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MYCN is a growth-driving gene that some neuroblastomas copy many times over; that amplification is one of the strongest signs the tumour is aggressive and sets the intensity of treatment.
MYCN encodes the N-myc transcription factor, a paralogue of MYC expressed in the developing neural crest. Amplification (many extra copies, detected by FISH) occurs in about 20 percent of neuroblastomas and places a child in the high-risk group of the INRG and COG classifications whatever the age or stage; it also defines a rare aggressive spinal ependymoma group and is amplified in some medulloblastomas and retinoblastomas. There is no approved MYCN-directed drug; the readout page carries the amplification rule and the risk groups that use it.
In plain words · MYCN is a growth-driving gene that some neuroblastomas copy many times over; that amplification is one of the strongest signs the tumour is aggressive and sets the intensity of treatment.
MYCN is a growth-driving gene that some neuroblastomas copy many times over; that amplification is one of the strongest signs the tumour is aggressive and sets the intensity of treatment.
N-myc dimerises with MAX and drives proliferation, ribosome biogenesis and metabolic programmes while repressing differentiation; amplified tumours depend on it and are being targeted indirectly through Aurora A, BET and CDK7 inhibitors.
No product in this corpus aims at MYCN (N-myc) yet. Transcription factors have no pocket to plug, so drugs either degrade them or block the partner protein they need to dock on DNA.
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated more often than chance); what a medicine would aim at or exploit is the altered form or its loss, absent from normal cells; no corpus medicine is aimed at it yet. HPA MYCN: RNA tissue enhanced (brain 6 nTPM, placenta 8 nTPM); no normal tissue stained high. Distribution: 1 cancer family in the corpus carries a prevalence row, label threshold or catalogue link for it (Childhood cancers (all types)); Open Targets associates it with 1 specific cancer type at or above 0.5 (basal cell carcinoma). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: Human Protein Atlas MYCN tissue; Open Targets ENSG00000134323 associations
First described 1985. Earliest sequence paper UniProt cites for the protein: Michitsch R.W. et al, Nucleic Acids Res, 1985, "Nucleotide sequence of the 3' exon of the human N-myc gene". Source.
What a pathology or genomic report can say about this target, each with the thresholds approvals use.
N-myc dimerises with MAX and drives proliferation, ribosome biogenesis and metabolic programmes while repressing differentiation; amplified tumours depend on it and are being targeted indirectly through Aurora A, BET and CDK7 inhibitors.
RNA: tissue enhanced (brain 6 nTPM, placenta 8 nTPM), detected in some normal tissues.
No normal tissue stained high.
RNA cancer enriched: Testicular Germ Cell Tumor 85 pTPM.
No cancer sample stained medium or high.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
Query for this target: (TITLE:"MYCN" OR ABSTRACT:"MYCN" OR TITLE:"N-myc" OR ABSTRACT:"N-myc" OR TITLE:"NMYC" OR ABSTRACT:"NMYC" OR TITLE:"bHLHe37" OR ABSTRACT:"bHLHe37") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about MYCN (N-myc), not a curated reading list.
Shares CIViC, IntOGen, Open Targets Platform and the tag biomarker-parent.
Shares CIViC and the tag biomarker-parent.
Shares CIViC and the tag biomarker-parent.
Shares CIViC, IntOGen, Open Targets Platform, Prostate cancer and the tag biomarker-parent.
Shares MYCN amplification, MYCN amplification, FISH / ISH (in situ hybridisation), High-risk neuroblastoma.
Shares Neuroblastoma (paediatric), CIViC, IntOGen, Open Targets Platform.
Shares Molecular characterisation of neuroendocrine prostate cancer and identification of new drug targets, Treatment-emergent neuroendocrine transformation (recognising it), CIViC, Prostate cancer.
Shares MYCN amplification, High-risk neuroblastoma, Neuroblastoma (paediatric).