Identification of Metastasis-Associated Metabolic Profiles of Tumors by 1H-HR-MAS-MRS

Gorad, Saurabh Sayajirao; Ellingsen, Christine; Bathen, Tone Frost; Mathiesen, Berit; Moestue, Siver Andreas; Rofstad, Einar K.

doi:10.1016/j.neo.2015.10.001

Cited by 6 publications

(3 citation statements)

References 55 publications

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“…Consistent with these results, distinct metabolic profiles were revealed between non-metastatic and metastatic cells of human R-18 melanoma cell line (established from a xenograft model) by proton high resolution magic angle spinning magnetic resonance spectroscopy ( 1 H-HR-MAS-MRS) (198). The metastatic tumors expressed higher levels of phosphocholine, creatine, and glycine, while lower levels of lactate were observed.…”

Section: From Primary Tumor To Metastasis: Metabolic Comparisonsupporting

confidence: 65%

Molecular and Metabolic Reprogramming: Pulling the Strings Toward Tumor Metastasis

et al. 2021

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Metastasis is a major hurdle to the efficient treatment of cancer, accounting for the great majority of cancer-related deaths. Although several studies have disclosed the detailed mechanisms underlying primary tumor formation, the emergence of metastatic disease remains poorly understood. This multistep process encompasses the dissemination of cancer cells to distant organs, followed by their adaptation to foreign microenvironments and establishment in secondary tumors. During the last decades, it was discovered that these events may be favored by particular metabolic patterns, which are dependent on reprogrammed signaling pathways in cancer cells while they acquire metastatic traits. In this review, we present current knowledge of molecular mechanisms that coordinate the crosstalk between metastatic signaling and cellular metabolism. The recent findings involving the contribution of crucial metabolic pathways involved in the bioenergetics and biosynthesis control in metastatic cells are summarized. Finally, we highlight new promising metabolism-based therapeutic strategies as a putative way of impairing metastasis.

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Section: From Primary Tumor To Metastasis: Metabolic Comparisonsupporting

confidence: 65%

Molecular and Metabolic Reprogramming: Pulling the Strings Toward Tumor Metastasis

et al. 2021

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“…The 5-year survival rate is 63% in patients with localized lung cancer, but it decreases to 35% if the cancer spreads to nearby tissue, and drops to approximately 7% if distant metastasis occurs [ 2 ]. Primary tumors and metastases show a variety of metabolic processes that are tightly linked to the characteristics of the tumor microenvironment [ 3 ]. More importantly, based on the various treatment responses of primary, metastatic, or recurrent tumors, understanding the metabolic status of the lesions would be a good means for predicting treatment responses [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Glycolytic Plasticity of Metastatic Lung Cancer Captured by Noninvasive 18F-FDG PET/CT and Serum 1H-NMR Analysis: An Orthotopic Murine Model Study

Chung

Hung

et al. 2023

Metabolites

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We aim to establish a noninvasive diagnostic platform to capture early phenotypic transformation for metastasis using 18F-FDG PET and 1H-NMR-based serum metabolomics. Mice with implantation of NCI-H460 cells grew only primary lung tumors in the localized group and had both primary and metastatic lung tumors in the metastatic group. The serum metabolites were analyzed using 1H-NMR at the time of PET/CT scan. The glycolysis status and cell proliferation were validated by Western blotting and staining. A receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic accuracy of SUVmean and serum metabolites in metastasis. In the metastatic mice, the SUVmean of metastatic tumors was significantly higher than that of primary lung tumors in PET images, which was supported by elevated glycolytic protein expression of HK2 and PKM2. The serum pyruvate level in the metastatic group was significantly lower than that in the localized group, corresponding to increased pyruvate-catalyzed enzyme and proliferation rates in metastatic tumors. In diagnosing localized or metastatic tumors, the areas under the ROC curves of SUVmean and pyruvate were 0.92 and 0.91, respectively, with p < 0.05. In conclusion, the combination of 18F-FDG PET and 1H-NMR-based serum metabolomics demonstrated the feasibility of a glycolytic platform for diagnosing metastatic lung cancers.

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“…The apparent diffusion coefficient (ADC), measured by DWI, reflects the structural limitation of tissue water molecule Brownian motion and is related to cell density. , The volume transfer constant ( K trans ) obtained from DCE-MR was reported to assess microvascular permeability changes after VEGF inhibitor therapy and informs on prognosis . Meanwhile, MRS, as a noninvasive method for obtaining in vivo biochemical and metabolic information, was shown to assess the hypoxia condition in metastasis via lactate (Lac) measurement .…”

Section: Introductionmentioning

confidence: 99%

Multimodal Imaging Response after the Singular or Combination Treatments of Vascular Endothelial Growth Factor Inhibitor and Immune Checkpoint Inhibitor

et al. 2022

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This study aims to dynamically assess tumor changes after variable treatments with vascular endothelial growth factor (VEGF) inhibitor and/or immune checkpoint inhibitor (ICI) using multimodal imaging of MRI and 18F-FDG PET/CT in a hepatocellular carcinoma (HCC) mice model. Based on different treatments, 24 mice were randomly divided into four groups: control (isotype-matched IgG antibody 10 mg/kg), VEGF inhibitor (sorafenib 50 mg/kg), ICI (anti-PD-L1 antibody 10 mg/kg), and combination groups (sorafenib 50 mg/kg + anti-PD-L1 antibody 10 mg/kg). Quantitative imaging assessments, including volume transfer constant (K trans), apparent diffusion coefficient (ADC), lactate/choline ratio, and the maximum standardized 18F-FDG uptake value ratio of tumor to muscle (SUVtumor/SUVmuscle ratio), were acquired at different time points (before treatment and 7, 14, and 21 days after treatment). Quantitative data were presented as the mean ± standard errors and two-way repeated-measure ANOVA tests were performed for intergroup and intertime point comparisons. After 21 days from the initiation of therapies, combination group showed the lowest tumor volume and weight, followed by ICI, VEGF inhibitor, and control group, with no significance between the VEGF inhibitor and control groups. In addition, K trans values significantly decreased, and the lactate/choline ratio and SUVtumor/SUVmuscle ratio were significantly elevated in the VEGF inhibitor group. ADC significantly increased in the ICI and combination groups, with no significant differences in ADC observed between the control and VEGF inhibitor groups, which showed a similar dynamic change to the tumor volume. Furthermore, K trans, lactate/choline ratio, and ADC were significantly correlated with CD31+ area, hypoxyprobe+ area, and apoptosis, respectively. Our results suggest that the singular treatment and combination of the VEGF inhibitor and ICI treatments for HCC present different multimodal imaging changes in accordance with the specific histopathological features. These findings might facilitate the formulation of better treatment response criteria; besides, we find ADC is probably an indicator easily to obtain for treatment response evaluation.

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Identification of Metastasis-Associated Metabolic Profiles of Tumors by 1H-HR-MAS-MRS

Cited by 6 publications

References 55 publications

Molecular and Metabolic Reprogramming: Pulling the Strings Toward Tumor Metastasis

Molecular and Metabolic Reprogramming: Pulling the Strings Toward Tumor Metastasis

Glycolytic Plasticity of Metastatic Lung Cancer Captured by Noninvasive 18F-FDG PET/CT and Serum 1H-NMR Analysis: An Orthotopic Murine Model Study

Multimodal Imaging Response after the Singular or Combination Treatments of Vascular Endothelial Growth Factor Inhibitor and Immune Checkpoint Inhibitor

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