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瘦素、脂肪细胞与乳腺癌:聚焦炎症与抗肿瘤免疫。

Leptin, adipocytes and breast cancer: Focus on inflammation and anti-tumor immunity.

机构信息

Clermont Université, Université d'Auvergne, UFR Pharmacie, 28 place Henri Dunant, 63000 Clermont-Ferrand, France; INRA, UMR 1019, ECREIN, CRNH Auvergne, 63000 Clermont-Ferrand, France.

Clermont Université, Université d'Auvergne, UFR Pharmacie, 28 place Henri Dunant, 63000 Clermont-Ferrand, France; INRA, UMR 1019, ECREIN, CRNH Auvergne, 63000 Clermont-Ferrand, France; Centre Jean-Perrin, CHU Gabriel-Montpied, Unité de Nutrition, 63003 Clermont-Ferrand, France.

出版信息

Life Sci. 2015 Nov 1;140:37-48. doi: 10.1016/j.lfs.2015.04.012. Epub 2015 May 6.

Abstract

More than one million new cases of breast cancer are diagnosed worldwide each year and more than 400,000 deaths are caused by the disease. The origin of this pathology is multifactorial and involved genetic, hormonal, environmental and nutritional factors including obesity in postmenopausal women. The role played by the adipose tissue and their secretions, ie adipokines, is beginning to be recognized. Plasma adipokine levels, which are modulated during obesity, could have “remote” effects on mammary carcinogenesis. Breast cancer cells are surrounded and locally influenced by an adipocyte microenvironment, which is probably more extensive in obese people. Hence, leptin appears to be strongly involved in mammary carcinogenesis and may contribute to the local pro-inflammatory mechanisms, especially in obese patients, who have increased metastatic potential and greater risk of mortality. This review presents the multifaceted role of leptin in breast cancer development and the different molecular pathways involved such as inflammation, oxidative stress and antitumor immunity.

摘要

每年全球有超过 100 万例乳腺癌新发病例,并有超过 40 万例患者死于该病。这种病理学的起源是多因素的,涉及遗传、激素、环境和营养因素,包括绝经后妇女的肥胖。脂肪组织及其分泌物(即脂联素)的作用开始得到认可。在肥胖期间被调节的血浆脂联素水平可能对乳腺发生具有“远程”作用。乳腺癌细胞被脂肪细胞微环境包围并局部受到影响,而在肥胖者中这种微环境可能更为广泛。因此,瘦素似乎强烈参与乳腺发生,并且可能有助于局部促炎机制,特别是在肥胖患者中,其具有增加的转移潜能和更大的死亡风险。本文综述了瘦素在乳腺癌发生发展中的多方面作用,以及涉及炎症、氧化应激和抗肿瘤免疫等不同的分子途径。

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