Abstract
Simple SummaryDeregulated tumor metabolism is known to shape the tumor microenvironment and directly affect the local immune response, promoting tumor growth, metastasis, and resistance to treatment. However, the metabolic profile or tumor cells, and therefore, the composition of their microenvironment, are highly variable among patients and even within the same tumor, resulting in heterogeneous response rates to oncologic therapies, making patient selection a key issue. This review article focuses on non-invasive imaging techniques that aim to visualize the crosstalk between tumor cells and their microenvironment in liver cancer mediated by tumor metabolism. In addition to improved tumor detection, such imaging tools may be able to provide a more accurate characterization of the individual tumor and ultimately improve understanding, as well as guide personalized treatment regimens for patients with liver cancer.With the increasing understanding of resistance mechanisms mediated by the metabolic reprogramming in cancer cells, there is a growing clinical interest in imaging technologies that allow for the non-invasive characterization of tumor metabolism and the interactions of cancer cells with the tumor microenvironment (TME) mediated through tumor metabolism. Specifically, tumor glycolysis and subsequent tissue acidosis in the realms of the Warburg effect may promote an immunosuppressive TME, causing a substantial barrier to the clinical efficacy of numerous immuno-oncologic treatments. Thus, imaging the varying individual compositions of the TME may provide a more accurate characterization of the individual tumor. This approach can help to identify the most suitable therapy for each individual patient and design new targeted treatment strategies that disable resistance mechanisms in liver cancer. This review article focuses on non-invasive positron-emission tomography (PET)- and MR-based imaging techniques that aim to visualize the crosstalk between tumor cells and their microenvironment in liver cancer mediated by tumor metabolism.
Highlights
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy, and primary liver cancer is the third most common cause of cancer-related death worldwide [1]
This review article focuses on non-invasive positron emission tomography (PET)- and MR-based imaging techniques that aim to visualize the crosstalk between tumor cells and their microenvironment in liver cancer mediated by tumor metabolism (Table 1)
For a subset of HCCs, which were moderately differentiated, these showed relatively high choline uptakes and a better detection rate with 11C-choline positron-emission tomography (PET) (75% detection sensitivity) as compared to poorly differentiated HCC with markedly lower choline uptake (25% detection sensitivity) [21]. This uptake behavior is inverse to the FDG-uptake; another study prospectively investigated the benefit of combining 11C-choline with 18F-FDG PET and showed a markedly increased sensitivity for detecting HCC of 93% [22]
Summary
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy, and primary liver cancer is the third most common cause of cancer-related death worldwide [1]. More comprehensive approaches to characterize and monitor the tumors metabolism are urgently needed [5] In this context, the individual physiological and biological variations of the tumor microenvironment (TME) are proposed to play an important role over the dynamic course of carcinogenesis and reflect the aggressiveness of cancer cells by their changing composition [6,7]. There is an unmet clinical need for novel imaging biomarkers that visualize the tumor and its microenvironmental characteristics, and thereby better reflect the true biochemical and pathological disease profile In this regard, metabolic pathways have gained increased interest as targets for imaging and therapies [7]. This review article focuses on non-invasive positron emission tomography (PET)- and MR-based imaging techniques that aim to visualize the crosstalk between tumor cells and their microenvironment in liver cancer mediated by tumor metabolism (Table 1)
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