Signaling Pathways That Drive <sup>18</sup>F-FDG Accumulation in Cancer.
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- Record sourced from PubMed, PMID 35241480.
- Also identified by DOI 10.2967/jnumed.121.262609.
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Abstract
<sup>18</sup>F-FDG measures glucose consumption and is an integral part of cancer management. Most cancer types upregulate their glucose consumption, yielding elevated <sup>18</sup>F-FDG PET accumulation in those cancer cells. The biochemical pathway through which <sup>18</sup>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 <sup>18</sup>F-FDG accumulation are less well understood. Understanding these signaling pathways could yield additional biologic insights from <sup>18</sup>F-FDG PET scans and could suggest new uses of <sup>18</sup>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.
Medical subject headings
- Fluorodeoxyglucose F18
- Neoplasms