Altered Pattern of Lipid Metabolism in Patients with Lung Cancer

Dessì, S.; Batetta, Barbara; Pulisci, D.; Spano, O.; Cherchi, R.; Lanfranco, Giacomo; Tessitore, Luciana; Costelli, P.; Baccino, Francesco M.; Anchis, C.; Pani, P.

doi:10.1159/000227088

Cited by 60 publications

(42 citation statements)

References 11 publications

(15 reference statements)

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“…A direct relationship between breast carcinoma and cholesterol metabolism has not been confirmed yet. However, this is not the case in the carcinoma of the colon and lung and in haematological neoplasia, where decrease in its serum concentration has been confirmed by several authors (Dessi et al 1992;Rose et al 1974;Spiegel et al 1982). In our experiment, no changes in the serum lipids in the carcinogen (NMU)-influenced animals were observed.…”

Section: Discussionsupporting

confidence: 61%

Chemoprevention of N-Methyl-N-Nitrosourea Induced Mammary Carcinogenesis with Raloxifene and Melatonin: Metabolic Changes in Female Rats

M¹,

Kubatka²,

Kalicka³

et al. 2002

Acta Vet. Brno

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Chamilová M., P. Kubatka, K. Kalická, E. Adámeková, B. Bojková, I. Ahlers, E. Ahlersová: Chemoprevention of N-methyl-N-nitrosourea Induced Mammary Carcinogenesis with Raloxifene and Melatonin: Metabolic Changes in Female Rats. Acta Vet. Brno 2002, 71: 235-242.The aim of this work was to determine the selected parameters of carbohydrate and lipid metabolism in the mammary carcinogenesis induced with N-methyl-N-nitrosourea (NMU) in two doses, each by 50 mg/kg of body weight with a 7-day interval between them within the postnatal days 43 and 54 in female Sprague-Dawley rats. Chemoprevention started with the administration of melatonin (MEL, 4 µg/ml in water, from 15.00 h to 08.00 h) 12 days and raloxifene (RAL 5 mg/kg, 2 × weekly) 10 days before the application of NMU. Twenty-four weeks following the NMU administration the animals were killed, and the incidence, latency, frequency and volume of tumours were evaluated. The animals were divided into: tumour-bearing (TB) and non-tumourbearing (NTB) with the influence of RAL, MEL and their combination. While RAL and RAL plus MEL significantly decreased the incidence and frequency of tumours, the effect of isolated MEL was substantially lower. In the serum, an increase in the concentration of serum glucose in TB and also NTB animals was observed. In the liver of both the TB and NTB animals, the content of cholesterol (CH) and triacylglycerols (TG) decreased and the contents of phospholipids (PL) increased. RAL decreased the contents of CH and PL in the liver of NTB animals and increased the concentration of TG in both groups of animals. Administration of RAL to NTB animals decreased the concentrations of malondialdehyde (MDA) in the serum and thymus, in the bone marrow also in TB animals. MEL decreased the concentration of MDA in the bone marrow of TB animals. MEL increased the concentrations of serum glucose and glycogen content in the heart muscle of NTB animals. RAL plus MEL decreased the concentration of serum TG and PL and decreased the contents of CH and PL in the liver of TB as well as NTB animals. In the thymus and liver, combination of RAL+MEL decreased the MDA content compared with the RAL alone in NTB animals.The co-effect of two or more substances will be probably the optimal way in prevention of cancer. The co-effect of RAL and MEL shows to be a prospective way for influencing the mammary tumors. Breast cancer, female rats, raloxifene, melatonin, chemopreventionThe hormonal therapy of the breast carcinoma is an inseparable part of the variety of therapeutic procedures. The substitution with estrogens has been considered for a long time as a dominant indication of therapy in postmenopausal women, and it has been recognized that approximately one third of women will have a benefit of this procedure. The use of estrogens protects these women against osteoporosis and decreases the cardiovascular risk, but on the other hand, increases the risk of breast and endometrium carcinoma (Col et al. 1997). With regard to the unfavourable effects of estrogens on ...

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Section: Discussionsupporting

confidence: 61%

Chemoprevention of N-Methyl-N-Nitrosourea Induced Mammary Carcinogenesis with Raloxifene and Melatonin: Metabolic Changes in Female Rats

M¹,

Kubatka²,

Kalicka³

et al. 2002

Acta Vet. Brno

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“…Case-control studies of newly diagnosed lung cancer have shown that HDL-cholesterol levels are reduced in lung cancer cases relative to levels observed in the control groups [7][8][9][10]. This association was found to be independent of type and stage of lung cancer [7], but not all adjusted for smoking or other confounders.…”

