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The associated risk stratification schema classifies tumors into low, intermediate, and high risk, depending on the stage of the tumor, as well as whether the tumor exhibits amplification of the MYCN gene and has favorable histologic features.
Conversely, the Mycn mRNA was increased in MPP cells (2.98-fold induction) (Figure 4), comparative with the results from the analysis in the endoglin/CD150 staining protocol (Figure 2).
Melaiu et al., "MYCN is an immunosuppressive oncogene dampening the expression of ligands for NK-cell-activating receptors in human high-risk neuroblastoma," OncoImmunology, vol.
CD44 is an adhesion molecule expressed on various cell types, and is an important participant in a number of signalling pathways.15 Data from descriptive studies showed CD44 expression in glial and neuronal cells can play a crucial role in nervous system pathology, such as response to injury and tumour invasion.16 Recently, two urinary tumour studies pointed to miR-34-a function as an anti-metastatic microRNA by directly targeting CD44.10,17 Another predicted target gene identified was MYCN, the most relevant gene for NB prognosis, progression and treatment, which was reported to change in parallel with miR-34-a.18
In the laboratory, the researchers found that cells with over-activated MYCN consumed more oxygen and depended on the production of heme to propagatecalled self-renewalas well as to become cancerous.
Furthermore, biological characteristics, including sensitivity to chemotherapy, might be lesion dependent because NSE immunohistochemistry in the primary lesion, uptake of [sup.123]I-MIBG in the primary lesion and metastatic sites, and MYCN amplification in the primary lesion and bone marrow aspirate were heterogeneous, and there was a higher residual tumor burden in the primary lesion compared with the renal lesion after auto-PBSCT (Figures 2(a)-2(h)).
In addition, expression of SSTR2 was not related to the p53 mutation and MYCN amplification status.
The top predicted transcription factors in our study, p53, MYC, and MYCN, are well-known upstream regulators involved in the process of carcinogenesis, since MYC and MYCN are oncogenes [21] and p53 is a tumor suppressor [22].
The genes sequenced were part of a custom, targeted next-generation sequencing amplicon panel testing for 68 hematologic malignancy-associated genes (ABL1, ASXL1, ATM, BCOR, BCORL1, BIRC3, BRAF CALR, CBL, CDKN2A, CEBPA, CSF1R, CSF3R, DDX3X, DNMT3A, ETV6, EZH2, FAM5C, FBXW7, FLT3, GATA2, GNAS, HNRNPK, IDH1, IDH2, IL7R, JAK2, KIT, KLHL6, KRAS, MAP2K1, MAPK1, MIR142, MPL, MYC, MYCN, MYD88, NF1, NOTCH1, NOTCH2, NPM1, NRAS, PDGFRA, PHF6, POT1, PRPF40B, PTEN, PTPN11, RAD21, RIT1, RUNX1, SETBP1, SF1, SF3A1, SF3B1, SMC1A, SRSF2, STAG2, TBL1XR1, TET2, TP53, TPMT, U2AF1, U2AF2, WT1, XPO1, ZMYM3, and ZRSR2) (TruSeq Custom Amplicon, Illumina Inc.) based on previously described analyses [12,13].
Neuroblastoma in adolescents and adults has been reported to lack MYCN oncogene amplification, which occurs in 20-30% of younger children.
The editors have organized the contributions that make up the main body of the text in seven parts devoted to genomic alterations, targeting MYCN, apoptosis and angioneogenesis, molecular-targeted therapy studies, immunology, minimal residual disease, and a wide variety of other related subjects.
Neuroblastoma cells can actively eliminate supernumerary MYCN gene copies by micronucleus formation--sign of tumour cell revertance?