The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
t(11;19)(q21;p13) translocation in mucoepidermoid carcinoma creates a novel fusion product that disrupts a Notch signaling pathway
Open accessAbstract
Truncation of Notch1 has been shown to cause a subtype of acute leukemia, and activation of Notch4 has been associated with mammary and salivary gland carcinomas of mice. Here we identify a new mechanism for disrupting Notch signaling in human tumorigenesis, characterized by altered function of a new ortholog of the Drosophila melanogaster Notch co-activator molecule Mastermind. We cloned the t(11;19) translocation that underlies the most common type of human malignant salivary gland tumor. This rearrangement fuses exon 1 from a novel gene of unknown function at 19p13, termed mucoepidermoid carcinoma translocated 1 (MECT1), with exons 2–5 of a novel member of the Mastermind-like gene family (MAML2) at 11q21 (ref. 3). Similar to D. melanogaster Mastermind and MAML1 (refs. 4,5), full-length MAML2 functioned as a CSL (CBF-1, suppressor of hairless and Lag-1)-dependent transcriptional co-activator for ligand-stimulated Notch. In contrast, MECT1–MAML2 activated transcription of the Notch target gene HES1 independently of both Notch ligand and CSL binding sites. MECT1–MAML2 induced foci formation in RK3E epithelial cells, confirming a biological effect for the fusion product. These data suggest a new mechanism to disrupt the function of a Notch co-activator in a common type of malignant salivary gland tumor.
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Cited by
Notch signaling: simplicity in design, versatility in function
Andersson, E. R., Sandberg, R., & Lendahl, U. (2011) · Development · doi:10.1242/dev.063610 · Cited by 950
The Varied Roles of Notch in Cancer
Aster, J. C., Pear, W. S., & Blacklow, S. C. (2017) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-052016-100127 · Cited by 710
Notch1 and Notch2 Have Opposite Effects on Embryonal Brain Tumor Growth
Fan, X., Mikolaenko, I., Elhassan, I., Ni, X., Wang, Y., Ball, D., Brat, D. J., Perry, A., & Eberhart, C. G. (2004) · Cancer Research · doi:10.1158/0008-5472.can-04-1446 · Cited by 382
Fouladi, M., Stewart, C. F., Olson, J., Wagner, L. M., Onar-Thomas, A., Kocak, M., Packer, R. J., Goldman, S., Gururangan, S., Gajjar, A., et al. (2011) · Journal of Clinical Oncology · doi:10.1200/jco.2011.35.7806 · Cited by 164
Fusion genes and chromosome translocations in the common epithelial cancers
Edwards, P. A. (2010) · The Journal of Pathology · doi:10.1002/path.2632 · Cited by 126
Metadata
- Authors
- Tonon, G., Modi, S., Wu, L., Kubo, A., Coxon, A. B., Komiya, T., O'Neil, K., Stover, K., El-Naggar, A., Griffin, J. D., Kirsch, I. R., & Kaye, F. J.
- Venue
- Nature Genetics
- Published
- 2003-01-21
- Volume
- 33
- Issue
- 2
- Pages
- 208-213
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W2060525726
- Cited by
- 567
- References
- 24
- FWCI
- 15.98
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: t(11;19)(q21;p13) translocation in mucoepidermoid carcinoma creates a novel fusion product that disrupts a Notch signaling pathway. https://app.cochat.ai/papers/10.1038/ng1083
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- Tonon, G., Modi, S., Wu, L., Kubo, A., Coxon, A. B., Komiya, T., O'Neil, K., Stover, K., El-Naggar, A., Griffin, J. D., Kirsch, I. R., & Kaye, F. J. (2003). t(11;19)(q21;p13) translocation in mucoepidermoid carcinoma creates a novel fusion product that disrupts a Notch signaling pathway. Nature Genetics. https://doi.org/10.1038/ng1083
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