Gwak Ho-Shin
Department of Cancer Control, National Cancer Center, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Korea.
Brain Tumor Res Treat. 2023 Jan;11(1):8-15. doi: 10.14791/btrt.2022.0045.
Brain metastases (BMs) often occur in patients with lung cancer, breast cancer, and melanoma and are the leading cause of morbidity and mortality. The incidence of BM has increased with advanced neuroimaging and prolonged overall survival of cancer patients. With the advancement of local treatment modalities, including stereotactic radiosurgery and navigation-guided microsurgery, BM can be controlled long-term, even in cases with multiple lesions. However, radiation/chemotherapeutic agents are also toxic to the brain, usually irreversibly and cumulatively, and it remains difficult to completely cure BM. Thus, we must understand the molecular events that begin and sustain BM to develop effective targeted therapies and tools to prevent local and distant treatment failure. BM most often spreads hematogenously, and the blood-brain barrier (BBB) presents the first hurdle for disseminated tumor cells (DTCs) entering the brain parenchyma. Nevertheless, how the DTCs cross the BBB and settle on relatively infertile central nervous system tissue remains unknown. Even after successfully taking up residence in the brain, the unique tumor microenvironment is marked by restricted aerobic glycolysis metabolism and limited lymphocyte infiltration. Brain organotropism, certain phenotype of primary cancers that favors brain metastasis, may result from somatic mutation or epigenetic modulation. Recent studies revealed that exosome secretion from primary cancer or over-expression of proteolytic enzymes can "pre-condition" brain vasculoendothelial cells. The concept of the "metastatic niche," where resident DTCs remain dormant and protected from systemic chemotherapy and antigen exposure before proliferation, is supported by clinical observation of BM in patients clearing systemic cancer and experimental evidence of the interaction between cancer cells and tumor-infiltrating lymphocytes. This review examines extant research on the metastatic cascade of BM through the molecular events that create and sustain BM to reveal clues that can assist the development of effective targeted therapies that treat established BMs and prevent BM recurrence.
脑转移瘤(BMs)常见于肺癌、乳腺癌和黑色素瘤患者,是发病和死亡的主要原因。随着先进神经影像学技术的发展以及癌症患者总体生存期的延长,BM的发病率有所上升。随着包括立体定向放射外科和导航引导显微手术在内的局部治疗方式的进步,即使在存在多个病灶的情况下,BM也能得到长期控制。然而,放疗/化疗药物对大脑也有毒性,通常是不可逆且累积性的,彻底治愈BM仍然很困难。因此,我们必须了解引发和维持BM的分子事件,以开发有效的靶向治疗方法和工具,防止局部和远处治疗失败。BM最常通过血液传播,血脑屏障(BBB)是播散性肿瘤细胞(DTCs)进入脑实质的第一道障碍。然而,DTCs如何穿过血脑屏障并在相对贫瘠的中枢神经系统组织中定居仍不清楚。即使成功在脑中定植后,独特的肿瘤微环境仍以有氧糖酵解代谢受限和淋巴细胞浸润有限为特征。脑器官嗜性,即原发性癌症的某些有利于脑转移的表型,可能源于体细胞突变或表观遗传调控。最近的研究表明,原发性癌症分泌的外泌体或蛋白水解酶的过度表达可“预处理”脑血管内皮细胞。“转移生态位”的概念,即驻留的DTCs在增殖前保持休眠状态,并免受全身化疗和抗原暴露的影响,这一概念得到了清除全身癌症患者BM的临床观察以及癌细胞与肿瘤浸润淋巴细胞相互作用的实验证据的支持。本综述通过创建和维持BM的分子事件,审视了关于BM转移级联的现有研究,以揭示有助于开发有效靶向治疗方法的线索,这些方法可治疗已形成的BM并预防BM复发。