Activation of the oncogenic transcription factor gene MYB is the key genomic event of<unk>  and seen in the vast majority of cases. Most commonly, MYB is activated through gene fusion with the transcription factor encoding NFIB gene as a result of a t(6;9) translocation. Alternatively, MYB is activated by copy number gain or by juxtaposition of enhancer elements in the vicinity of the MYB gene. In a subset of<unk> s, the closely related MYBL1 gene is fused to NFIB or to other fusion partners. MYB drives proliferation of<unk>  cells and regulates genes involved in cell cycle control, DNA replication and repair, and RNA processing. Thus, the MYB oncogene is a potential diagnostic and therapeutic target in<unk> .<unk>  has a relatively quiet genome with few recurrent copy number alterations or point mutations, consistent with the view that MYB and MYBL1 are the main oncogenic drivers of the disease.
Adenoid cystic carcinoma
Bartholin gland carcinoma
Sebaceous carcinoma
Medulloepithelioma
Ceruminous adenoma
Lymphoepithelioma
Laryngeal papillomatosis
Basal cell adenoma