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Analysis of MYB expression and MYB-NFIB gene fusions in adenoid cystic carcinoma and other salivary neoplasms

Artikel i vetenskaplig tidskrift
Författare L. B., 2nd Brill
W. A. Kanner
Andre Fehr
Ywonne Andrén
C. A. Moskaluk
T. Loning
Göran Stenman
H. F., Jr. Frierson
Publicerad i Modern Pathology
Volym 24
Nummer/häfte 9
Sidor 1169-76
ISSN 1530-0285
Publiceringsår 2011
Publicerad vid Institutionen för biomedicin, avdelningen för patologi
Sidor 1169-76
Språk en
Länkar dx.doi.org/10.1038/modpathol.2011.8...
Ämnesord Adult, Aged, Carcinoma, Adenoid Cystic/*genetics/metabolism, Female, Genes, myb, Humans, Immunohistochemistry, Male, Middle Aged, Oncogene Proteins v-myb/*biosynthesis/genetics, Oncogene Proteins, Fusion/*genetics, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Salivary Gland Neoplasms/*genetics/metabolism, Tumor Markers, Biological/analysis/genetics, Young Adult
Ämneskategorier Cell- och molekylärbiologi

Sammanfattning

Recent studies have shown that the recurrent t(6;9)(q22-23;p23-24) translocation in adenoid cystic carcinoma results in a novel fusion of the MYB proto-oncogene with the transcription factor gene NFIB. To determine the frequency of this finding, we used RT-PCR assays of the MYB and MYB-NFIB fusion transcripts, and immunohistochemistry for the MYB protein, to study adenoid cystic carcinomas and other epithelial tumors of the salivary glands, and head and neck region. MYB-NFIB fusion transcript was detected in 25 of 29 (86%) frozen adenoid cystic carcinoma tumor samples, and in 14 of 32 (44%) formalin-fixed paraffin-embedded adenoid cystic carcinoma tumor specimens. In contrast, the MYB-NFIB fusion was not expressed in non-adenoid cystic carcinoma neoplasms of the head and neck, confirming the high specificity of the MYB-NFIB fusion. Adenoid cystic carcinomas from various anatomic sites, including salivary gland, sinonasal cavity, tracheobronchial tree, larynx, breast, and vulva were repeatedly fusion-positive, indicating that adenoid cystic carcinomas located in different anatomic sites not only have important morphologic features in common, but also probably evolve through activation of the same molecular pathways. Studies of the expression of MYB revealed that 89% of the tumors, including both fusion-positive and fusion-negative cases, overexpressed MYB RNA. Similarly, 82% of adenoid cystic carcinomas stained positive for MYB protein, compared with 14% of non-adenoid cystic carcinoma neoplasms, indicating that MYB immunostaining may be useful for the diagnosis of adenoid cystic carcinoma, but that neoplasms sometimes in the differential diagnosis are also labeled. The latter are, however, fusion-negative. In summary, our studies show that MYB activation through gene fusion or other mechanisms is a major oncogenic event in adenoid cystic carcinoma occurring at various anatomic sites. In addition to being a diagnostically useful biomarker for adenoid cystic carcinoma, MYB and its downstream effectors are also novel potential therapeutic targets.

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