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ABSTRACTSince English has become the dominant global language, research efforts have mostly concentrated on spoken English as a lingua franca (ELF). Written ELF is largely under-researched both in relation to translation and otherwise. This study examines ‘before and after’ texts made available by the European Parliament’s Editing Unit. The original texts were written by non-native English speakers (before) and subsequently revised by native English editors (after) with a view to delivering consistent edited source texts as a basis for translation into different EU languages. In a pre-study, 12 texts (and their edited versions) were scrutinised for potentialtranslation problems. In the main study, three of the 12 originals and their three edited counterparts were translated by six professional translators. A mixed-method approach was adopted: product-based analysis of the translations for actualtranslation problems combined with screen-recording-prompted retrospective translator comments and screen-recording-based indicators for the time taken to translate edited and non-edited segments. The results suggest that there is a sufficiently large number of challenges arising from non-standard source segments to prolong translational decision-making and provoke inadequate solutions.

Telomerase reactivation and immortalization are critical for human carcinoma progression. However, little is known about the mechanisms controlling this crucial step, due in part to the paucity of experimentally tractable model systems that can examine human epithelial cell immortalization as it might occur in vivo. We achieved efficient non-clonal immortalization of normal human mammary epithelial cells (HMEC) by directly targeting the 2 main senescence barriers encountered by cultured HMEC. The stress-associated stasis barrier was bypassed using shRNA to p16INK4; replicative senescence due to critically shortened telomeres was bypassed in post-stasis HMEC by c-MYCtransduction. Thus, 2 pathologically relevant oncogenic agents are sufficient to immortally transform normal HMEC. The resultant non-clonal immortalized lines exhibited normal karyotypes. Most human carcinomas contain genomically unstable cells, with widespread instability first observed in vivoin pre-malignant stages; in vitro, instability is seen as finite cells with critically shortened telomeres approach replicative senescence. Our results support our hypotheses that: (1) telomere-dysfunction induced genomic instability in pre-malignant finite cells may generate the errors required for telomerase reactivation and immortalization, as well as many additional “passenger” errors carried forward into resulting carcinomas; (2) genomic instability during cancer progression is needed to generate errors that overcome tumor suppressive barriers, but not required per se; bypassing the senescence barriers by direct targeting eliminated a need for genomic errors to generate immortalization. Achieving efficient HMEC immortalization, in the absence of “passenger” genomic errors, should facilitate examination of telomerase regulation during human carcinoma progression, and exploration of agents that could prevent immortalization.