da Cunha Júnior Ademar Dantas, Zanette Dalila Luciola, Pericole Fernando Vieira, Olalla Saad Sara Teresinha, Barreto Campello Carvalheira José
Division of Oncology, Department of Internal Medicine, Faculty of Medical Sciences, State University of Campinas (UNICAMP), Campinas, SP, Brazil.
Hematology and Oncology Clinics, Cancer Hospital of Cascavel, União Oeste de Estudos e Combate ao Câncer (UOPECCAN), Cascavel, PR, Brazil.
Adv Hematol. 2021 Jan 18;2021:6615684. doi: 10.1155/2021/6615684. eCollection 2021.
Obesity is increasingly associated with the transformation of monoclonal gammopathy of undetermined significance (MGUS) into multiple myeloma MM). Obesity, MGUS, and MM share common etiopathogenesis mechanisms including altered insulin axis and the action of inflammatory cytokines. Consistent with this interconnection, metformin could predominantly exert inhibition of these pathophysiological factors and thus be an attractive therapeutic option for MGUS. Despite the possible clinical significance, only a limited number of epidemiological studies have focused on obesity as a risk factor for MGUS and MM. This review describes multiple biological pathways modulated by metformin at the cellular level and their possible impacts on the biology of MGUS and its progression into MM.
肥胖与意义未明的单克隆丙种球蛋白病（MGUS）向多发性骨髓瘤（MM）的转变日益相关。肥胖、MGUS和MM具有共同的病因发病机制，包括胰岛素轴改变和炎性细胞因子的作用。与此种相互联系相一致，二甲双胍可能主要对这些病理生理因素发挥抑制作用，因此是MGUS一种有吸引力的治疗选择。尽管具有潜在的临床意义，但仅有少数流行病学研究关注肥胖作为MGUS和MM的危险因素。本综述描述了二甲双胍在细胞水平调节的多种生物学途径及其对MGUS生物学特性及其向MM进展的可能影响。
