Background Adenoid cystic carcinoma is a locally aggressive salivary gland neoplasm which has a poor long term prognosis. A chromosomal translocation involving the genes encoding the transcription factors MYB and NFIB has been recently discovered in these tumors. Methods MYB translocation and protein expression was studied in 37 adenoid cystic carcinomas, 112 other salivary gland neoplasms, and 409 non salivary gland neoplasms by FISH and immunohistochemistry. MYB translocation and expression status in adenoid cystic carcinoma was correlated with clinicopathologic features including outcome, with a median follow up of 77.1 months (range: 23.2–217.5) for living patients. Results A balanced translocation between MYB and NFIB is present in 49% of adenoid cystic carcinomas but is not identified in other salivary gland tumors or non-salivary gland neoplasms. There is no apparent translocation of MYB in 35% of the cases. Strong Myb immunostaining is very specific for adenoid cystic carcinomas but is only present in 65% of all cases. Interestingly, Myb immunostaining is confined to the basal cell component though the translocation is present in all the cells. Neoplasms with MYB translocation demonstrate a trend towards higher local relapse rates, but the results are not statistically significant with current case numbers. Conclusions MYB translocation and expression are useful diagnostic markers for a subset of adenoid cystic carcinomas. The presence of the translocation may be indicative of local aggressive behavior but a larger cohort may be required to demonstrate statistical significance.

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The genome of the replication-defective avian myeloblastosis virus (AMV) contains an inserted cellular sequence (amy) that is part of the oncogene responsible for acute myeloblastic leukemia in chickens infected with AMV. Three antisera raised against distinct synthetic peptides predicted from the long open reading frame of amy specifically precipitated the same 48-kilodalton protein (p48amn) from leukemic myeloblasts but not from normal hematopoietic tissue, fibroblasts, or from fibroblasts infected with the AMV helper virus, MAV-1 (myeloblastosis-associated virus type 1). p48arv is not glycosylated or phosphorylated and does not appear to act as a protein kinase in vitro. The same three antisera that recognized p48a"v also specifically precipitated a common 110-kilodalton protein from normal uninfected hematopoietic tissue. This normal cellular homologue of the AMV leukemogenic protein, plIOProtomv, was not present in normal fibroblasts, MAV-1 infected fibroblasts, or, interestingly, in some leukemic myeloblasts. We conclude that p48aamv is the leukemogenic product of an altered, transduced, partial protooncogene. Short helper-virus sequences provide its carboxyl terminus and also may provide the amino terminus.

Antibodies directed against a bacterial fusion protein that contains the domain encoded by the highly evolutionarily conserved 5' one-third of the v-myb oncogene of avian myeloblastosis virus (AMV) detect the protein products of various members of the myb gene family. Immunoprecipitation or immunoblot analyses with these antibodies yielded the following information. First, the products of the v-myb oncogenes of AMV (p48v-myb) and of E26 virus (p135gag-mybets) contain this highly conserved amino acid sequence, as previously hypothesized. Second, p75c mYb, the product of the chicken c-myb protooncogene, also contains this protein domain. Third, these antibodies have identified the products of the human, murine, and Drosophila c-myb genes, which were all found to be nuclear proteins of Mr 75,000-80,000. The human c-myb protein product is present in immature cells of the erythroid, myeloid, and lymphoid lineages.