Testis specific gene expression drives disease progression and Rituximab resistance in lymphoma

Activation of cancer promoting genes or silencing of tumour suppressors is often due to aberrant expression of transcription factors or transcriptional regulators; interestingly, the expression of many of these transcriptional regulators is usually restricted to male germ cells (Rousseaux et al, 2013; Simpson et al, 2005). The similarities between germ cell development and cancer have long been noted and resulted in the identification of a number of cancer/testis antigens such as the MAGE family members (Simpson et al, 2005). Although the biological function of many of the cancer/testis antigens is poorly understood, some are known to act as transcriptional regulators. These discoveries spawned the idea that aberrant expression of germ line genes in somatic cells triggers the activation of a gametogenic programme that drives tumourigenesis. A number of these testis/cancer genes comprise epigenetic regulators that play a key role in male genome reprogramming. BRDT, one such regulator, plays a critical function in