The role of serum neuron-specific enolase in patients with prostate cancer: a systematic review of the recent literature

Muoio, Barbara; Pascale, Mariarosa; Ricevuto, Enrico

doi:10.5301/ijbm.5000286

Cited by 20 publications

(17 citation statements)

References 43 publications

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“…NSE is a highly specific marker for neurons and peripheral neuroendocrine cells, used as a biomarker for aggressive forms of neuroendocrine tumors and small cell carcinoma [27,28]. Elevated NSE serum levels have also been observed in neuroendocrine subtypes of prostate carcinoma [29,30]. While only a small proportion of prostate cancer patients represent neuroendocrine features at the beginning of disease [31], more patients develop these under therapy [24].…”

Section: Discussionmentioning

confidence: 99%

Neuron-specific enolase has potential value as a biomarker for [18F]FDG/[68Ga]Ga-PSMA-11 PET mismatch findings in advanced mCRPC patients

et al. 2020

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Background: PSMA-targeted radioligand therapy (PSMA-RLT) yielded impressive results in the metastasized castration-resistant prostate carcinoma (mCRPC) setting. High expression of PSMA is essential for successful PSMA-RLT. However, some patients develop [ 18 F]FDG-avid lesions with low or no PSMA expression ([ 18 F]FDG/[ 68 Ga]Ga-PSMA-11 mismatch findings on PET/CT) in the course of treatment. Those lesions are not affected by PSMA-RLT and a change in therapy management is needed. To enable early mismatch detection, possible blood parameters as indicators for the occurrence of [ 18 F]FDG/[ 68 Ga]Ga-PSMA-11 mismatch findings on PET/CT were evaluated. Methods: Retrospective study of N = 66 advanced mCRPC patients with dual [ 68 Ga]Ga-PSMA-11 and [ 18 F]FDG PET/ CT imaging within 4 weeks, who were referred for or received [ 177 Lu]Lu-PSMA-617 radioligand therapy. Prostatespecific antigen (PSA), neuron-specific enolase (NSE), gamma-glutamyltransferase (GGT), and alkaline phosphatase (ALP) were tested as indicators for the occurrence of [ 18 F]FDG/[ 68 Ga]Ga-PSMA-11 mismatch findings. Additional to absolute values, relative changes (ΔPSA, ΔNSE, ΔGGT, ΔALP) over a period of 4 ± 1 weeks prior to [ 18 F]FDG PET/CT were analyzed. Results: In total, 41/66 (62%) patients revealed at least one [ 18 F]FDG/[ 68 Ga]Ga-PSMA-11 mismatch finding on PET/ CT. These mismatch findings were detected in 13/41 (32%) patients by screening for and in 28/41 (68%) patients during PSMA-RLT. NSE serum level (55.4 ± 44.6 μg/l vs. 18.5 ± 8 μg/l, p < 0.001) and ΔNSE (93.8 ± 124.5% vs. 2.9 ± 39.5%, p < 0.001) were significantly higher in the mismatch group than in the non-mismatch group. No significant differences were found for serum PSA (p = 0.424), ΔPSA (p = 0.417), serum ALP (p = 0.937), ΔALP (p = 0.611), serum GGT (p = 0.773), and ΔGGT (p = 0.971). For NSE and ΔNSE, the maximum value of the Youden index in ROC analysis was at a cutoff level of 26.8 μg/l (sensitivity 78%, specificity 96%) and at + 13.9% (sensitivity 84%, specificity 75%), respectively. An introduced scoring system of both parameters achieved a sensitivity of 90% and a specificity of 88% for the occurrence of [ 18 F]FDG/[ 68 Ga]Ga-PSMA-11 mismatch.

