Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 123, Issue 7, Pages 2783-2785Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI69070
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Funding
- NCI NIH HHS [P30 CA044579] Funding Source: Medline
- NIDCR NIH HHS [RC1-DE020687, RC1 DE020687, RFP NHLBI-DE-09-10] Funding Source: Medline
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Adenoid cystic carcinoma (ACC), a relatively rare malignancy usually of salivary gland origin, has a signature v-myb avian myeloblastosis viral oncogene homolog-nuclear factor I/B (MYB-NFIB) gene fusion that activates MYB transcriptional regulatory activity. A new study in this issue by Stephens et al. is a comprehensive genomic mutation profiling analysis of this neoplasm and documents a common theme of alteration in chromatin regulatory genes. Also, mutations in SPEN (split ends, homolog of Drosophila), which encodes an RNA-binding coregulatory protein, suggest that other changes in transcriptional regulation may involve the NOTCH, FGFR, or other signaling pathways in which SPEN participates. Since there is a low prevalence of mutations in common oncogenes and tumor-suppressor genes, it is likely that alterations primarily in specific transcriptional regulatory genes, augmented by changes in chromatin structure, drive the neoplastic process in ACC.
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