Carcinogenesis and Aging

Anisimov, Vladimir N.

doi:10.1016/s0065-230x(08)60684-3

Cited by 54 publications

(15 citation statements)

References 146 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In summary, the decline in gastric cancer observed during modernization across developed nations [1,5] may reflect not only the progressive disappearance of H. pylori [12], especially cagA + strains [13], but, as transmission becomes less intense, this may reflect a change in the average age of acquisition [11], in the number of different strains acquired [47], or in their preadaptation to particular hosts [42,43].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Early-Life Family Structure and Microbially Induced Cancer Risk

et al. 2007

View full text Add to dashboard Cite

BackgroundCancer may follow exposure to an environmental agent after many decades. The bacterium Helicobacter pylori, known to be acquired early in life, increases risk for gastric adenocarcinoma, but other factors are also important. In this study, we considered whether early-life family structure affects the risk of later developing gastric cancer among H. pylori + men.Methods and FindingsWe examined a long-term cohort of Japanese-American men followed for 28 y, and performed a nested case-control study among those carrying H. pylori or the subset carrying the most virulent cagA+ H. pylori strains to address whether family structure predicted cancer development. We found that among the men who were H. pylori+ and/or cagA + (it is possible to be cagA+ and H. pylori − if the H. pylori test is falsely negative), belonging to a large sibship or higher birth order was associated with a significantly increased risk of developing gastric adenocarcinoma late in life. For those with cagA+ strains, the risk of developing gastric cancer was more than twice as high (odds ratio 2.2; 95% confidence interval 1.2–4.0) among those in a sibship of seven or more individuals than in a sibship of between one and three persons.ConclusionsThese results provide evidence that early-life social environment plays a significant role in risk of microbially induced malignancies expressing five to eight decades later, and these findings lead to new models to explain these interactions.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Cancer is generally a disease of old age with mortality rates increasing with each succeeding decade of life [1]. However, for many forms of cancer, the relevant risks are conferred by exposure to environmental agents decades earlier [2,3].…”

Section: Introductionmentioning

confidence: 99%

Early-Life Family Structure and Microbially Induced Cancer Risk

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Indeed, polyploidy is a common feature of senescent cells and post-mitotic cells [66], suggesting that some intrinsic factor prevents such cells, endowed with a functional DNA-replication machinery, from achieving mitosis.…”

Section: Discussionmentioning

confidence: 99%

Continued Stabilization of the Nuclear Higher-Order Structure of Post-Mitotic Neurons In Vivo

et al. 2011

View full text Add to dashboard Cite

BackgroundCellular terminal differentiation (TD) correlates with a permanent exit from the cell cycle and so TD cells become stably post-mitotic. However, TD cells express the molecular machinery necessary for cell proliferation that can be reactivated by experimental manipulation, yet it has not been reported the stable proliferation of any type of reactivated TD cells. Neurons become post-mitotic after leaving the ventricular zone. When neurons are forced to reenter the cell cycle they invariably undergo cell death. Wider evidence indicates that the post-mitotic state cannot solely depend on gene products acting in trans, otherwise mutations in the corresponding genes may lead to reentry and completion of the cell cycle in TD cells, but this has not been observed. In the interphase, nuclear DNA of metazoan cells is organized in supercoiled loops anchored to a nuclear nuclear matrix (NM). The DNA-NM interactions define a higher-order structure in the cell nucleus (NHOS). We have previously compared the NHOS of aged rat hepatocytes with that of early post-mitotic rat neurons and our results indicated that a very stable NHOS is a common feature of both senescent and post-mitotic cells in vivo.Principal FindingsIn the present work we compared the NHOS in rat neurons from different post-natal ages. Our results show that the trend towards further stabilization of the NHOS in neurons continues throughout post-natal life. This phenomenon occurs in absence of overt changes in the post-mitotic state and transcriptional activity of neurons, suggesting that it is independent of functional constraints.ConclusionsApparently the continued stabilization of the NHOS as a function of time is basically determined by thermodynamic and structural constraints. We discuss how the resulting highly stable NHOS of neurons may be the structural, non-genetic basis of their permanent and irreversible post-mitotic state.

show abstract

“…25 Administration of phenformin failed influence the mean life span in LIO rats. 73,74 At the same time, the mean life span of the last decile of survivors was increased by 10%, and maximum life span was increased by 3 months (+10%) as compared with the controls. The treatment with phenformin slightly decreased the body weight of rats in comparison with the control.…”

Section: Effect Of Antidiabetic Drugs On Longevitymentioning

confidence: 84%

“…Long-term treatment with phenformin significantly inhibited (by fourfold) the incidence of spontaneous mammary adenocarcinomas in female C3H/Sn mice. 25 The treatment with phenformin was followed by a 1.6-fold decrease in total spontaneous tumor incidence in rats, 73,74 whereas total tumor incidence was decreased by 49.5% in buformin-treated rats. 74,75 The anticarcinogenic effect of antidiabetic biguanides has been demonstrated in several models of induced carcinogenesis (TABLE 2).…”

Section: Effect Of Antidiabetic Drugs On Carcinogenesismentioning

confidence: 99%

Central and Peripheral Effects of Insulin/IGF‐1 Signaling in Aging and Cancer: Antidiabetic Drugs as Geroprotectors and Anticarcinogens

Anisimov

Berstein

Popovich

et al. 2005

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors both in aging and in the development of cancer. Insulin/insulin-like growth factor 1 (IGF-1) signaling molecules linked to longevity include DAF-2 and insulin receptor (InR) and their homologues in mammals and to inactivation of the corresponding genes followed by increased life span in nematodes, fruit flies, and mice. It is possible that the life-prolonging effect of caloric restriction are due to decreasing IGF-1 levels. A search of pharmacological modulators of life span-extending mutations in the insulin/IGF-1 signaling pathway and mimetics of effects of caloric restriction could be a direction in the regulation of longevity. Some literature and our own observations suggest that antidiabetic drugs could be promising candidates for both life span extension and prevention of cancer.

show abstract

Carcinogenesis and Aging

Cited by 54 publications

References 146 publications

Early-Life Family Structure and Microbially Induced Cancer Risk

Early-Life Family Structure and Microbially Induced Cancer Risk

Continued Stabilization of the Nuclear Higher-Order Structure of Post-Mitotic Neurons In Vivo

Central and Peripheral Effects of Insulin/IGF‐1 Signaling in Aging and Cancer: Antidiabetic Drugs as Geroprotectors and Anticarcinogens

Contact Info

Product

Resources

About