in areas where Burkitt’s lymphoma is endemic (e.g., Mombasa and Kisumu). Commenting further on the report by Khan,2Iwish to point out that this disease has not been recorded in Kenya in a nonAfrican child over the past 8 years. The statement that the British type of leukaemia appears " in Kenya with roughly the " same frequency as in Britain is correct if applied only to the relatively small European and Asian community. Leukxmia is rare in Kenya African children. Dalldorf et al.,3 comparing the incidence of leukaemia and lymphoma in African children in Kenya, have suggested that lymphatic malignancies of young children which are usually leukxmia in North America are characteristically tumorous in East Africa. Department of Head and Neck Surgery, Kenyatta National Hospital, PETER CLIFFORD. P.O. Box 30024, Nairobi.
THE GEOGRAPHY OF MULTIPLE SCLEROSIS SIR,-As the tempo quickens in the effort to solve the strange geography of multiple sclerosis4 about which you have written (July 9), epidemiologists should not overlook the considered belief of several observers 5-8 that multiple sclerosis is either a psychosomatic disorder, or has a predominant psychosomatic component; after twenty years of study I have no doubt on this point. This does not exclude the relevance of autoimmunity for which there is accumulating evidence, or of increased platelet stickiness-the first of these is strongly influenced by the emotional state (what could be more " psychosomatic than autoclasis ?), while the second falls into Cannon’s theory of " flight and fight". Assessment of cultural patterns of social behaviour, of attitudes within the family to marriage, to children, and to parents, 1 Cft, R. A., Wright, D. H., Clifford, P. Blood, 1963, 20, 243. "
2 Khan, A. G. J. Lar. Otol. 1964, 78, 480. 3 Dadorf, G., Linsell, C. A., Barnhart, F. E., Martyn,
R.
Perspect. Biol.
Med. 1964, 7, 435.
4 McAlpine, D., Lumsden,
C. E., Acheson, E. D. A Reappraisal. Edinburgh, 1965. 5 Inman, W. S. Br. J. med. Psychol. 1948, 21, 135. 6 Groen, J. J. Mt Sinai Hosp. 1951, 18, 71. 7 Jonez, H. D. Ann. Allergy, 1951, 9, 653. 8 lley, J. W. Lancet, 1952 i, 1305.
Multiple Sclerosis:
and of the influence of taboos and religion in certain subcultures on emotional maturation and emotional release, especially of aggression, seems at first sight prohibitive. But I think an attempt on these lines should be made because it is in this area of emotional conflict that one has seen multiple sclerosis flourish. I am not at all surprised that the rate of incidence falls when Northern Europeans emigrate. They leave behind not only the northern fogs, but also the cold cramp of cloying family ties which have possibly become unhealthily prevalent in our culture, and in its place find the challenge of survival in expanding societies. This could also have some bearing on the unproven higher incidence in smaller communities or in those long-settled with traditions or rigidity. At the same time the effect of climate on social behaviour and attitudes can hardly be doubted. Crude though they are, inventories are improving, and it should be possible to design one to measure some of these things. Meanwhile more information on membership of religious sects and social class would be helpful-my current impression is of an undue incidence of multiple sclerosis in social classes n and III, which is much in accord with the findings of Miller et al.that it is hish in I and II. Ipswich and East Suffolk Hospital, J. W. PAULLEY. Ipswich, Suffolk. ’
MALIGNANT CELLULAR EVOLUTION SiR,—The hypothesis by Dr. Ravenholt 10 gives a refreshing view of malignant growth seen as a part of the total picture of cell growth, rather than as mysterious cells possessed of a devil. Certain additions to, or extensions of, Dr. Ravenholt’s theories may be in order. He defines a mutagen as " any agent which acts specifically to increase heritable change during cell division ". In a letter in the same issue of The Lancet, Dr. Reid 11 mentions the possibility that cervical cancer may be initiated by " the presence of deoxyribonucleic acid of sperm origin in the host cell acting as a mutagen ". If nuclear material from a sperm cell can enter another cell and act as a mutagen, it would seem possible that material from other adjacent cells might act likewise. In biology, the union of cells or parts of cells, which are not " sex cells, is spoken of as conjugation ". This process of conjugation is an occasional supplement to the usual asexual reproduction in many unicellular organisms. Such a process seems equally possible in multicellular organisms. It would be much more difficult to observe, but this is no argument for its non-existence. Perhaps, with excessive damage and repeated " repair, producing many generations of Dr. Ravenholt’s serial reproduction ", the cells of the body may exhaust their vitality and weaken their genetic pattern. They may then be stimulated to proliferation by a sort of conjugation with nuclear materials from adjacent body cells, thus initiating malignant growth. Williamsburg, Virginia, U.S.A.
JANET C. KIMBROUGH.
VIRUS INDUCTION OF AUTOIMMUNE DISEASE AND NEOPLASIA SIR,-Autoimmune leukxmogenesis has been rather thoroughly discussed by Professor Stanley and Dr. Walters 12 and Professor Dameshek.13 In 1961 I found lymphoid cells, deriving from the cell population of a murine lymphoma, which caused either typical runt disease or malignant lymphoma (with leukaemic generalisation) in recipient newborn mice.14 Some mice which survived chronic runt disease later developed leukaemia.15 Just how 9. Miller, H., Ridley, A., Schapira, K. Br. med. J. 10. Ravenholt, R. T. Lancet, 1966, i, 523. 11. Reid, B. L. ibid. p. 548. 12. Stanley, N. F., Walters, N. I. M. ibid. p. 962. 13. Dameshek, W. ibid. p. 1268. 14. Sinkovics, J. G. J. Infect. Dis. 1962, 110, 282. 15 Sinkovics, J. G. Arch. Virusforsch. 1962, 12, 143.
1960, ii, 243.