Inflammation, ageing and cancer

Vasto, Sonya; Carruba, Giuseppe; Lio, Domenico; Colonna‐Romano, Giuseppina; Bona, Danilo Di; Candore, Giuseppina; Caruso, Calogero

doi:10.1016/j.mad.2008.06.003

Cited by 117 publications

(110 citation statements)

References 79 publications

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“…An increase in somatic mutations has been documented in aged cells, and presumably relates to cumulative lifetime exposure to endogenous and exogenous DNA damaging agents, as well as to an accumulation of mutations during DNA replication [59,62]. However, as previously stated, in oldest old individuals cancer prevalence does not increase, but declines, despite the longer exposure to exogenous and endogenous factors causing cancer.…”

Section: Cancer and Ageingmentioning

confidence: 81%

“…However, incidence and mortality rates of most human cancers consistently increase up to age 90, but they plateau and decline thereafter, suggesting that centenarians are protected from developing cancer. Accordingly, cancer deaths account for 40% from age 50 to 70 and less than 4% for centenarian people [59]. Actually, centenarians, their offspring and siblings have better chances to escape major age related disease including cancer [60]; autoptic studies clearly show that, in centenarians, the cause of death by cancer and metastatic spread are lower than expected [61].…”

Section: Cancer and Ageingmentioning

confidence: 99%

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Low Grade Inflammation as a Common Pathogenetic Denominator in Age-Related Diseases: Novel Drug Targets for Anti-Ageing Strategies and Successful Ageing Achievement

Candore

Caruso

Jirillo³

et al. 2010

CPD

127

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Nowadays, people are living much longer than they used to do, however they are not free from ageing. Ageing, an inexorable intrinsic process that affects all cells, tissues, organs and individuals, is a post-maturational process that, due to a diminished homeostasis and increased organism frailty, causes a reduction of the response to environmental stimuli and, in general, is associated to an increased predisposition to illness and death. However, the high incidence of death due to infectious, cardiovascular and cancer diseases underlies a common feature in these pathologies that is represented by dysregulation of both instructive and innate immunity. Several studies show that a low-grade systemic inflammation characterizes ageing and that inflammatory markers are significant predictors of mortality in old humans. This pro-inflammatory status of the elderly underlies biological mechanisms responsible for physical function decline and agerelated diseases such as Alzheimer's disease and atherosclerosis are initiated or worsened by systemic inflammation. Understanding of the ageing process should have a prominent role in new strategies for extending the health old population. Accordingly, as extensively discussed in the review and in the accompanying related papers, investigating ageing pathophysiology, particularly disentangling agerelated low grade inflammation, is likely to provide important clues about how to develop drugs that can slow or delay ageing.

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Section: Cancer and Ageingmentioning

confidence: 81%

Section: Cancer and Ageingmentioning

confidence: 99%

Low Grade Inflammation as a Common Pathogenetic Denominator in Age-Related Diseases: Novel Drug Targets for Anti-Ageing Strategies and Successful Ageing Achievement

Candore

Caruso

Jirillo³

et al. 2010

CPD

127

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“…[1][2][3][4] Physical activity may have beneficial anti-inflammatory effects as evidence from epidemiological studies has consistently demonstrated an inverse association between physical activity and markers of low grade systemic inflammation. [5][6][7] The anti-inflammatory effects of exercise may partly explain the well-documented cardio-protective effects of physical activity.…”

Section: Introductionmentioning

confidence: 99%

Prospective association of TV viewing with acute phase reactants and coagulation markers: English Longitudinal Study of Ageing

2015

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“…1 Continuous exposure to inflammatory cytokines is known to cause tumorigenesis; 2 thus controlling chronic inflammation is crucial to prevent tumor progression, particularly in the elderly. 3 By contrast, tumors developed due to mutations are thought to be largely driven by intrinsic signals emerging from damage to tumor-initiating genes, formation of chimeric proteins due to translocation or loss of tumor suppressor genes. 4 Osteosarcoma is a rare malignancy but the most common bone sarcoma in children and adolescents.…”

Section: Introductionmentioning

confidence: 99%

TNFα promotes osteosarcoma progression by maintaining tumor cells in an undifferentiated state

et al. 2013

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Chronic inflammation is frequently associated with tumorigenesis in elderly people. By contrast, young people without chronic inflammation often develop tumors considered independent of chronic inflammation but driven instead by mutations. Thus, whether inflammation has a significant role in tumor progression in tumors driven by mutations remains largely unknown. Here we show that TNFa is required for the tumorigenesis of osteosarcoma, the most common tumor in children and adolescents. We show that transplantation of AX osteosarcoma cells, which harbor mutations driving c-Myc overexpression and Ink4a-deficiency, in wildtype mice promotes lethal tumorigenesis accompanied by ectopic bone formation and multiple metastases, phenotypes seen in osteosarcoma patients. Such tumorigenesis was completely abrogated in TNFa-deficient mice. AX cells have the capacity to undergo osteoblastic differentiation; however, that activity was significantly inhibited by TNFa treatment, suggesting that TNFa maintains AX cells in an undifferentiated state. TNFa inhibition of AX cell osteoblastic differentiation occurred through ERK activation, and a pharmacological TNFa inhibitor effectively inhibited both AX cell tumorigenesis and increased osteoblastic gene expression and increased survival of tumor-bearing mice. Lethal tumorigenesis of AX cells was also abrogated in IL-1a/IL-1b doubly deficient mice. We found that both TNFa and IL-1 maintained AX cells in an undifferentiated state via ERK activation. Thus, inflammatory cytokines are required to promote tumorigenesis even in mutation-induced tumors, and TNFa/IL-1 and ERK may represent therapeutic targets for osteosarcoma.

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Inflammation, ageing and cancer

Cited by 117 publications

References 79 publications

Low Grade Inflammation as a Common Pathogenetic Denominator in Age-Related Diseases: Novel Drug Targets for Anti-Ageing Strategies and Successful Ageing Achievement

Low Grade Inflammation as a Common Pathogenetic Denominator in Age-Related Diseases: Novel Drug Targets for Anti-Ageing Strategies and Successful Ageing Achievement

Prospective association of TV viewing with acute phase reactants and coagulation markers: English Longitudinal Study of Ageing

TNFα promotes osteosarcoma progression by maintaining tumor cells in an undifferentiated state

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