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Hans Schilder
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Editor- In his editorial on stress and cancer Mcgee states that "prospective longitudinal designs would be a good place to start" (BMJ, 319:1015-1016). Such studies have been done long since. In 20, 30, 30 and 35 year prospective designs increased cancer devlopment was observed in persons characterized by respectively depression1, perceived lack of closeness to parents2, being 'loners' as opposed to acting out and emotional expressiveness3, ambivalent and avoidant interpersonal relationships as opposed to well adjusted ones, as measured with the Rorschach Interaction scale4. One of the prevalent hypotheses in psycho- oncology is that repression of emotions unfavourable affects cancer development 5. It is conceivable that even when more stressful life events would have occurred in people subsequently turning out to be cancer patients, these patients would recall less such events as they may not have experienced the event as intense and thus as seemingly not as stressful as their controls. Still, inherent to the concept of repression, an effect of the event would be there. The subject, however, is even more complicated as seemingly identical 'objective stressful' events have different meaning and thus different effects in different people. In line with the concept of repression it is not surprising that use of a projective measure like the Rorschach test yielded strong prospective results. Prospective studies using fruitful parameters take up to decades; indeed, the word is that Bedell Thomas (2) postponed her retirement to see the outcomes of her study, originating as it did in 1947. Longer survival of cancer patients after psychotherapy having been observed since6,7, as well as temporarily halting of tumour progression during psychotherapy by DeVries and us8, it is likely that intervention studies deserve our emphasis right now, favourably also using frequent assessment of tumormarkers to adequately detect possible relationships between what's going on in life (and in counselling) and in the body. Still, those interested in cancer onset rather than treatment, might, theoretically at least, extend the realm of intervention-studies to prevention-studies, using the parameters of the aforementioned prospective designs to locate persons at risk. Johannes N. Schilder, psycho-oncologist 1.Persky VM, Kempthorne-Rawson J, Shekelle RB. Personailty and risk of cancer: 20-Year follow-up of the Western Electric Study. Psychosom Med 1987;49:435-449. 2.Bedell Thomas C, Duszynski KR, Shaffer JW. Family attitudes reported in youth as potential predictors for cancer. Psychosom Med 1979;41:287-302.
3.Shaffer JW, Graves PL, Swank RT, Pearson ThA. Clustering of personality traits on youth and the subsequent development of cancer among physicians. J Beh Med 1987;10:441-447. 4.Graves PL, Phil M. Mead LA, Pearson ThA. The Rorschach Interaction scale as a potential predictor in cancer. Psychosom Med 1986;48:549-563. 5.Jensen MR. Psychobiological factors predicting the course of breast cancer. J Personal 1987;55:317-342 (and 451). 6.Spiegel D, Bloom J, Kraemer H, Gottheil E. effects of pscyhosocial treatment on survival of patients with metastatic breast cancer. Lancet 1989;2:888-891. 7.Fawzy IF, Fawzy NW, Hyun ChS,Elashoff R, Guthrie D, Fahey JL, Morton DL. Malignant Melanoma; effects of an early structured psychiatric intervention, coping, and affective state on recurrence and survival 6 years later. Arch Gen Psychiatry 1993;50:681- 689. 8.DeVries MJ, Schilder JN, Mulder CL, Vrancken AME, Remie ME, Garssen B. Phase II study of psychotherapeutic intervention in advanced cancer. Psycho-Oncology 1997;6:129-137. |
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A G Dalgleish, Chair Department of Oncology St George''''s Hospital Medical School
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Dear Dr Smith The title of your leading editorial, Does Stress Cause Cancer? subtitled, There's No Good Evidence of a Relation Between Stressful Events and Cancer, by Rob McGee (1) comes to this conclusion reviewing the recent literature and the paper by Protheroe et al in the same issue (2). It is important to note that this conclusion is about breast cancer and its effect on presentation. It would be misleading to believe that this would apply to all cancers, and in particular to a tendency to relapse. Using an intracellular cytokine assay that measures the ability of patients own peripheral blood to produce interleukine-2 (a cell mediated cytokine) or interleukine-4 (humoral associated cytokine), we noted patients with a strong cell mediated response whether or not induced with immunotherapy, tend to do better than those that do not, and in the case where this was induced by vaccination an improved survival was seen compared to those who did not make a cell medicated associated cytokine response (3). We have subsequently used this assay longitudinally and have also noted that a sudden decline in IL-2 production and/or elevation of IL-4 production has been the forerunner of relapsed disease (unpublished observations). Prior to their relapse, at least four patients who had previously been stable for several months, have volunteered that they were under severe stress at work prior to evidence of clinical relapse. It remains a strong possibility that inspite of your editorials conclusion, that stress may well play an important role in some cancers particularly with regard to the likelihood of relapse, and that formal studies addressing this question are justified. Professor A G Dalgleish References 1. McGee R. Does stress cause cancer. BMJ 1999; 7216:1015-1016. 2. Protheroe D et al. Stressful life events and difficulties and onset of breast cancer: case-control study. BMJ 1999; 7216: 1027-1030. 3. Maraveyas A, et al (1999) Possible improved survival of patients with Stage IV AJCC melanoma receiving SRL 172 immunotherapy: Correlation with induction of increased levels of intracellular interleukin 2 in peripheral blood lymphocytes. Annals of Oncology 10.7. 817 - 824 |
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