Using body temperature, food and water consumption as biomarkers of disease progression in mice with Eμ-myc lymphoma.
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ABSTRACT:
SUBMITTER: Hunter JE
PROVIDER: S-EPMC3929895 | biostudies-other | 2014 Feb
REPOSITORIES: biostudies-other
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Project description:Mice housed in an enriched environment (EE) have inhibited tumor development because of eustress (positive stress) stimulation. However, the mechanisms underlying increased cancer resistance in EEs remain unclear; this may be due to poor reproducibility of the results because of the complicated EE assembly requirements. In this study, we examined the effects of a simplified EE (sEE) model, consisting only of a nesting shelter and a running wheel, on cancer development in mice. We found that, similar to the complex EE, the sEE promoted motor function and alleviated anxiety in mice. Moreover, the mice housed in the sEE showed inhibited tumor growth and metastasis in addition to a higher average body temperature (especially at the point of transition from light to darkness). Furthermore, mice in the sEE had a decreased brown adipose tissue (BAT) mass, with a significant upregulation of the Ucp1 and Adrb3 genes (which encode uncoupling protein 1 and ?-adrenergic receptor, respectively) observed in the BAT at the point of transition from light to darkness. An antibody against the immune checkpoint protein programmed cell death 1 was also found to have an additive effect with the sEE against tumor development. Our findings indicate that the established sEE model may be a useful tool for studying the antitumor effects of eustress and can potentially introduce new avenues for cancer prevention and treatment.
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Project description:The tumor microenvironment is a dynamic and interactive supporting network of various components, including blood vessels, cytokines, chemokines, and immune cells, which sustain the tumor cell's survival and growth. Murine models of lymphoma are useful to study tumor biology, the microenvironment, and mechanisms of response to therapy. Lymphomas are heterogeneous hematologic malignancies, and the complex microenvironment from which they arise and their multifaceted genetic basis represents a challenge for the generation and use of an appropriate murine model. So, it is important to choose the correct methodology. Recently, we supported the first evidence on the pro-oncogenic action of IBTK in Myc-driven B cell lymphomagenesis in mice, inhibiting apoptosis in the pre-cancerous stage. We used the transgenic E?-myc mouse model of non-Hodgkin's lymphoma and Ibtk hemizygous mice to evaluate the tumor development of Myc-driven lymphoma. Here, we report that the allelic loss of Ibtk alters the immunophenotype of Myc-driven B cell lymphomas, increasing the rate of pre-B cells and affecting the tumor microenvironment in E?-myc mice. In particular, we observed enhanced tumor angiogenesis, increasing pro-angiogenic and lymphangiogenic factors, such as VEGF, MMP-9, CCL2, and VEGFD, and a significant recruitment of tumor-associated macrophages in lymphomas of Ibtk+/- E?-myc compared to Ibtk+/+ E?-myc mice. In summary, these results indicate that IBTK haploinsufficiency promotes Myc tumor development by modifying the tumor microenvironment.
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Project description:PARP1 has been shown to regulate EBV latency. However, the therapeutic effect of PARP1 inhibitors on EBV+ lymphomagenesis has not yet been explored. Here, we show that PARPi BMN-673 has a potent anti-tumor effect on EBV-driven LCL in a mouse xenograft model. We found that PARP1 inhibition induces a dramatic transcriptional reprogramming of LCLs driven largely by the reduction of the MYC oncogene expression and dysregulation of MYC targets, both in vivo and in vitro. PARP1 inhibition also reduced the expression of viral oncoprotein EBNA2, which we previously demonstrated depends on PARP1 for activation of MYC. Further, we show that PARP1 inhibition blocks the chromatin association of MYC, EBNA2, and tumor suppressor p53. Overall, our study strengthens the central role of PARP1 in EBV malignant transformation and identifies the EBNA2/MYC pathway as a target of PARP1 inhibitors and its utility for the treatment of EBNA2-driven EBV-associated cancers.