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Section: Discussionmentioning

confidence: 99%

Neuron-specific enolase has potential value as a biomarker for [18F]FDG/[68Ga]Ga-PSMA-11 PET mismatch findings in advanced mCRPC patients

et al. 2020

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“…Serum NE markers such as NSE and CgA have been reported to be prognostic in patients with mCRPC [ 61 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 ]. Their role as predictors of response in unselected mCRPC patients is still under investigation, with some reports suggesting such a role [ 93 ].…”

Section: Ongoing Research and Future Perspectivesmentioning

confidence: 99%

Neuroendocrine and Aggressive-Variant Prostate Cancer

Spetsieris

Boukovala

Patsakis

et al. 2020

Cancers

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In prostate cancer, neuroendocrine (NE) differentiation may rarely present de novo or more frequently arises following hormonal therapy in patients with castration-resistant prostate cancer (CRPC). Its distinct phenotype is characterized by an aggressive clinical course, lack of responsiveness to hormonal therapies and poor prognosis. Importantly, a subset of CRPC patients exhibits an aggressive-variant disease with very similar clinical and molecular characteristics to small-cell prostate cancer (SCPC) even though tumors do not have NE differentiation. This aggressive-variant prostate cancer (AVPC) also shares the sensitivity of SCPC to platinum-based chemotherapy albeit with short-lived clinical benefit. As optimal treatment strategies for AVPC remain elusive, currently ongoing research efforts aim to enhance our understanding of the biology of this disease entity and improve treatment outcomes for our patients. This review is an overview of our current knowledge on prostate cancer with NE differentiation and AVPC, with a focus on their clinical characteristics and management, including available as well as experimental therapeutic strategies.

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“…Elevated serum NSE is currently considered to be a strong marker of progressive and metastatic CRPC. 19 In addition, a high level of serum NSE strongly predicts a worsened prognosis of CRPC patients. 20 Thus, the downregulation of NSE by EPOR knockdown suggests that the EPO signaling pathway promotes the neuroendocrine transmission of PCa by interacting with functional EPOR.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of erythropoietin and erythropoietin receptor in castration-resistant progression of prostate cancer

Wang

Chen

et al. 2020

Asian J Androl

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Hypoxia-induced erythropoietin signaling plays an important role in tumor growth and invasion. In the present study, we investigated the contribution of erythropoietin signaling pathway to castration-resistant prostate cancer and the development of a neuroendocrine phenotype. Immunohistochemical staining showed that the erythropoietin and erythropoietin receptor scores in castration-resistant prostate cancer and androgen-dependent prostate cancer were 7.55 versus 4.5 and 7.45 versus 5.9, respectively ( P < 0.001). Furthermore, a cell proliferation assay was conducted, and the differential expression of erythropoietin and erythropoietin receptor in LNCaP cells and hypoxia-induced LNCaP cells was evaluated using western blot and quantitative real-time PCR. The proliferation capacity of hypoxia-induced LNCaP cells was similar in cultures of both fetal bovine serum and charcoal-stripped fetal bovine serum, suggesting that LNCaP cells acquired hypoxia-induced androgen-independent growth. After 2 weeks of hypoxic culture, LNCaP cells showed a neuroendocrine cell change and increased expression of neuron-specific enolase, erythropoietin, and erythropoietin receptor; knockdown of erythropoietin receptor reversed the hypoxia-induced upregulation of neuron-specific enolase in the LNCaP cells. In conclusion, the concurrent upregulation of erythropoietin and erythropoietin receptor in castration-resistant prostate cancer suggests that the erythropoietin/erythropoietin receptor autocrine loop plays an important role in the progression of castration resistance and is responsible for the development of a neuroendocrine phenotype.

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The role of serum neuron-specific enolase in patients with prostate cancer: a systematic review of the recent literature

Cited by 20 publications

References 43 publications

Neuron-specific enolase has potential value as a biomarker for [18F]FDG/[68Ga]Ga-PSMA-11 PET mismatch findings in advanced mCRPC patients

Neuron-specific enolase has potential value as a biomarker for [18F]FDG/[68Ga]Ga-PSMA-11 PET mismatch findings in advanced mCRPC patients

Neuroendocrine and Aggressive-Variant Prostate Cancer

Upregulation of erythropoietin and erythropoietin receptor in castration-resistant progression of prostate cancer

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