Section: Introductionmentioning

confidence: 92%

HDL-cholesterol and the incidence of lung cancer in the Atherosclerosis Risk in Communities (ARIC) study

et al. 2008

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This study examined prospectively the association of baseline plasma HDL-cholesterol levels with incidence of lung cancer in 14,547 members of the Atherosclerosis Risk in Communities (ARIC) cohort. There were 259 cases of incident lung cancer identified during follow-up from 1987 through 2000. Results of this study indicated a relatively weak inverse association of HDL-cholesterol with lung cancer that was dependent on smoking status. The hazard ratio of lung cancer incidence in relation to low HDL-cholesterol, adjusted for race, gender, exercise, alcohol consumption, body mass index, triglycerides, age, and cigarette pack-years of smoking, was 1.45 (95% confidence interval 1.10, 1.92). This association was observed among former smokers (hazard ratio: 1.77, 95% confidence interval 1.05, 2.97), but not current smokers. The number of cases among never smokers in this study was too small (n=13) for meaningful interpretation of effect estimates. Excluding cases occurring within 5 years of baseline did not appreciably change the point estimates, suggesting lack of reverse causality. The modest association of low plasma HDL-cholesterol with greater incident lung cancer observed in this study is in agreement with existing case-control studies.

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“…[41][42][43][44][45] Crucially, when examined, many such defects correlate with the degree of inflammatory activity in these disease processes. These observations support the notion that common mechanisms link immune dysregulation and metabolic dysfunction across a range of diseases that share common cellular and molecular effector pathways.…”

Section: Evidence Of Similar Metabolic Perturbances In Other Chronic mentioning

confidence: 99%

Explaining How “High-Grade” Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis

et al. 2003

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Abstract-There is intense interest in mechanisms whereby low-grade inflammation could interact with conventional and novel vascular risk factors to promote the atheromatous lesion. Patients with rheumatoid arthritis (RA), who by definition manifest persistent high levels of inflammation, are at greater risk of developing cardiovascular disease. Mechanisms mediating this enhanced risk are ill defined. On the basis of available evidence, we argue here that the systemic inflammatory response in RA is critical to accelerated atherogenesis operating via accentuation of established and novel risk factor pathways. By implication, long-term suppression of the systemic inflammatory response in RA should be effective in reducing risk of coronary heart disease. Key Words: immune system Ⅲ risk factors Ⅲ atherosclerosis C onsiderable evidence indicates that patients with rheumatoid arthritis (RA) are at greater risk of developing coronary heart disease (CHD). 1 Seventeen of 21 relevant observational studies show an increased standardized morality ratio in RA and that life expectancy is shortened by 3 to 18 years. Pooled analysis of these studies suggests a 70% increase in risk of death in RA patients. Life expectancy is especially shortened in RA patients treated in specialist referral centers, where the prognosis is comparable to that of triple-vessel CHD or stage 4 Hodgkin's disease. 1 Cardiovascular disease accounts for 35% to 50% of excess mortality in RA patients, with cerebrovascular disease being the second leading cause of death. Intriguingly, most evidence suggests that classic risk factors do not explain excess vascular disease in RA. In an 8-year follow-up of 236 RA patients, a 3.96-fold (95% CI 1.86 to 8.43) higher incidence of cardiovascular events relative to a community-dwelling cohort was noted. 2 However, this risk ratio was only minimally attenuated (to 3.17 [95% CI 1.33 to 6.36]) by adjustment for conventional risk factors. These clinical epidemiological observations strongly suggest that mechanisms other than classic risk factors promote accelerated atherogenesis in RA, and responsible candidate pathways are explored in this review. Inflammation as a Candidate Pathway for CHDIt is firmly established that systemic markers of inflammation, albeit at considerably lower levels than those apparent in RA, independently predict CHD events in men and women with or without existing heart disease. 3,4 The levels of cytokines and other inflammatory mediators detected in CHD are such that high-sensitivity assays rather than conventional assays are required. This concept of inflammatory-driven atherogenesis is consistent with the plaque composition of unstable coronary lesions, with an abundance of inflammatory molecules and immune cells at the shoulder region that act to erode the collagen cap that separates the atheromatous material of the plaque from blood. 4 This appearance is similar to that of inflammatory synovitis in RA. 5 However, whereas in RA, C-reactive protein (CRP) is a powerful measure of synovial infla...

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Altered Pattern of Lipid Metabolism in Patients with Lung Cancer

Cited by 60 publications

References 11 publications

Chemoprevention of N-Methyl-N-Nitrosourea Induced Mammary Carcinogenesis with Raloxifene and Melatonin: Metabolic Changes in Female Rats

Chemoprevention of N-Methyl-N-Nitrosourea Induced Mammary Carcinogenesis with Raloxifene and Melatonin: Metabolic Changes in Female Rats

HDL-cholesterol and the incidence of lung cancer in the Atherosclerosis Risk in Communities (ARIC) study

Explaining How “High-Grade” Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis

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