MYCN


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MYCN

A gene on chromosome 2p24.3 that encodes a DNA-binding transcription factor.
 
Molecular pathology
MYCN mutation causes Feingold syndrome; MYCN is amplified in various tumours, especially in neuroblastomas.
References in periodicals archive ?
7] Human genes: MYCN, v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (avian); GALNT3, UDP-N-acetyl-[alpha]-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase 3 (GALNAC-T3); B2M, [[beta].
of tissues 122 Stage 1, 2, 3, 4S 66 (54) 4 56 (46) Age at diagnosis <18 months 56 (46) [greater than or equal to] 18 months 66 (54) MYCN status Not amplified 96 (79) Amplified 26 (21) No.
For MYCN amplification detection, we used a MYCN probe and compared it also against the centromeric probe for chromosome 9.
14) Hybridization signals for the MYCC and MYCN probes were counted in more than 100 nuclei, and the number of chromosome 9 centromeric signals was reported for each nucleus; increases in the number of signals greater than 5 were recorded as amplifications.
With the probes used, each green spot corresponded to the centromere of a single chromosome 9, and each red spot corresponded to the specific probe for MYCC or MYCN (Figure 1, A and B, respectively, and Figure 2).
In this model, although established metastatic neuroblasts exhibit a similar MYCN amplification compared with stage 4 disease-derived neuroblasts, a considerably higher MYCN expression is observed that is consistent with their aggressive biological behavior (10).
Our analysis of GALNTI3 mRNA transcripts in various NB cell lines, as well as in favorable and high-risk neuroblastic tumors, showed that GALNTI3 is highly expressed in malignant neuroblasts but is not correlated with MYCN amplification and/or expression (data not shown).
Coactivation of the MDR1 and MYCN in human neuroblastoma during the metastatic process in the nude mouse.
Patient 19, a 6-year-old boy diagnosed with a stage 4 NB with a 1p deletion and no MYCN amplification, repeatedly tested negative at different time points during therapy.
In all PB and BM samples (n = 6) from patient 26, a 6-month-old girl with a stage 4 NB without MYCN amplification or 1p deletion, residual NB cells were detected by IC, TH QPCR, and/or ELAVL4 QPCR.
MYCN amplification was measured in 49 neuroblastomas, in which the presence of oncogene amplification had previously been tested by a competitive PCR assay based on the use of a synthetic internal standard, as previously described (18,32).
We tested the reproducibility of the external calibration curves for [beta]-actin and MYCN gene determination, evaluating the slope and the correlation coefficient of experimental fitting of the calibration curve in each experiment.