Transcriptomic and functional studies of fusion oncogene-driven salivary gland tumors

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These findings highlight the role of NFIB as a fusion partner gene in both benign and malignant SGTs and indicate that NFIB can activate both PLAG1 and HMGA2 by gene

Previous studies of PA have revealed recurrent chromosomal rearrangements that activate the key oncogenes PLAG1 and HMGA2 by gene fusion events.. Here, detailed studies of

lar localization of peroxidase activity in different submandibular glands, and to study the mechanisms for release of the enzyme. The following questions were initially raised

Without the lysine residue involved in ATP binding in the D2 domain one would expect considerably lower hydrolytic activity, and as seen in figure 3.13, this is very much the

Recent studies show that mutation in these channels could lead to loss of selectivity of these channel allowing ions like Na + to pass in producing same effect like K + leading

Here we have used a combination of genomic techniques, including spectral karyotryping, FISH and high-resolution oligonucleotide array CGH, to (i) identify novel gene

Key words: chromosome translocation, fusion oncogene, MYB, NFIB, CRTC1, MAML2, salivary gland, breast, adenoid cystic carcinoma, mucoepidermoid carcinoma,