Breast cancer is a major cause of death globally, and particularly in developed countries. Breast cancer is influenced by cholesterol membrane content, by affecting the signaling pathways modulating cell growth, adherence, and migration. Furthermore, steroid hormones are derived from cholesterol and these play a key role in the pathogenesis of breast cancer. Although most findings have reported an inverse association between serum high‐density lipoprotein (HDL)‐cholesterol level and the risk of breast cancer, there have been some reports of the opposite, and the association therefore remains unclear. HDL is principally known for participating in reverse cholesterol transport and has an inverse relationship with the cardiovascular risk. HDL is heterogeneous, with particles varying in composition, size, and structure, which can be altered under different circumstances, such as inflammation, aging, and certain diseases. It has also been proposed that HDL functionality might have a bearing on the breast cancer. Owing to the potential role of cholesterol in cancer, its reduction using statins, and particularly as an adjuvant during chemotherapy may be useful in the anticancer treatment, and may also be related to the decline in cancer mortality. Reconstituted HDLs have the ability to release chemotherapeutic drugs inside the cell. As a consequence, this may be a novel way to improve therapeutic targeting for the breast cancer on the basis of detrimental impacts of oxidized HDL on cancer development.

High‐density lipoprotein (HDL) function rather than level may better predict cardiovascular disease (CVD). However, the contribution of the impaired antioxidant function of HDL that is associated with increased HDL lipid peroxidation (HDLox) to the development of clinical CVD remains unclear. We have investigated the association between serum HDLox with incident CVD outcomes in Mashhad cohort. Three‐hundred and thirty individuals who had a median follow‐up period of 7 years were recruited as part of the cohort. The primary end point was cardiovascular event, including myocardial infarction, stable angina, unstable angina, or coronary revascularization. In both univariate/multivariate analyses adjusted for traditional CVD risk factors, HDLox was an independent risk factor for CVD (odds ratio, 1.62; 95% confidence interval, 1.41–1.86; p < 0.001). For every increase in HDLox by 0.1 unit, there was an increase in CVD risk by 1.62‐fold. In an adjusted analysis, there was a >2.5‐fold increase in cardiovascular risk in individuals with HDLox higher than cutoff point of 1.06 compared to those with lower scores, suggesting HDLox > 1.06 is related to the impaired HDL oxidant function and in turn exposed to elevated risk of CVD outcomes (hazard ratio, 2.72; 95% CI, 1.88–3.94). Higher HDLox is a surrogate measure of reduced HDL antioxidant function that positively associated with cardiovascular events in a population‐based cohort.

Background The efficiency of high‐density lipoprotein (HDL) to efflux cholesterol contributes to the reverse cholesterol transport (RCT) pathway as one of HDL’s proposed functions and depends on the ability of HDL to uptake cholesterol. We aimed to investigate cholesterol uptake capacity (CUC) by a newly developed assay in samples from the MASHAD (Mashhad Stroke and Heart Atherosclerotic Disorders) cohort study. Method The study population comprised 153 individuals developed CVD diagnosed by a specialist cardiologist, over 6 years of follow‐up, and 350 subjects without CVD. We used a modified CUC method to evaluate the functionality of HDL in serum samples. Result The CUC assay was highly reproducible with values for inter‐ and intra‐assay variation of 13.07 and 6.65, respectively. The mean serum CUC was significantly lower in the CVD group compared to control (p = 0.01). Although, there were no significant differences in serum HDL‐C between the groups and there was no significantly association with risk of progressive CVD. Multivariate logistic regression analysis showed that there was a significantly negative association between CUC and risk of CVD after adjustment for confounding parameters (OR = 0.57, 95% CI = 0.38–0.87, p = 0.009). The CUC was also inversely and independently associated with the risk of CVD event using Cox proportional hazards models analysis (HR = 0.62; 95% CI = 0.41–0.94, p = 0.02). We determined the optimum cutoff value of 1.7 a.u for CUC in the population. Furthermore, the CUC value was important in determining the CVD risk stratification derived from data mining analysis. Conclusions Reduced HDL functionality, as measured by CUC, appears to predict CVD in population sample from north‐eastern Iran.

Cardiovascular disease (CVD) is the leading cause of mortality globally. There are few useful markers available for CVD risk stratification that has proven clinical utility. Scavenger receptor B type I (SR‐BI) is a cell surface protein that plays a major role in cholesterol homeostasis through its interaction with high‐density lipoprotein‐cholesterol (HDL‐C) esters (CE). HDL delivers CE to the liver through selective uptake by the SR‐BI. SR‐BI also regulates the inflammatory response. It has been shown that SR‐BI overexpression has beneficial, protective effects in atherogenesis, and there is considerable interest in developing antiatherogenic strategies that involve SR‐BI‐mediated increases in reverse cholesterol transport through HDL and/or low‐density lipoprotein. Further investigations are essential to explore the clinical utility of this approach. Moreover, there is growing evidence showing associations between genetic variants with modulation of SR‐BI function that may, thereby, increase CVD risk. The aim of the current review was to provide an overview of the possible molecular mechanisms by which SR‐BI may affect CVD risk, and the clinical implications of this, with particular emphasis on preclinical studies on genetic changes of SR‐BI and CVD risk.

A randomized clinical trial high-density lipoprotein (HDL) cholesterol uptake capacity (CUC) is reduced in patients with metabolic syndrome (MetS). We have assessed the effect of crocin supplementation on HDL CUC in patients with MetS. Forty-four subjects with MetS were randomly allocated to one of two groups: one group received placebo and the other group received crocin at a dose of 30 mg (two tablets of 15 mg per day) for 8 weeks. Serum biochemical parameters were measured using an AutoAnalyzer BT3000 (BioTechnica). The modified CUC method is a cell free, simple, and high-throughput assay that used to evaluate HDL CUC of serum samples. The decision tree analysis was undertaken using JMP Pro (SAS) version 13. The mean age of the crocin and placebo groups were 38.97 ± 13.33 and 43.46 ± 12.77 years, respectively. There was a significant increase in serum HDL CUC in the crocin group compared to that of the placebo group in patients with MetS (p-value< 0.05). The decision tree analysis showed that serum HDL functionality was more important variable than HDL-C level in predicting patients with hypertension at baseline