Salas Jessica R, Clark Peter M
Department of Molecular and Medical Pharmacology, UCLA, Los Angeles, California.
Department of Molecular and Medical Pharmacology, UCLA, Los Angeles, California
J Nucl Med. 2022 May;63(5):659-663. doi: 10.2967/jnumed.121.262609. Epub 2022 Mar 3.
F-FDG measures glucose consumption and is an integral part of cancer management. Most cancer types upregulate their glucose consumption, yielding elevated F-FDG PET accumulation in those cancer cells. The biochemical pathway through which F-FDG accumulates in cancer cells is well established. However, beyond well-known regulators such as c-Myc, PI3K/PKB, and HIF1α, the proteins and signaling pathways that cancer cells modulate to activate the facilitated glucose transporters and hexokinase enzymes that drive elevated F-FDG accumulation are less well understood. Understanding these signaling pathways could yield additional biologic insights from F-FDG PET scans and could suggest new uses of F-FDG PET in the management of cancer. Work over the past 5 years, building on studies from years prior, has identified new proteins and signaling pathways that drive glucose consumption in cancer. Here, we review these recent studies and discuss current limitations to our understanding of glucose consumption in cancer.
F-FDG可测量葡萄糖消耗,是癌症管理的一个重要组成部分。大多数癌症类型会上调其葡萄糖消耗,导致这些癌细胞中F-FDG PET的积聚增加。F-FDG在癌细胞中积聚的生化途径已得到充分证实。然而,除了诸如c-Myc、PI3K/PKB和HIF1α等知名调节因子外,癌细胞为激活促进葡萄糖转运蛋白和己糖激酶而调节的蛋白质和信号通路,驱动F-FDG积聚增加,人们对此了解较少。了解这些信号通路可能会从F-FDG PET扫描中获得更多生物学见解,并可能提示F-FDG PET在癌症管理中的新用途。在过去5年的研究基础上,基于多年前的研究,已经确定了驱动癌症中葡萄糖消耗的新蛋白质和信号通路。在此,我们回顾这些最新研究,并讨论目前我们对癌症中葡萄糖消耗理解的局限性。