Hostname: page-component-78c5997874-t5tsf Total loading time: 0 Render date: 2024-11-19T04:26:49.528Z Has data issue: false hasContentIssue false

Cancer and Senescence: Is There a Biological Link?

Published online by Cambridge University Press:  01 August 2014

P.R.J. Burch*
Affiliation:
Department of Medical Physics, University of Leeds, The General Infirmary, Leeds, UK
*
Department of Medical Physics, University of Leeds, The General Infirmary, Leeds LSI 3EX, UK

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

It is shown that sex- and age-specific death rates from all causes of death other than neoplasms have features that resemble those of corresponding rates for all neoplasms. The same generalization holds in connexion with specific neoplastic and non-neoplastic disorders. In both categories of disease many age-patterns suggest that the rate-governing mechanism for their occurrence is stochastic in character; a rather small number of random events, generally fewer than ten, suffice for their initiation. It is not immediately obvious how a widespread degenerative disorder, sometimes involving an astronomical number of target cells, can be initiated by only a few random events. We infer that all such disorders, together with natural cancers, are autoaggressive in nature. They are initiated by random somatic mutations in comparator stem cells of the central system of growth control. Mutant stem cells propagate forbidden clones of cells that attack target cells at one or multiple sites. (In certain disorders, the presence of an extrinsic precipitator in the host in essential to the propagation of forbidden clones). Autoaggressive attacks have consequences that range from the destruction of target cells to their transformation with invasive proliferation. Senescence can be regarded as the cumulative effect of predominantly late-onset autoaggressive disorders. The relevance of studies of twins to this unified theory is discussed.

Type
Research Article
Copyright
Copyright © The International Society for Twin Studies 1984

References

REFERENCES

1.Benditt, EP, Benditt, JM (1973): Evidence for a monoclonal origin of human atherosclerotic plaques. Proc Natl Acad Sci USA 70: 17531756.CrossRefGoogle ScholarPubMed
2.Burch, PRJ (1968): An Inquiry Concerning Growth, Disease and Ageing. Edinburgh: Oliver & Boyd; Buffalo, N.Y.: University of Toronto Press(1969).Google Scholar
3.Burch, PRJ (1968): Genetic aspects of rheumatic and arthritic diseases. In Duthie, JJR, Alexander, WRM (eds): Rheumatic Diseases. Pfizer Medical Mongraphs 3. Edinburgh University Press, p 2950.Google Scholar
4.Burch, PRI (1976): The Biology of Cancer. A New Approach. Lancaster: MTP Press Ltd; Baltimore: University Park Press.Google Scholar
5.Burch, PRJ (1979): Huntington's disease: types, frequency and progression. In Chase, TN, Wexler, NS, Barbeau, A (eds): Advances in Neurology, Vol 23. New York: Raven Press, p 4357.Google Scholar
6.Burch, PRJ (1980): Ischaemic heart disease: epidemiology, risk factors and cause. Cardiovasc Res 14:307338.Google Scholar
7.Burch, PRJ (1983): The Surgeon General's “Epidemiologic Criteria for Causality”. A critique. J Chron Dis 36:821836.CrossRefGoogle Scholar
8.Burch, PRJ, Burwell, RG (1965): Self and not-self: a clonal induction approach to immunology. Q Rev Biol 40:252279.CrossRefGoogle Scholar
9.Burch, PRJ, Jackson, D, Fairpo, CG, Murray, JJ (1973): Gingival recession (“getting long in the tooth”), colorectal cancer: degenerative and malignant changes as errors of growth-control. Mech Ageing Dev 2:251273.Google Scholar
10.Burch, PRJ, Murray, JJ, Jackson, D (1971): The age-prevalence of arcus senilis, greying of hair, and baldness. Etiological considerations. J Gerontol 26:364372.Google Scholar
11.Burnet, FM (1959): The Clonal Selection Theory of Acquired Immunity. London: Cambridge University Press.CrossRefGoogle Scholar
12.Burwell, RG (1963): The role of lymphoid tissue in morphostasis. Lancet 2:6974.CrossRefGoogle ScholarPubMed
13.Carakushansky, G, Berthier, C (1976): The de Lange syndrome in one of twins. J Med Genet 13: 404406.CrossRefGoogle Scholar
14.Carmelli, D, Andersen, S (1981): A longevity study of twins inthe Mormon genealogy. In Gedda, L, Parisi, P, Nance, WE (eds): Twin Research 3: Part C, Epidemiological and Clinical Studies. New York: Alan R Liss, p 187200.Google Scholar
15.Karp, L, Bryant, JI, Tagatz, G, Giblett, F, Fialkow, PJ (1975): The occurrence of gonadal dysgenesis in association with monozygotic twinning. J Med Genet 12:7078.CrossRefGoogle ScholarPubMed
16.Pedersen, IK, Philip, J, Sele, V, Starup, J (1980): Monozygotic twins with dissimilar phenotypes and chromosome complements. Acta Obstet Gynecol Scand 59:459462.CrossRefGoogle ScholarPubMed
17.Registrar General (1982): Mortality Statistics, Cause, 1980, England and Wales. Office of Population Censuses and Surveys. London: HMSO.Google Scholar
18.Schmidt, R, Sobel, EA, Nitowsky, HM, Dar, H, Allen, FH (1976): Monozygotic twins discordant for sex. J Med Genet 13:6468.CrossRefGoogle ScholarPubMed
19.US Surgeon General (1982): The Health Consequences of Smoking. Cancer. Rockville: US Department of Health and Human Services.Google Scholar