Priority Research Papers:

The impact of the MYB-NFIB fusion proto-oncogene in vivo

Oliver R. Mikse, Jeremy H. Tchaicha, Esra A. Akbay, Liang Chen, Roderick T. Bronson, Peter S. Hammerman and Kwok-Kin Wong _

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Oncotarget. 2016; 7:31681-31688. https://doi.org/10.18632/oncotarget.9426

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Oliver R. Mikse1,2,3, Jeremy H. Tchaicha1,2,3, Esra A. Akbay1,2,3, Liang Chen1,2,3, Roderick T. Bronson4, Peter S. Hammerman1,2,5 and Kwok-Kin Wong1,2,3,6

1 Department of Medicine, Dana Farber Cancer Institute, Boston, Massachusetts, USA

2 Harvard Medical School, Boston, Massachusetts, USA

3 Ludwig Institute for Cancer, Cambridge, Massachusetts, USA

4 Department of Microbiology and Immunobiology, Division of Immunology, Harvard Medical School, Boston, Massachusetts, USA

5 The Broad Institute, Cambridge, Massachusetts, USA

6 Belfer Institute for Applied Cancer Science, Boston, Massachusetts, USA

Correspondence to:

Kwok-Kin Wong, email:

Keywords: MYB-NFIB, adenoid cystic carcinoma, breast, salivary, GEMM

Received: November 30, 2015 Accepted: April 11, 2016 Published: May 18, 2016


Recurrent fusion of the v-myb avian myelobastosis viral oncogene homolog (MYB) and nuclear factor I/B (NFIB) generates the MYB-NFIB transcription factor, which has been detected in a high percentage of individuals with adenoid cystic carcinoma (ACC). To understand the functional role of this fusion protein in carcinogenesis, we generated a conditional mutant transgenic mouse that expresses MYB-NFIB along with p53 mutation in tissues that give rise to ACC: mammary tissue, salivary glands, or systemically in the whole body. Expression of the oncogene in mammary tissue resulted in hyperplastic glands that developed into adenocarcinoma in 27.3% of animals. Systemic expression of the MYB-NFIB fusion caused more rapid development of this breast phenotype, but mice died due to abnormal proliferation in the glomerular compartment of the kidney, which led to development of glomerulonephritis. These findings suggest the MYB-NFIB fusion is oncogenic and treatments targeting this transcription factor may lead to therapeutic responses in ACC patients.

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