Immunology Laboratory, Victor Babes National Institute of Pathology, Bucharest, Romania.
Pathology Department, Colentina University Hospital, Bucharest, Romania.
Adv Exp Med Biol. 2024;1460:851-867. doi: 10.1007/978-3-031-63657-8_28.
The significant increase in the incidence of obesity represents a global health crisis. Obesity is actually a multi-organ disease affecting the entire organism; hence, skin is no exception. As the functional alterations in the adipose tissue are contributing factors to many diseases, including cancer, recently, the link between the development of melanoma skin cancer and obesity gains increased attention. Besides several other factors, the increase of adipose stromal/stem cells (ASCs) impacts cancer progression. Moreover, increased production of cytokines and growth factors done by ASCs induces tumorigenesis and metastasis. The chronic inflammatory state that is sustained by this metabolic imbalance favors skin malignancies, melanoma included. Cutaneous melanoma, as an aggressive skin cancer, has both intrinsic and extrinsic risk factors where sun exposure and lifestyles are the main environmental factors inducing this skin cancer. With the advent of recent targeted and immune-based therapies in melanoma, the link between obesity and the efficacy of these therapies in melanoma remains controversial. A recent molecular relationship between the melanocortin pathway appending to both melanin synthesis and obesity was established. The biology of adipokines, molecules secreted by the adipose tissue, is linked to inflammation, and their molecular pathways can be involved in angiogenesis, migration, invasion, and proliferation of melanoma cells. In melanoma cells, among the most noticeable metabolic reprogramming characteristics is an increased rate of lipid synthesis. Lipid mediators impact classical oncogenic pathways, affecting melanoma progression. The chapter will tackle also the practical implications for melanoma prevention and treatment, namely, how metabolic manipulation can be exploited to overcome immunosuppression and support immune checkpoint blockade efficacy.
肥胖发病率的显著增加代表了全球健康危机。肥胖实际上是一种影响整个机体的多器官疾病;因此,皮肤也不例外。由于脂肪组织的功能改变是包括癌症在内的许多疾病的促成因素,最近,黑色素皮肤癌的发展与肥胖之间的联系引起了更多的关注。除了其他几个因素外,脂肪基质/干细胞 (ASC) 的增加会影响癌症的进展。此外,ASC 产生的细胞因子和生长因子增加会导致肿瘤发生和转移。这种代谢失衡导致的慢性炎症状态有利于皮肤恶性肿瘤,包括黑色素瘤。黑色素瘤作为一种侵袭性皮肤癌,既有内在风险因素,也有外在风险因素,其中阳光暴露和生活方式是导致这种皮肤癌的主要环境因素。随着黑色素瘤中最近靶向和免疫治疗方法的出现,肥胖与这些疗法在黑色素瘤中的疗效之间的联系仍然存在争议。最近确立了黑素皮质素途径与黑色素合成和肥胖之间的分子关系。脂肪细胞因子(由脂肪组织分泌的分子)的生物学与炎症有关,其分子途径可参与黑色素瘤细胞的血管生成、迁移、侵袭和增殖。在黑色素瘤细胞中,最显著的代谢重编程特征之一是脂质合成率的增加。脂质介质影响经典的致癌途径,影响黑色素瘤的进展。本章还将探讨黑色素瘤预防和治疗的实际意义,即代谢操纵如何被利用来克服免疫抑制并支持免疫检查点阻断的疗效。