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Background: Breast cancer (BrCa) is one of the leading causes of cancer-related deaths. There are several factors for getting BrCa, including some changeable factors related to lifestyle like unhealthy dietary patterns, so modifying them can prevent one third of the complications and deaths caused by BrCa. Therefore, we decided to investigate the relationship between Healthy Beverage Index (HBI) and the risk of BrCa. Methods: In this hospital-based case–control study, 253 patients with BrCa and 267 non-BrCa controls were enrolled. Food consumption was recorded to calculate the HBI score using a semi-quantitative Food Frequency Questionnaire (FFQ). Additionally, by using binary logistic regression analysis with adjustment for confounders, the relationship between HBI and the risk of BrCa were assessed. HBI was established by Duffey et al. and is used to evaluate the overall quality of beverage intake and identify changes in consumption. Results: Mean ± SD of age and BMI of the study participants were 47.92 ± 10.33 years and 29.43 ± 5.51 kg/m2, respectively. Patients with BrCa considerably outperformed controls in terms of waist circumference (WC), age at first pregnancy, history of abortion, and number of children(Pvalue < 0.05). Compared with those in the lowest quartile of HBI, subjects in the highest quartile had higher intake of energy, carbohydrate, protein, fat, fiber, sodium, potassium, calcium, magnesium, zinc, vitamin C, E, B9, fruits, vegetables, fish and nut as well as lower BMI and WC (Pvalue < 0.05). After adjustment for potential confounders, individuals in highest compared to lowest quartile of HBI had significantly lower risk of BrCa for total population (odds ratio (OR): 0.40; 95% confidence interval (95%CI): 0.21–0.76, Pvalue < 0.05), premenopausal (OR: 0.38; 95% CI: 0.16–0.92, Pvalue = 0.013), and postmenopausal (OR: 0.27; 95% CI: 0.10–0.78, Pvalue = 0.023). Conclusion: Findings of this study suggested that higher HBI score decreased the risk of BrCa. However, further investigation is needed. [ABSTRACT FROM AUTHOR]

Simple Summary: Xeroderma pigmentosum (XP) is a very rare recessive disease caused by the incapacity to resolve ultraviolet-induced DNA lesions through Nucleotide Excision Repair (NER). Some XP patients suffer from aggressive skin carcinoma and melanoma at a very early age (<8). Our previous results show that primary XP fibroblasts isolated from healthy, non-photo-exposed skin negatively impact the extracellular matrix and the activation of the innate immune system. Here, we show for the first time that XP group C primary fibroblasts also play a major role in cancer cell invasion ex vivo and in vivo through the overexpression of Hepatocyte Growth Factor/Scatter Factor (HGF/SF) in the absence of genotoxic attacks. Using inhibitors of the activation of the HGF/SF pathway counteracted the effects of XP fibroblasts on the growth of cancer cells, suggesting new perspectives in the care of XP patients. Xeroderma pigmentosum (XP) is a very rare recessive disease caused by the incapacity to resolve ultraviolet-induced DNA lesions through Nucleotide Excision Repair (NER). Most XP patients suffer from aggressive skin carcinoma and melanoma at a very early age (<8). Our previous results showed that primary XP fibroblasts isolated from healthy (non-photo-exposed) skin negatively impact the extracellular matrix and fail to activate the innate immune system. Here, we show for the first time that XP-C fibroblasts also play a major role in cancer cell invasion ex vivo and in vivo through the overexpression of Hepatocyte Growth Factor/Scatter Factor (HGF/SF) in the absence of genotoxic attacks. The use of inhibitors of the activation of the HGF/SF pathway counteracted the effects of XP fibroblasts on the growth of cancer cells, suggesting new perspectives in the care of XP patients. [ABSTRACT FROM AUTHOR]

