57 research outputs found
La thérapie génique (perpectives, applications et essais cliniques en cancérologie)
No full textLILLE2-BU Santé-Recherche (593502101) / SudocSudocFranceF
Effects of Intentional Weight Loss on Markers of Oxidative Stress, DNA Repair and Telomere Length - a Systematic Review
No full textBackground: Altered levels of markers of oxidative stress, DNA repair, and telomere integrity have been detected in obese individuals and may underlie the pathogenesis of obesity-related diseases. However, whether or not such effects are reversed by intentional weight loss has not been systematically reviewed. Methods: A literature search in PubMed/Medline identified 2,388 articles of which 21 studies (randomized controlled trial (RCT) (n = 10) and non-randomized intervention studies (n = 11)) were classified as testing the effects of intentional weight loss on i) oxidative stress (n = 15), ii) DNA repair (n = 2), and iii) telomere length (n = 4). Results: Across a broad range of intervention designs, diet-, exercise-, surgery-, balloon-induced weight loss regimens decreased oxidative stress measures. Studies investigating DNA repair capacity or telomere length as endpoints after weight loss were less common in number and yielded null or inconsistent results, respectively. Conclusion: While this systematic review supports a role for intentional weight loss in reducing obesity-associated oxidative stress, it is not clear whether the effects are primary outcomes or secondary to improvement in obesity-associated insulin resistance and/or chronic inflammation. Although the lack of effect of intentional weight loss on DNA repair capacity might be anticipated given that oxidative stress is reduced, additional studies are needed. The inconsistent effects of weight loss on telomere length or DNA repair suggest the need for a re-assessment of intervention designs and assay methodology to definitively address this topic
Effects of Intentional Weight Loss on Markers of Oxidative Stress, DNA Repair and Telomere Length - a Systematic Review
No full text<b><i>Background:</i></b> Altered levels of markers of oxidative stress, DNA repair, and telomere integrity have been detected in obese individuals and may underlie the pathogenesis of obesity-related diseases. However, whether or not such effects are reversed by intentional weight loss has not been systematically reviewed. <b><i>Methods:</i></b> A literature search in PubMed/Medline identified 2,388 articles of which 21 studies (randomized controlled trial (RCT) (n = 10) and non-randomized intervention studies (n = 11)) were classified as testing the effects of intentional weight loss on i) oxidative stress (n = 15), ii) DNA repair (n = 2), and iii) telomere length (n = 4). <b><i>Results:</i></b> Across a broad range of intervention designs, diet-, exercise-, surgery-, balloon-induced weight loss regimens decreased oxidative stress measures. Studies investigating DNA repair capacity or telomere length as endpoints after weight loss were less common in number and yielded null or inconsistent results, respectively. <b><i>Conclusion:</i></b> While this systematic review supports a role for intentional weight loss in reducing obesity-associated oxidative stress, it is not clear whether the effects are primary outcomes or secondary to improvement in obesity-associated insulin resistance and/or chronic inflammation. Although the lack of effect of intentional weight loss on DNA repair capacity might be anticipated given that oxidative stress is reduced, additional studies are needed. The inconsistent effects of weight loss on telomere length or DNA repair suggest the need for a re-assessment of intervention designs and assay methodology to definitively address this topic.</jats:p
Energy balance and gastrointestinal cancer: risk, interventions, outcomes and mechanisms
No full textSignals from the Adipose Microenvironment and the Obesity–Cancer Link—A Systematic Review
No full textAbstract
Obesity and its associated metabolic dysregulation are established risk factors for many cancers. However, the biologic mechanisms underlying this relationship remain incompletely understood. Given the rising rates of both obesity and cancer worldwide, and the challenges for many people to lose excess adipose tissue, a systematic approach to identify potential molecular and metabolic targets is needed to develop effective mechanism-based strategies for the prevention and control of obesity-driven cancer. Epidemiologic, clinical, and preclinical data suggest that within the growth-promoting, proinflammatory microenvironment accompanying obesity, crosstalk between adipose tissue (comprised of adipocytes, macrophages and other cells) and cancer-prone cells may occur via obesity-associated hormones, cytokines, and other mediators that have been linked to increased cancer risk and/or progression. We report here a systematic review on the direct “crosstalk” between adipose tissue and carcinomas in humans. We identified 4,641 articles with n = 20 human clinical studies, which are summarized as: (i) breast (n = 7); (ii) colorectal (n = 4); (iii) esophageal (n = 2); (iv) esophageal/colorectal (n = 1); (v) endometrial (n = 1); (vi) prostate (n = 4); and (vii) ear-nose-throat (ENT) cancer (n = 1). Findings from these clinical studies reinforce preclinical data and suggest organ-dependent crosstalk between adipose tissue and carcinomas via VEGF, IL6, TNFα, and other mechanisms. Moreover, visceral white adipose tissue plays a more central role, as it is more bioenergetically active and is associated with a more procancer secretome than subcutaneous adipose tissue. Efforts to eavesdrop and ultimately interfere with this cancer-enhancing crosstalk may lead to new targets and strategies for decreasing the burden of obesity-related cancers. Cancer Prev Res; 10(9); 494–506. ©2017 AACR.</jats:p
Associations of combined physical activity and body mass index groups with colorectal cancer survival outcomes
No full textBACKGROUND: Physical activity and BMI have been individually associated with cancer survivorship but have not yet been studied in combinations in colorectal cancer patients. Here, we investigate individual and combined associations of physical activity and BMI groups with colorectal cancer survival outcomes.
