Corrections to: ‘‘Age distribution of cancer in mice’’

Harding, Charles; Pompei, Francesco; Wilson, Richard E.

doi:10.1177/0748233710386410

Cited by 5 publications

(6 citation statements)

References 9 publications

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“…These data do not exclude other potential causes, such as the "weeding out of the susceptible" (8,10,11). It is also notable that cancer incidence rates do not decelerate in mice (20). This fact, combined with our discovery of a major difference between mice and humans with respect to normal cell division rates, provides further evidence for the causal relationship between cancer incidence and the replicative mutations that occur when normal stem cells divide (22,(28)(29)(30)(31).…”

Section: Discussionmentioning

confidence: 85%

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Cell division rates decrease with age, providing a potential explanation for the age-dependent deceleration in cancer incidence

Tomasetti

Poling

Roberts

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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A new evaluation of previously published data suggested to us that the accumulation of mutations might slow, rather than increase, as individuals age. To explain this unexpected finding, we hypothesized that normal stem cell division rates might decrease as we age. To test this hypothesis, we evaluated cell division rates in the epithelium of human colonic, duodenal, esophageal, and posterior ethmoid sinonasal tissues. In all 4 tissues, there was a significant decrease in cell division rates with age. In contrast, cell division rates did not decrease in the colon of aged mice, and only small decreases were observed in their small intestine or esophagus. These results have important implications for understanding the relationship between normal stem cells, aging, and cancer. Moreover, they provide a plausible explanation for the enigmatic age-dependent deceleration in cancer incidence in very old humans but not in mice.

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Section: Discussionmentioning

confidence: 85%

“…Cell Division Rates Do Not Decelerate in Laboratory Mice. Although cancer incidence decelerates at advanced age in humans, no deceleration occurs in mice (20). We wondered whether this difference might reflect differences in stem cell division rates in older individuals of the 2 species (21,22).…”

Section: Significancementioning

confidence: 98%

Cell division rates decrease with age, providing a potential explanation for the age-dependent deceleration in cancer incidence

Tomasetti

Poling

Roberts

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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“…Miyaishi et al32 found that, in 331 F344/N rats, all animals that survived for >30 months died of cancer. Unfortunately, it has been discovered that the results reported by Pompei et al,36 who found a mortality peak in BALB/C mice, are entirely incorrect 37…”

Section: Discussionmentioning

confidence: 94%

“…Unfortunately, it has been discovered that the results reported by Pompei et al, 36 who found a mortality peak in BALB/C mice, are entirely incorrect. 37 Although previous work and our results evidence a decline in the age-specific incidence and mortality of most cancers at very old ages, this does not explain why such a decline would occur.…”

Section: Comparison With Previous Resultsmentioning

confidence: 99%

Peak and decline in cancer incidence, mortality, and prevalence at old ages

Harding

Pompei

Wilson

2011

Cancer

Self Cite

104

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BACKGROUND: Cancer incidence and mortality increase with age through much of adulthood, but earlier work has found that these rates decline among the very elderly. To compare incidence and mortality at the oldest ages, the authors investigated both in the same large population, which comprised 9.5% of the United States in 2000. The authors also report age-specific prevalence among the elderly, which has received little attention. METHODS: Twentythree cancer types were studied in men, and 24 cancer types were studied in women. Patient records were obtained from the SEER 9 cancer registries, and population figures were taken from the 2000 US Census. The authors explored the reliability of census data on the oldest old, which has been questioned. RESULTS: Age-specific incidence, prevalence, and mortality results are presented for the years 1998 to 2002. Incidence and mortality usually decreased or plateaued at very old ages. Prevalence usually decreased swiftly at ages >90 years. When there was statistical power, incidence normally peaked between ages 75 years and 90 years, dropping abruptly afterward. With several large exceptions, peak incidence and mortality coincided within AE5 years. Both rates often trended toward zero among centenarians, who may be asymptomatic or insusceptible. CONCLUSIONS: The current results were found to be consistent with autopsy and survival studies. Most age-specific models of carcinogenesis are based on cancer rate data for ages <85 years. The authors argue that these models could not fit the current results without fundamental modification and outline biologic mechanisms for such modification, mostly cellular and tissue senescence. They also recommend caution to researchers who use census data on the very elderly. Cancer 2012;118:1371-

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“…Several factors likely contribute to the diminished incidence in older adults, including that the data may not be as reliable for older individuals (3). This explanation is insufficient, however, as studies in animal models demonstrate the same pattern (4). A second contributing factor is variation among individuals in intrinsic cancer susceptibility, also referred to as frailty (5).…”

Section: Introductionmentioning

confidence: 99%

Host Age Is a Systemic Regulator of Gene Expression Impacting Cancer Progression

et al. 2015

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Aging is the major determinant of cancer incidence, which, in turn, is likely dictated in large part by processes that influence the progression of early subclinical (occult) cancers. However, there is little understanding of how aging informs changes in aggregate host signaling that favor cancer progression. In this study, we provide direct evidence that aging can serve as an organizing axis to define cancer progression-modulating processes. As a model system to explore this concept, we employed adolescent (68 days), young adult (143 days), middle-aged (551 days), and old (736 days) C57BL/6 mice as syngeneic hosts for engraftment of Lewis lung cancer to identify signaling and functional processes varying with host age. Older hosts exhibited dysregulated angiogenesis, metabolism, and apoptosis, all of which are associated with cancer progression. TGFβ1, a central player in these systemic processes, was downregulated consistently in older hosts. Our findings directly supported the conclusion of a strong host age dependence in determining the host tumor control dynamic. Furthermore, our results offer initial mechanism-based insights into how aging modulates tumor progression in ways that may be actionable for therapy or prevention.

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Corrections to: ‘‘Age distribution of cancer in mice’’

Cited by 5 publications

References 9 publications

Cell division rates decrease with age, providing a potential explanation for the age-dependent deceleration in cancer incidence

Cell division rates decrease with age, providing a potential explanation for the age-dependent deceleration in cancer incidence

Peak and decline in cancer incidence, mortality, and prevalence at old ages

Host Age Is a Systemic Regulator of Gene Expression Impacting Cancer Progression

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