Decline in Human Cancer Incidence Rates at Old Ages: Age-Period-Cohort Considerations

Arbeev, Konstantin G.; Ukraintseva, Svetlana V.; Arbeeva, Lyubov S.; Yashin, Anatoli I.

doi:10.4054/demres.2005.12.11

Cited by 13 publications

(11 citation statements)

References 38 publications

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“…As discussed by Macunovich (1998) and based on my own literature survey, ageperiod-cohort analyses in demography have been implemented in a large amount of literature (Arbeev et al 2005;Brass 1974;Clayton and Schifflers 1987;Mason 1978, 1985;Foster 1990;Namboodiri 1981;Ni Bhrolchain 1992;Page 1977;Pullum 1980;Wilmoth 1990;Wright and Maxim 1987). The following three studies are noteworthy, but no existing study can be compared with my study.…”

Section: Introductionmentioning

confidence: 92%

“…However, the main problem with their method is that its methodological usefulness depends on strong prior information about the constraint, and estimates of model effect coefficients are sensitive to the arbitrary choice of the identifying constraint (Yang et al 2004). Recently, Arbeev et al (2005) applied a nonlinear age-period-cohort model developed by James and Segal (1982) to obtain declining U.S. cancer incidence rates at old ages. However, the age-period-cohort model proposed in this paper is a linear model.…”

Section: Introductionmentioning

confidence: 98%

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Age–Period–Cohort Decomposition of U.S. and Japanese Birth Rates

Fukuda

2008

Popul Res Policy Rev

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Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 98%

Age–Period–Cohort Decomposition of U.S. and Japanese Birth Rates

Fukuda

2008

Popul Res Policy Rev

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“…The model might also explain the decline in the incidence of cancer after the 8th decade of life [43] (see mathematic formulation in Supplementary Information). While very old persons have accumulated first-stage mutational hits at the stem cell level, because of their short telomeres, they are less likely to sustain through clonal expansion the 2 nd Hit.…”

Section: The Potential Resolution Of the Cancer-telomere Length Paradoxmentioning

confidence: 99%

Mutations, Cancer and the Telomere Length Paradox

2017

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Individuals with short telomeres should be at increased risk for cancer, since short telomeres lead to genomic instability— a hallmark of cancer. However, individuals with long telomeres also display an increased risk for major cancers, thus creating a cancer-telomere length paradox. The two-stage clonal expansion model we propose is based on the thesis that a series of mutational hits (1st Hit) at the stem-cell level generates a clone with replicative advantage. A series of additional mutational hits (2nd Hit) transforms the expanding clone into cancer. By proposing that the 1st Hit is largely telomere length-independent, while the 2nd Hit is largely telomere length-dependent, we resolve the paradox, highlighting a regulatory role of telomeres in cancer.

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“…[1][2][3][4][5][6] In contrast, immunity appears to decline with age and low-level chronic inflammation becomes commonplace. 7,8 Interestingly, however, cancer incidence rates begin to decelerate and plateau at age 85, 5 and rates of diagnosis of a number of cancers peak many years before. Incidence rates of testicular cancer, for example, are greatest between the ages of 25 and 35, falling thereafter, whilst male bowel cancer incidence rates fall throughout the ninth decade of life.…”

Section: Introductionmentioning

confidence: 98%

Failing to adapt – the ageing immune system's role in cancer pathogenesis

Jones

2011

Rev. Clin. Gerontol.

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A person's risk of developing cancer rises exponentially with age, an increase that is widely considered to result from cumulative exposure to mutagenic agents. However, cancer incidence rates decelerate and plateau beyond 85 years of age and numerous malignant pathologies peak in incidence during early or middle life, indicating an important role for additional factors in controlling the timing and nature of cancer development. Given that immune function is known to decrease with age, malignant neoplastic change may be induced by increased chronic infection and the onset of a pervasive low grade inflammatory environment. This article discusses in detail the ageing immune system's role in cancer pathogenesis and demonstrates that key polymorphisms coding for relatively low pro-inflammatory cytokine production act to protect some populations from age-induced neoplastic transformation.

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Decline in Human Cancer Incidence Rates at Old Ages: Age-Period-Cohort Considerations

Cited by 13 publications

References 38 publications

Age–Period–Cohort Decomposition of U.S. and Japanese Birth Rates

Age–Period–Cohort Decomposition of U.S. and Japanese Birth Rates

Mutations, Cancer and the Telomere Length Paradox

Failing to adapt – the ageing immune system's role in cancer pathogenesis

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