Primary cutaneous lymphomas (PCLs) are a heterogeneous group of lymphoproliferative disorders caused by the accumulation of neoplastic T or B lymphocytes in the skin. Sézary syndrome (SS) is an aggressive and rare form of cutaneous T cell lymphoma (CTCL) characterized by an erythroderma and the presence of atypical cerebriform T cells named Sézary cells in skin and blood. Most of the available treatments for SS are not curative, which means there is an urgent need for the development of novel efficient therapies. Recently, targeting cancer metabolism has emerged as a promising strategy for cancer therapy. This is due to the accumulating evidence that metabolic reprogramming highly contributes to tumor progression. Genes play a pivotal role in regulating metabolic processes, and alterations in these genes can disrupt the delicate balance of metabolic pathways, potentially contributing to cancer development. In this review, we discuss the importance of targeting energy metabolism in tumors and the currently available data on the metabolism of Sézary cells, paving the way for potential new therapeutic approaches aiming to improve clinical outcomes for patients suffering from SS. [ABSTRACT FROM AUTHOR]

Background: UV skin exposure is an important matter of public health, as the worldwide rising prevalence of skin cancers indicates. However, a wide majority of commercially available sunscreens are responsible for ocean ecosystem damages such as coral reef degradation and phytoplankton mortality. Aims: To answer the urge for new eco‐friendly UV filters, we studied the use of lecithin‐based multilamellar liposomes (MLLs) of controlled size and elasticity as a bio‐sourced and biodegradable alternative to classic sunscreens. These parameters control allows different skin layers targeting. Methods: The performance of two different MLLs compositions and a commercially available SPF50+ water‐resistant liposomal sunscreen was compared on skin explants. SC‐MLLs target the stratum corneum and Epi‐MLLs the whole epidermis. Preparations were applied prior to skin irradiation. Their efficiencies were evaluated histologically (hematoxylin and eosin staining plus cyclobutane pyrimidine dimer [CPD] immunostaining) and by skin barrier quality assessment (trans‐epithelial electrical resistance). Adhesiveness to the skin was also investigated. Results: Altogether, ex vivo results indicate MLLs offer a solar protection as effective as a SPF50+ water‐resistant liposomal sunscreen but with a better skin adhesiveness and an improved skin barrier function. Conclusion: Lecithin‐based MLLs of controlled physicochemical parameters can be used as a new eco‐friendly and water‐resistant agent for solar protection. The stratum corneum targeted action of SC‐MLLs appears to be more interesting, as SC‐MLLs exhibit an overall better performance than Epi‐MLLs at a lower cost. The skin barrier improvement showcased could be of interest to people suffering from dry skin or skin barrier impairment related disease. [ABSTRACT FROM AUTHOR]

Metabolic reprogramming is a common hallmark of cancer, but a large variability in tumor bioenergetics exists between patients. Using high-resolution respirometry on fresh biopsies of human lung adenocarcinoma, we identified 2 subgroups reflected in the histologically normal, paired, cancer-adjacent tissue: high ([OX.sup.+]) mitochondrial respiration and low ([OX.sup.-]) mitochondrial respiration. The [OX.sup.+] tumors poorly incorporated [[sup.18]F]fluorodeoxy-glucose and showed increased expression of the mitochondrial trifunctional fatty acid oxidation enzyme (MTP; HADHA) compared with the paired adjacent tissue. Genetic inhibition of MTP altered [OX.sup.+] tumor growth in vivo. Trimetazidine, an approved drug inhibitor of MTP used in cardiology, also reduced tumor growth and induced disruption of the physical interaction between the MTP and respiratory chain complex I, leading to a cellular redox and energy crisis. MTP expression in tumors was assessed using histology scoring methods and varied in negative correlation with [[sup.18]F]fluorodeoxy-glucose incorporation. These findings provide proof-of-concept data for preclinical, precision, bioenergetic medicine in oxidative lung carcinomas., Introduction Lung cancer is the leading cause of cancer death worldwide. Causative gene alterations have been identified in various signaling pathways including the MAPK, PI3K, oxidative stress response, RNA splicing, [...]