Role of telomere length in human carcinogenesis (Review)

Tsatsakis, Aristidis; Oikonomopoulou, T.; Νikolouzakis, Τaxiarchis Κonstantinos; Vakonaki, Elena; Tzatzarakis, Manolis; Flamourakis, Matthaios; Renieri, Elisavet; Fragkiadaki, Persefoni; Iliaki, E.; Bachlitzanaki, Maria; Karzi, Vasiliki; Katsikantami, Ioanna; Kakridonis, Fotios; Hatzidaki, Eleftheria; Tolia, Maria; Svistunov, Andrey; Spandidos, Demetrios A.; Nikitovic, Dragana; Tsiaoussis, John; Berdiaki, Aikaterini

doi:10.3892/ijo.2023.5526

Cited by 26 publications

(18 citation statements)

References 261 publications

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“…Li & Ma, 2022), gastric cancer (Z. Wang et al, 2018), and lung cancer (Doherty et al, 2018; Tsatsakis et al, 2023). A longer telomere could result in prolonged cell survival, subsequently elevating the probability of accumulating mutations associated with cancer (Aviv et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Is exposure to pesticides associated with biological aging? A systematic review and meta-analysis

Zuo,

Sasitharan,

Di Tanna

et al. 2024

Preprint

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Objective: Exposure to pesticides is a risk factor for various diseases, yet its association with biological aging remains unclear. We aimed to systematically investigate the relationship between pesticide exposure and biological aging. Methods: PubMed, Embase and Web of Science were searched from inception to August 2023. Observational studies investigating the association between pesticide exposure and biomarkers of biological aging were included. Three-level random-effect meta-analysis was used to synthesize the data. Risk of bias was assessed by the Newcastle-Ottawa Scale. Results: Twenty studies evaluating the associations between pesticide exposure and biomarkers of biological aging in 10,368 individuals were included. Sixteen reported telomere length and four reported epigenetic clocks. Meta-analysis showed no statistically significant associations between pesticide exposure and the Hannum clock (pooled β = 0.27; 95%CI: -0.25, 0.79), or telomere length (pooled Hedges'g = -0.46; 95%CI: -1.10, 0.19). However, the opposite direction of effect for the two outcomes showed an indication of possible accelerated biological aging. After removal of influential effect sizes or low-quality studies, shorter telomere length was found in higher-exposed populations. Conclusion: The existing evidence for associations between pesticide exposure and biological aging is limited due to the scarcity of studies on epigenetic clocks and the substantial heterogeneity across studies examining telomere length. High-quality studies incorporating more biomarkers of biological aging, focusing more on active chemical ingredients of pesticides and accounting for potential confounders are needed to enhance our understanding of the impact of pesticides on biological aging.

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Section: Discussionmentioning

confidence: 99%

Is exposure to pesticides associated with biological aging? A systematic review and meta-analysis

Zuo,

Sasitharan,

Di Tanna

et al. 2024

Preprint

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“…Telomere length plays a critical role in maintaining genomic stability and preventing cellular senescence or apoptosis [ 30 , 31 ]. Shortened telomeres are commonly observed in various cancer types and are generally associated with genomic instability and tumor progression [ 32 – 34 ]. Our findings add to the existing body of evidence by highlighting the importance of telomere length in hematopoietic malignancies.…”

Section: Discussionmentioning

confidence: 99%

Genetically determined telomere length as a risk factor for hematological malignancies: evidence from Mendelian randomization analysis

Fang,

Zhang,

Ren

et al. 2024

Aging

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Background: Over the past years, the exact correlation between telomere length and hematological malignancies was still not fully understood. Methods: We performed a two-sample Mendelian randomization study to investigate the causal relationship between telomere length and hematological malignancies. We selected genetic instruments associated with telomere length. The genetic associations for lymphoid and hematopoietic malignant neoplasms were obtained from the most recent publicly accessible FinnGen study R9 data. Inverse variant weighted (IVW) analysis was adopted as the primary method, and we also performed the weighted-median method and the MR-Egger, and MRPRESSO methods as sensitive analysis. Results: Significant associations have been observed between telomere length and primary lymphoid (IVW: OR = 1.52, P = 2.11 × 10 −6 ), Hodgkin lymphoma (IVW: OR = 1.64, P = 0.014), non-Hodgkin lymphoma (IVW: OR = 1.70, P = 0.002), B-cell lymphoma (IVW: OR = 1.57, P = 0.015), non-follicular lymphoma (IVW: OR = 1.58, P = 1.7 × 10 −3 ), mantle cell lymphoma (IVW: OR = 3.13, P = 0.003), lymphoid leukemia (IVW: OR = 2.56, P = 5.92E-09), acute lymphocytic leukemia (IVW: OR = 2.65, P = 0.021) and chronic lymphocytic leukemia (IVW: OR = 2.80, P = 8.21 × 10 −6 ), along with multiple myeloma (IVW: OR = 1.85, P = 0.016). Conclusion: This MR study found a significant association between telomere length and a wide range of hematopoietic malignancies. But no substantial impact of lymphoma and hematopoietic malignancies on telomere length has been detected.

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“…Multiple pathways are involved in the development of cancer, including the upregulation of pro-oncogenes and the suppression of onco-suppressor genes, as reviewed extensively elsewhere ( 66 - 73 ). In oncogenesis, the shift from a cell's original state to a malignant state is a process that requires the cell to surmount its anti-oncogenic milestones ( 74 , 75 ). Cancer is caused by various genetic and epigenetic alterations in (stem) cells, primarily involving mutations, deletions, inversions, amplifications and chromosome translocations resulting, among others, in an altered oncogene activity ( 66 , 76 - 78 ).…”

Section: Cancer Hallmarks and The Determination Of The Phases Of Onco...mentioning

confidence: 99%

Role of stress in the pathogenesis of cancer (Review)

Lempesis,

Georgakopoulou,

Papalexis

et al. 2023

Int J Oncol

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Stress is a state of disrupted homeostasis, triggered by intrinsic or extrinsic factors, the stressors, which are counteracted by various physiological and behavioural adaptive responses. Stress has been linked to cancer development and incidence for decades; however, epidemiological studies and clinical trials have yielded contradictory results. The present review discusses the effects of stress on cancer development and the various underlying mechanisms. Animal studies have revealed a clear link between stress and cancer progression, revealing molecular, cellular and endocrine processes that are implicated in these effects. Thus, stress hormones, their receptor systems and their intracellular molecular pathways mediate the effects of stress on cancer initiation, progression and the development of metastases. The mechanisms linking stress and cancer progression can either be indirect, mediated by changes in the cancer microenvironment or immune system dysregulation, or direct, through the binding of neuroendocrine stress-related signalling molecules to cancer cell receptors. Stress affects numerous anti- and pro-cancer immune system components, including host resistance to metastasis, tumour retention and/or immune suppression. Chronic psychological stress through the elevation of catecholamine levels may increase cancer cell death resistance. On the whole, stress is linked to cancer development and incidence, with psychological stressors playing a crucial role. Animal studies have revealed a better link than human ones, with stress-related hormones influencing tumour development, migration, invasion and cell proliferation. Randomized controlled trials are required to further evaluate the long-term cancer outcomes of stress and its management.

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Role of telomere length in human carcinogenesis (Review)

Cited by 26 publications

References 261 publications

Is exposure to pesticides associated with biological aging? A systematic review and meta-analysis

Is exposure to pesticides associated with biological aging? A systematic review and meta-analysis

Genetically determined telomere length as a risk factor for hematological malignancies: evidence from Mendelian randomization analysis

Role of stress in the pathogenesis of cancer (Review)

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