Butyrylcholinesterase as a Blood Biomarker in Neuroblastoma
| Autor: | Jake A. Luther, Janina Baranowska-Kortylewicz, Don W. Coulter, Stephen P. Enke, Vivek Verma, Angela D. Boettner, Zbigniew P. Kortylewicz |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty medicine.medical_treatment 03 medical and health sciences Mice Neuroblastoma 0302 clinical medicine Species Specificity Internal medicine medicine Animals Humans Butyrylcholinesterase Chemotherapy business.industry Case-control study Infant Hematology Plasma levels medicine.disease Response to treatment Disease Models Animal 030104 developmental biology Endocrinology Oncology 030220 oncology & carcinogenesis Case-Control Studies Child Preschool Pediatrics Perinatology and Child Health Biomarker (medicine) Heterografts Female Signal transduction business Biomarkers Signal Transduction |
| Zdroj: | Journal of pediatric hematology/oncology. 39(4) |
| ISSN: | 1536-3678 |
| Popis: | Blood-based biomarkers are important in the detection of the disease and in the assessment of responses to therapy. In this study, butyrylcholinesterase was evaluated as a potential biomarker in newly diagnosed neuroblastoma (NB) patients at diagnosis and longitudinally during treatment. Plasma butyrylcholinesterase activities in age-matched and sex-matched children were used as controls. Pretreatment butyrylcholinesterase levels in NB subjects are on an average 2 times lower than butyrylcholinesterase levels in healthy subjects. Significantly, butyrylcholinesterase activities are ∼40% lower in MYCN-amplified as compared with nonamplified disease. As the course of chemotherapy progresses, butyrylcholinesterase activities recover and normalize to control values. The evident response to treatment indicates that plasma butyrylcholinesterase is a good biomarker of tumor response to therapy. Depressed butyrylcholinesterase levels in NB subjects are not caused by hepatic deficits suggesting a specific role for butyrylcholinesterase in NB. Further examination of the mechanism of altered butyrylcholinesterase production require an animal model that best approximates human condition. Studies in mice show that murine NB allografts significantly reduce butyrylcholinesterase activity in plasma. This finding correlates with changes observed in NB patients. In contrast, human NB xenografts produce the opposite effect, that is, butyrylcholinesterase plasma levels rise as the xenograft size increases. In the absence of any liver damage, dissimilarities between butyrylcholinesterase production in murine and human NB models suggest species-specific signaling pathways. This disparity also suggests that human NB xenograft mouse models do not approximate the human disease. |
| Databáze: | OpenAIRE |
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