Although Burkitt’s lymphoma is thankfully fairly rare in the general population, it is the most common form of malignancy in children in Equatorial Africa and is very frequent in immunocompromised persons, such as those suffering from AIDS. It is invariably accompanied by an increase in the expression of a particular gene, the so-called c-myc gene. An increased level of c-myc is not usually enough to cause cancer and most patients also have alterations to another gene. The groups of Dr. Veronika Sexl at the University of Veterinary Medicine, Vienna (Vetmeduni Vienna), and Dr. Dagmar Stoiber at the Ludwig Boltzmann Institute for Cancer Research, Vienna, have recently provided important new information on how the nature of the additional alterations shapes the course and onset of disease. The results are published in the October 27, 2011 issue of the journal Blood and are of immediate relevance to lymphoma treatment. The human c-myc gene encodes a transcription factor (MYC) involved in the regulation of a vast number of other genes – it has been estimated that the transcription of about one in six genes is somehow under the control of MYC. Perhaps because of MYC’s wide range of targets, mutations of the c-myc gene are frequently associated with a variety of tumors, not only with Burkitt’s lymphoma. Mutations that lead to excessive amounts of the MYC protein are particularly threatening. It has long been known that Burkitt’s lymphoma only develops when MYC is mutated or overexpressed, although experiments in mice have shown that some animals live quite happily and healthily with higher levels of the MYC protein. This observation is consistent with the “second hit” model for the origin of cancer: as well as a change to c-myc, a second gene must also be disturbed before disease is initiated.
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