Tumor Cell Metabolism Imaging

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Molecular imaging of tumor metabolism has gained considerable interest, since preclinical studies have indicated a close relationship between the activation of various oncogenes and alterations of cellular metabolism. Furthermore, several clinical trials have shown that metabolic imaging can significantly impact patient management by improving tumor staging, restaging, radiation treatment planning, and monitoring of tumor response to therapy. In this review, we summarize recent data on the molecular mechanisms underlying the increased metabolic activity of cancer cells and discuss imaging techniques for studies of tumor glucose, lipid, and amino acid metabolism. Key Words: glucose metabolism; amino acid metabolism; lipid metabolism; PET; optical imaging; MRI

J Nucl Med 2008; 49:43S-63S

DOI: 10.2967/jnumed.107.045930

Imaging of tumor cell metabolism has been remarkably successful in recent years. Numerous studies have demonstrated that malignant tumors can be detected with high sensitivity and specificity by imaging their increased metabolic rates for glucose, amino acids, or lipids. PET with the glucose analog ^sup 18^F-FDG has become a routine clinical test for staging and restaging of malignant lymphoma (1) and most solid tumors (2), ^sup 11^C-choline and ^sup 18^F-fluorocholine are used at many European centers for detection of recurrent prostate cancer (3), and various radiolabeled amino acids have been shown to be clinically useful for brain tumor imaging (4,5). This success of metabolic imaging is perhaps unexpected, since the metabolic pathways targeted by these imaging probes are present in virtually all cells in the human body. Therefore, one would have predicted tumor cell metabolism imaging to provide an unspecific signal of limited use in clinical oncology. However, recent studies have revealed that oncogenic signaling and tumor cell metabolism are closely interrelated. For example, malignant transformation by various oncogenes or loss of tumor suppressor genes has been shown to result in quantitative and qualitative alterations of glucose metabolism (6,7). Conversely, genes involved in mitochondrial metabolism have been found to also function as tumor suppressor genes (. In addition, the tumor environment causes specific adaptations of cellular metabolism that increase the uptake of metabolic substrates (9).

Several modalities can be used in humans for tumor cell metabolism imaging, including SPECT, PET, and magnetic resonance spectroscopy (MRS). Metabolic imaging is increasingly combined with CT and MRI for precise anatomic localization (3,10,11). These multimodality imaging approaches are now becoming the standard for staging and restaging of cancer patients and for evaluation and prediction of treatment response and may contribute to determining the prognosis of patients.

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