Abstract
Neuroblastoma is the most common extracranial malignant solid tumor in children. This disease displays a remarkable heterogeneity in clinical behavior, ranging from spontaneous regression to rapid progression and resistance to therapy. Recent evidence has shown that microRNAs are often involved in regulation of tumor development and progression. MiR-885-5p has a tumor suppressive role in neuroblastoma, interfering with cell cycle progression and cell survival. MiR-885-5p leads to the accumulation of p53 protein and activates p53-mediated pathway of cell cycle arrest, resulting in upregulation of its targets. We have analyzed association of miR-885-5p expression in 58 neuroblastoma tumors with different clinical characteristics and disease outcome. In tumor samples of patients with unfavorable clinical characteristics lower miR-885-5p expression levels were observed. Event-free survival analysis showed that low miR-885-5p expression was tightly associated with a significantly poorer outcome than in those with high expression of miR-885-5p. In this study, evidence is presented on miR-885-5p dysregulation in neuroblastoma. As follows, along with other clinical features, it can be used as an independent prognostic and possibly therapeutic approach for optimization of neuroblastoma treatment.
Highlights
Neuroblastoma (NB) is a malignant tumor of the sympathetic nervous system reaching 11.7 % of all malignancies in children and taking fourth place in structure of cancer mortality after acute leukemia, central nervous system tumors and malignant lymphomas [5]
Howe ver, ~40 % of NB rapidly progress despite multimodal treatment regimens. This high clinical heterogeneity reflects a complexity of genomic abnormalities that are characteri zed for NB tumors [7]
It was found that the value of miR-885-5p expression in tumor cells of patients with NB varied in a wide range
Summary
Neuroblastoma (NB) is a malignant tumor of the sympathetic nervous system reaching 11.7 % of all malignancies in children and taking fourth place in structure of cancer mortality after acute leukemia, central nervous system tumors and malignant lymphomas [5]. Age distribution of the disease is heterogeneous and frequency of tumor detection decreases with age. A characteristic feature of NB is its clinical heterogeneity – from localized tumors to widespread forms and early hematogenous metastasing. Howe ver, ~40 % of NB rapidly progress despite multimodal treatment regimens. This high clinical heterogeneity reflects a complexity of genomic abnormalities that are characteri zed for NB tumors [7]. Multiple segmental aberrations of chromosomes and individual gene amplification, particular MYCN oncogene, are inherent for aggressive NB. Amplification of MYCN gene is observed in ~25 % of primary tumors and is associated with rapid tumor progression
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
