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[Our results also suggest that, whereas EGFr and Ha-ras, both of which act in the same signal transduction cascade, stimulated urothelial hyperplasia, they were not synergistic in urothelial tumorigenesis, and EGFr overexpression can cooperate with p53 and pRB dysfunction (as occurring in SV40T transgenic mice) to promote bladder tumor growth.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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Gene-disease associations inferred from text-mining the literature.
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