Judith Scheliga focuses on elucidating the biochemical pathways controlled by eIF3e and on linking its loss during breast carcinogenesis to its potential role in stress-specific translation and apoptosis. The putative tumor suppressor Int6/eIF3e, a conserved subunit of the translation initiation factor eIF3, was first identified as an integration site for the mouse mammary tumor virus (MMTV), whereupon a truncated, oncogenic version of the protein is expressed (designated Int6sh), leading to mammary tumor formation. Several studies have implicated the protein in breast tumorigenesis, while the underlying mechanism remains unknown.