METHODS: Self-reported physical activity levels (MET hrs/wk) were assessed using an adapted version of the International Physical Activity Questionnaire (IPAQ) at baseline in 931 patients with stage I-III colorectal cancer and classified into \u27highly active\u27 and\u27not-highly active\u27(≥ / \u3c 18 MET hrs/wk). BMI (kg/m
RESULTS: \u27Not-highly active\u27 compared to \u27highly active\u27 and \u27overweight\u27/ \u27obese\u27 compared to \u27normal weight\u27 patients had a 40-50% increased risk of death or recurrence (HR: 1.41 (95% CI: 0.99-2.06), p = 0.03; HR: 1.49 (95% CI: 1.02-2.21) and HR: 1.51 (95% CI: 1.02-2.26), p = 0.04, respectively). \u27Not-highly active\u27 patients had worse disease-free survival outcomes, regardless of their BMI, compared to \u27highly active/normal weight\u27 patients. \u27Not-highly active/obese\u27 patients had a 3.66 times increased risk of death or recurrence compared to \u27highly active/normal weight\u27 patients (HR: 4.66 (95% CI: 1.75-9.10), p = 0.002). Lower activity thresholds yielded smaller effect sizes.
CONCLUSION: Physical activity and BMI were individually associated with disease-free survival among colorectal cancer patients. Physical activity seems to improve survival outcomes in patients regardless of their BMI
Clinical characteristics and outcomes of colorectal cancer in the ColoCare Study: Differences by age of onset
No full textEarly-onset colorectal cancer has been on the rise in Western populations. Here, we compare patient characteristics between those with early- (\u3c50 years) vs. late-onset (≥50 years) disease in a large multinational cohort of colorectal cancer patients
0555: Arrhythmic risk stratification and prognostic value of programmed ventricular stimulation in arrhythmogenic right ventricular cardiomyopathy/dysplasia
No full textBackgroundThe role of programmed ventricular stimulation (PVS) in arrhythmic risk stratification is unclear in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D).ObjectiveTo determine clinical factors associated with inducibility of PVS and determine its pronostic value in the overall population and in three risk groups.MethodsBetween 2000 and 2010, 150 consecutive patients systematically benefited PVS at diagnosis. Predictors for PVS inducibility were studied. Risk factors for arrhythmic events were then determined by Cox regression in the entire population and in three risk groups.ResultsVT inducibility was significantly higher for males (p=0.007), symptomatic patients (p<0.001) especially those with syncope (p=0.004), patients who had spontaneous ventricular tachycardia (VT) (p<0.001) and right (p<0.001) or left (p=0.03) ventricular dysfunction.Abstract 0555 - Figure 1. Decision treeAfter a follow up of 48±32 months, we recorded 31 ventricular arrhythmias and 10 sudden cardiac deaths (SCD). Male gender, symptoms, syncope, sustained VT, right or left ventricular dysfunction and positive PVS were associated with ventricular arrhythmias. PVS had a 50% of sensibility on predicting SCD. The presence of a history of an aborted SCD, syncope or non tolerated VT identified high-risk subjects whereas asymptomatic patients represented a low risk group whatever PVS results were. Inducibility at PVS was associated with a higher rate of events in the intermediate risk group. A decision tree based on our analyses is shown on figure 1 above.ConclusionPVS inducibility is associated with the occurrence of sustained ventricular arrythmia but not with the occurrence of SCD. History of aborted SCD, syncope or non tolerated VT isolate a high risk group of patients whereas asymptomatic patients are at low risk. PVS seems to be interesting in the intermediate risk group for predicting ventricular arrhythmias
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