Latency periods in neoplastic diseases

Our plain-English summary of Latency periods in neoplastic diseases, by A.P. Polednak (American Journal of Epidemiology, 1974).

The study

• Author: A.P. Polednak
• Journal: American Journal of Epidemiology
• Published: 1974;100(5):354-6
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

In this short commentary, the author discussed what the latency period between exposure to a presumed causal agent and the detection of, or death from, a cancer means. It followed a review of latency distributions by Armenian and Lilienfeld. The author argued that the meaning of latency depends on the causal model that applies to a particular cancer. The first was a "cumulative exposure" model, illustrated by cigarette smoking and lung cancer, in which accumulated insults produce cell changes that are reversible up to a critical point. Citing Burbank, the author noted an estimated population latency period of about 30 years. The second was a "one insult, co-carcinogenic" model, illustrated by pulmonary scars and lung cancer, in which an initiator interacts with a promoting factor during a critical period. The author said that pulmonary infection and scarring in adults, and apical scarring possibly caused by air pollution, needed study in relation to lung cancer. Cervical cancer, for which a one-insult model had been suggested, was also discussed, along with what each model implies for explanations based on DNA modification. Finally, the author noted that other causal mechanisms could bring cases with unusual latency periods into the data, affecting averages and dispersions more than medians. As an example, a latency of over 70 years had been suggested for one case of mesothelioma after asbestos exposure, but only if asbestos caused the disease.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This 1974 article was a short commentary, not a study with its own data. The author responded to a review by Armenian and Lilienfeld of the time between exposure to a suspected cause and the detection of, or death from, a cancer (the latency period). The author argued that what a latency period means depends on how a particular cancer is thought to be caused, and described two models. In a "cumulative exposure" model, illustrated with cigarette smoking and lung cancer, repeated insults cause cell changes that can be reversed up to a threshold point. In a "one insult, co-carcinogenic" model, illustrated with lung scars and lung cancer, a starting event must interact with a second factor. Cervical cancer was also discussed. Asbestos appeared only once. Citing other researchers, the author noted that a latent period of over 70 years had been suggested in one case of mesothelioma after asbestos exposure, but only if that exposure caused the disease. The author argued that such unusual cases can distort averages of latency periods, while the median is less affected.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Commentary on causal models and the meaning of latency periods in cancer, with no original data
• Exposure: Discussed conceptually: cigarette smoking and lung cancer, pulmonary scars or infection and lung cancer, and a presumed initiator in cervical cancer. Asbestos exposure and mesothelioma were mentioned once, citing another study.
• Main results:
  • The author's argument: in a cumulative exposure model, latency could partly reflect the time needed for accumulated insults to produce a neoplasm. This would involve a threshold, with cell changes reversible up to a point.
  • The author's argument: in a one insult, co-carcinogenic model, the outcome depends on an interaction between an initiator (such as scar formation) and a promoting factor.
  • Citing McDonald and McDonald, not this article's own finding: a latent period of over 70 years had been suggested in a case of mesothelioma after asbestos exposure, but only if that exposure was responsible for the disease.
  • The author's argument: cases with unusual latency periods, caused by other mechanisms but attributed to one agent, could affect averages and dispersions of latency periods. The median would be less affected.
• The authors' conclusion: The author concluded that in most human cancers causal mechanisms are little understood, so the meaning of the latency period could vary with the mechanism involved.

Topics

Medical terms in this study, explained in our Lexicon: Latency, Cumulative Exposure, Lung Cancer, Carcinogenic, Mesothelioma, Asbestos Exposure.

Related studies

• Inorganic particles in human tissues and their association with neoplastic disease — A.M. Langer (1974)
• Cancer survival and prevalence in Australia: period estimates from 1982 to 2010 — Australian Institute of Health and Welfare (2013)
• Latency period for mesothelioma — A. Chovil, C. Stewart (1979)
• Cell proliferation and carcinogenesis may share a common basis of permeable plasma membrane clusters — J.A. Beech (1992)
• Expression of Gab1 lacking the pleckstrin homology domain is associated with neoplastic progression — H. Kameda, J.I. Risinger, et al. (2001)
• The latency period of mesothelioma among a cohort of British asbestos workers (1978-2005) — G. Frost (2013)

Browse more research in American Journal of Epidemiology, or return to medical research.