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Project description:The idea that increasing salt intake increases drinking and urine volume is widely accepted. We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men living under ultra-long-term controlled conditions.Over the course of 2 separate space flight simulation studies of 105 and 205 days' duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d). All other nutrients were maintained constant. We studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte and water balance.A 6-g/d increase in salt intake increased urine osmolyte excretion, but reduced free-water clearance, indicating endogenous free water accrual by urine concentration. The resulting endogenous water surplus reduced fluid intake at the 12-g/d salt intake level. Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorption via the renal concentration mechanism. Mineralocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osmolyte and water surplus by relative urine dilution. A 6-g/d increase in salt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucocorticoid release. The projected effect of salt-driven hormone rhythm modulation corresponded well with the measured decrease in water intake and an increase in urine volume with surplus osmolyte excretion.Humans regulate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus body water, and precise surplus excretion.Federal Ministry for Economics and Technology/DLR; the Interdisciplinary Centre for Clinical Research; the NIH; the American Heart Association (AHA); the Renal Research Institute; and the TOYOBO Biotechnology Foundation. Food products were donated by APETITO, Coppenrath und Wiese, ENERVIT, HIPP, Katadyn, Kellogg, Molda, and Unilever.
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Project description:IntroductionControversies surround the issue if chronic consumption of a high-sugar diet is detrimental to health or not. This study investigates whether lifelong consumption of a higher sucrose diet will induce overeating, and obesity, and cause metabolic dysfunctions such as hyperglycemia and dyslipidaemia in C57BL/6N mice, compared to a lower sucrose diet.MethodsMale C57BL/6N mice at 3 weeks of age were randomized into consuming a diet with 25 or 10% kcal from sucrose for the rest of their lives. Body weight, food and water intake, fasting blood glucose, insulin, and lipid levels were measured at regular intervals. At the end of the study, organs and tissues were collected and gene expression was measured.ResultsThere was no discernible difference in the impact on food intake, body composition, glucose and lipid homeostasis, liver triglyceride content, life expectancy, as well as gene expression related to intermediary metabolism between mice fed a diet with 10 vs. 25% kcal as sucrose over their lifespan. We also showed that switching from a 25% kcal diet to a 10% kcal diet at different life stages, or vice versa, did not appear to affect these outcomes of interest.DiscussionThe results from our study suggest that lifelong consumption of a higher sugar diet generally did not induce overeating and obesity, disrupt carbohydrate metabolism and lipid homeostasis, and reduce life expectancy compared with a lower sugar diet. Our unorthodox findings disagreed with the popular belief that higher sugar consumption is detrimental to health, which should be confirmed in future studies.
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Project description:ObjectiveThe association between organic food consumption and biomarkers of inflammation, C-reactive protein (CRP) and cystatin C (CysC) was explored in this cross-sectional analysis of older adults.DesignDietary data and organic food consumption was collected in 2013 from a FFQ. Alternative Mediterranean diet score (A-MedDiet) was calculated as a measure of healthy eating. Biomarkers CRP and CysC were collected in serum or plasma in 2016. We used linear regression models to assess the associations between organic food consumption and CRP and CysC.SettingThis cross-sectional analysis uses data from the nationally representative, longitudinal panel study of Americans over 50, the Health and Retirement Study.ParticipantsThe mean age of the analytic sample (n 3815) was 64·3 (se 0·3) years with 54·4 % being female.ResultsLog CRP and log CysC were inversely associated with consuming organic food after adjusting for potential confounders (CRP: β = -0·096, 95 % CI 0·159, -0·033; CysC: β = -0·033, 95 % CI -0·051, -0·015). Log CRP maintained statistical significance (β = -0·080; 95 % CI -0·144, -0·016) after additional adjustments for the A-MedDiet, while log CysC lost statistical significance (β = -0·019; 95 % CI -0·039, 0·000). The association between organic food consumption and log CRP was driven primarily by milk, fruit, vegetables and cereals, while log CysC was primarily driven by milk, eggs and meat after adjustments for A-MedDiet.ConclusionsThese findings support the hypothesis that organic food consumption is inversely associated with biomarkers of inflammation CRP and CysC, although residual confounding by healthy eating and socioeconomic status cannot be ruled out.
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