Telomere biology and translational research

Mason, Philip J.; Perdigones, Nieves

doi:10.1016/j.trsl.2013.08.009

Cited by 38 publications

(41 citation statements)

References 83 publications

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“…Telomeres are particularly sensitive to ROS because they are rich in guanine residues, and guanine can be oxidized to 8 hydroxyguanine, which is unstable (Mason and Perdigones 2013). Both pentavalent and trivalent antimonial compounds induce the generation of ROS in human and murine cell line (Mann et al 2006; Mookerjee Basu et al 2006; Rais et al 2000; Wyllie and Fairlamb 2006).…”

Section: Discussionmentioning

confidence: 99%

Urinary antimony and leukocyte telomere length: An analysis of NHANES 1999–2002

Scinicariello

Buser

2016

Environmental Research

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Telomeres are repetitive DNA sequences (TTAGGG) at the end of chromosomes. Cells with critically short telomeres enter replicative senescence and apoptosis. Several in vitro studies report that antimony causes cell apoptosis in human leukocyte cell lines. The goal of this analysis was to investigate whether there is an association between antimony exposure and leukocyte telomere length (LTL) among US adults aged 20 and older based on the National Health and Nutrition Examination Survey (NHANES) 1999–2002. We used multivariate linear regression to analyze the association of urinary antimony with LTL. LTL was log-natural transformed and the results were re-transformed and presented as percent differences. After adjustment for potential confounders, individuals in the 3rd and 4th quartiles of urinary antimony had statistically significantly shorter LTL (−4.78%, 95% CI: −8.42, −0.90; and −6.11%, 95% CI: −11.04, −1.00, respectively) compared to the lowest referent quartile, with evidence of a dose-response relationship (p-value for trend = 0.03). Shorter LTL with antimony was driven by middle aged (40–59 years) and older (60–85 years) adult groups. The association may be biologically plausible because of reported oxidative stress and apoptosis effects of antimony on blood cells, effects known to shorten telomere length.

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Section: Discussionmentioning

confidence: 99%

Urinary antimony and leukocyte telomere length: An analysis of NHANES 1999–2002

Scinicariello

Buser

2016

Environmental Research

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“…Most melanocytic nevi carry BRAF mutations, whereas TERT promoter mutations and CDKN2A alterations are detected in later stages 9,41 . The loss of CDKN2A has been suggested to be a key step in escape of melanocytes from BRAF-induced senescence; the acquisition of the TERT promoter mutations and consequent increased telomerase activity can be hypothesized to facilitate stabilization of the transformed genome following telomeric crisis through reversal of telomeric loss as a consequence of increase telomerase activity 42,43 . Thus, alterations in BRAF or NRAS, CDKN2A and TERT promoter can be presumed to represent unique driver mutations en route to melanoma development.…”

Section: Tert Promoter Mutationsmentioning

confidence: 99%

Telomerase reverse transcriptase promoter mutations in primary cutaneous melanoma

Nagore²,

et al. 2014

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We previously reported a disease segregating causal germline mutation in a melanoma family and recurrent somatic mutations in metastasized tumours from unrelated patients in the core promoter region of the telomerase reverse transcriptase (TERT) gene. Here we show that the TERT promoter mutations, besides causing an increased gene expression, associate with increased patient age, increased Breslow thickness and tumour ulceration in 287 primary melanomas. The mutations are more frequent at both intermittently and chronically sun-exposed sites than non-exposed sites and tend to co-occur with BRAF and CDKN2A alterations. The association with parameters generally connected with poor outcome, coupled with high recurrence and mechanistic relevance, raises the possibility of the eventual use of TERT promoter mutations in the disease management.

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“…DNA sequences are lost with each replication cycle, and telomeres serve as a buffer that protects the chromosome from losing critical DNA (34, 35). Telomeres shorten with each cell division, and on average older individuals have shorter telomeres than younger individuals (36).…”

Section: Introductionmentioning

confidence: 99%

“…Telomeres shorten with each cell division, and on average older individuals have shorter telomeres than younger individuals (36). Telomere shortening beyond a critical threshold initiates the DNA damage response pathway and induces replicative senescence or apoptosis (9, 34, 37). …”

Section: Introductionmentioning

confidence: 99%

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Alterations of Mitochondrial DNA Copy Number and Telomere Length With Early Adversity and Psychopathology

Tyrka

Parade

Price

et al. 2016

Biological Psychiatry

227

177

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Background Telomere shortening and alterations of mitochondrial biogenesis are involved in cellular aging. Childhood adversity is associated with telomere shortening, and several investigations have shown short telomeres in psychiatric disorders. Recent studies have examined whether mitochondria might be involved in neuropsychiatric conditions; findings are limited and no prior work has examined this in relation to stress exposure. Methods Two-hundred and ninety healthy adults provided information on childhood parental loss and maltreatment and completed diagnostic interviews. Participants were categorized into four groups based upon the presence or absence of childhood adversity and the presence or absence of lifetime psychopathology (depressive, anxiety, and substance use disorders). Telomere length and mtDNA copy number were measured from leukocyte DNA by qPCR. Results Childhood adversity and lifetime psychopathology were each associated with shorter telomeres (p < .01) and higher mtDNA copy numbers (p < .001). Significantly higher mtDNA copy numbers and shorter telomeres were seen in individuals with major depression, depressive disorders, and anxiety disorders, as well as those with parental loss and childhood maltreatment. A history of substance disorders was also associated with significantly higher mtDNA copy numbers. Conclusion This study provides the first evidence of an alteration of mitochondrial biogenesis with early life stress and with anxiety and substance use disorders. We replicate prior work on telomere length and psychopathology, and show that this effect is not secondary to medication use or comorbid medical illness. Finally, we show that early life stress and psychopathology are each associated with these markers of cellular aging.

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Telomere biology and translational research

Cited by 38 publications

References 83 publications

Urinary antimony and leukocyte telomere length: An analysis of NHANES 1999–2002

Urinary antimony and leukocyte telomere length: An analysis of NHANES 1999–2002

Telomerase reverse transcriptase promoter mutations in primary cutaneous melanoma

Alterations of Mitochondrial DNA Copy Number and Telomere Length With Early Adversity and Psychopathology

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