Correlation between MYC gene rearrangement and MYC protein expression suggests that MYC regulation is more complex than previously known

Since its discovery in the 1970's, MYC oncoprotein has been continuing to fascinate the scientific world and there is a growing interest in the role of MYC in the genesis and prognosis of cancer. Initially MYC was identified as the cellular homologue of the MC29 transforming avian retrovirus. Shortly hereafter, additional related sequences were identified, suggesting that MYC might be part of a larger family of genes. The constellation of MYC effects on genes involved in proliferation has led to the concept of MYC-driven lymphomas, that include Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL), and lymphomas that share morphologic features of DLBCL and BL, officially termed B-cell lymphoma, unclassifiable, with features intermediate between DLBCL and BL (BCLU). Other lymphomas showing MYC over-expression comprises Plasmablastic lymphoma and Plasmacytoma, Double hit/triple hit lymphomas and Anaplastic lymphomas Kinase-positive Large B-cell Lymphoma. MYC aberrations can be detected by standard cytogenetics, interphase fluorescence in situ hybridization (FISH), comparative genomic hybridization and most recently immunohistochemistry. By comparing expression profiles of MYC gene rearrangement and MYC protein expression has came up that MYC gene rearrangements do not necessarily correlate with MYC protein expression. In fact, by applying immunoistochemistry, the frequency of MYC protein expression appears much higher than what is detected by FISH standard method. Therefore, nowadays the key problem in the hematopathology field is to define the clinical impact of the double-expressor lymphoma status. The updated World Health Organization (WHO) of tumours of hematopoietic and lymphoid tissues asses that the status of double or triple lymphoma should rely only on molecular biology findings and not on immunohistochemistry results.