Evaluation of Bone Metastases by 18F-Choline PET/CT in a Patient with Castration-Resistant Prostate Cancer Treated with Radium-223

Scalzi, Piera; Baiocco, Cinzia; Genovese, Sabrina; Trevisan, Antonella; Sirotovà, Zuzana; Poti, C.

doi:10.5301/uro.5000206

Cited by 7 publications

(5 citation statements)

References 10 publications

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“…In addition, the cell membrane phospholipid choline can be abnormally metabolized and internalized in tumor cells overexpressing choline kinase (352). This abnormal regulation of the phospholipid metabolism has been observed in situ in cancer cells metastatic to bone (290,348), as visualized by FCH-PET scanning of prostate cancer bone metastases (Figure 8). Autophagy could be another potential source of energy for tumor cells in bone (233).…”

Section: Fueling Expansion -Reprogramming Energy Metabolism To Facilitate Bone Metastasis Progressionmentioning

confidence: 85%

Bone metastasis: mechanisms, therapies, and biomarkers

Clézardin

Coleman

Puppo

et al. 2021

Physiological Reviews

235

160

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Skeletal metastases are frequent complications of many cancers, causing bone complications (fractures, bone pain, disability), which negatively affect the patient's quality of life. Here, we first discuss the burden of skeletal complications in cancer bone metastasis. We then describe the pathophysiology of bone metastasis. Bone metastasis is a multistage process; long before the development of clinically detectable metastases, circulating tumor cells settle and enter a dormant state in normal vascular and endosteal niches present in the bone marrow, which provide immediate attachment and shelter, and only become active years later as they proliferate and alter the functions of bone-resorbing (osteoclasts) and bone-forming (osteoblasts) cells, promoting skeletal destruction. The molecular mechanisms involved in mediating each of these steps are described and we also explain how tumor cells interact with a myriad of interconnected cell populations in the bone marrow, including a rich vascular network, immune cells, adipocytes and nerves. We discuss metabolic programs that tumor cells could engage with to specifically grow in bone. We also describe the progress and future directions of existing bone-targeted agents and report emerging therapies that have arisen from recent advances in our understanding of the pathophysiology of bone metastases. Finally, we discuss the value of bone turnover biomarkers in detection and monitoring of progression and therapeutic effects in patients with bone metastasis.

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Section: Fueling Expansion -Reprogramming Energy Metabolism To Facilitate Bone Metastasis Progressionmentioning

confidence: 85%

Bone metastasis: mechanisms, therapies, and biomarkers

Clézardin

Coleman

Puppo

et al. 2021

Physiological Reviews

235

160

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“…Radium-223 clinical trials evaluated efficacy of the drug in mCRPC patients according to baseline ALP levels, assessed changes in ALP dynamics during treatment, and examined the potential of ALP as a prognostic biomarker [64][65][66][94][95][96][97][98][99][100][101]. Due to its mechanism of action and the effect of radium-223 on ALP levels during treatment, numerous ALP data were available from mCRPC clinical trials with this agent.…”

Section: Radium-223mentioning

confidence: 99%

“…Case reports have correlated changes in skeletal tumor activity on 18 F-choline positron emission tomography/computed tomography ( 18 F-choline PET/CT) imaging with ALP levels in patients treated with radium-223 [99,100]. In these cases, reduction of bone-metastatic disease on 18 F-choline PET/CT corresponded with decreases in ALP levels.…”

Section: Radium-223mentioning

confidence: 99%

“…In patients with mCRPC, changes in ALP level may reflect changes in bone turnover and osteoblastic activity indicative of the extent of bone-metastatic disease [12,17,20]. Decreases in ALP levels were reported to correspond with reduction of bone-metastatic disease on 18 F-choline PET/CT imaging [99,100]. More data are needed to evaluate imaging changes and ALP assessments.…”

Section: Using Alp As a Biomarkermentioning

confidence: 99%

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Alkaline Phosphatase in Metastatic Castration-Resistant Prostate Cancer: Reassessment of an Older Biomarker

et al. 2018

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Since most patients with metastatic castration-resistant prostate cancer (mCRPC) have bone metastases, it is important to understand the potential impact of therapies on prognostic biomarkers, such as ALP. Clinical studies involving mCRPC life-prolonging agents (i.e., sipuleucel-T, abiraterone, enzalutamide, docetaxel, cabazitaxel, and radium-223) have shown that baseline ALP level is prognostic for overall survival, and may be a better prognostic marker for overall survival than prostate-specific antigen in patients with bone-dominant mCRPC. Mechanism of action differences between therapies may partly explain ALP dynamics during treatment. ALP changes can be interpreted within the context of other parameters while monitoring disease activity to better understand the underlying pathology. This review evaluates the current role of ALP in mCRPC.

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“…The degree of BM is indicated by changes in bone turnover and osteoblastic activity, which are reflected in changes in ALP levels [38][39][40]. Increased levels of ALP were seen in PCa patients with BM, and decreases in ALP levels were also observed in PCa patients with BM after radium-233 radionuclide therapy [41,42]. However, due to its correlation with several non-neoplastic illnesses, including liver cancer and cholecystitis [43], serum total ALP (TALP) shows low sensitivity in the diagnosis of PCa BM, and the cut-off (C/O) value of TALP varies widely in different researches [44].…”

Section: Alkaline Phosphatase (Alp)mentioning

confidence: 99%

Biomarkers for Prostate Cancer Bone Metastasis Detection and Prediction

Ying

Mao

Sheng

et al. 2023

JPM

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Prostate cancer (PCa) causes deaths worldwide, ranking second after lung cancer. Bone metastasis (BM) frequently results from advanced PCa, affecting approximately 90% of patients, and it also often results in severe skeletal-related events. Traditional diagnostic methods for bone metastases, such as tissue biopsies and imaging, have substantial drawbacks. This article summarizes the significance of biomarkers in PCa accompanied with BM, including (1) bone formation markers like osteopontin (OPN), pro-collagen type I C-terminal pro-peptide (PICP), osteoprotegerin (OPG), pro-collagen type I N-terminal pro-peptide (PINP), alkaline phosphatase (ALP), and osteocalcin (OC); (2) bone resorption markers, including C-telopeptide of type I collagen (CTx), N-telopeptide of type I collagen (NTx), bone sialoprotein (BSP), tartrate-resistant acid phosphatase (TRACP), deoxypyridinoline (D-PYD), pyridoxine (PYD), and C-terminal pyridinoline cross-linked telopeptide of type I collagen (ICTP); (3) prostate-specific antigen (PSA); (4) neuroendocrine markers, such as chromogranin A (CgA), neuron-specific enolase (NSE), and pro-gastrin releasing peptide (ProGRP); (5) liquid biopsy markers, such as circulating tumor cells (CTCs), microRNA (miRNA), circulating tumor DNA (ctDNA), and cell-free DNA (cfDNA) and exosomes. In summary, some of these markers are already in widespread clinical use, while others still require further laboratory or clinical studies to validate their value for clinical application.

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Evaluation of Bone Metastases by 18F-Choline PET/CT in a Patient with Castration-Resistant Prostate Cancer Treated with Radium-223

Cited by 7 publications

References 10 publications

Bone metastasis: mechanisms, therapies, and biomarkers

Bone metastasis: mechanisms, therapies, and biomarkers

Alkaline Phosphatase in Metastatic Castration-Resistant Prostate Cancer: Reassessment of an Older Biomarker

Biomarkers for Prostate Cancer Bone Metastasis Detection and Prediction

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