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[In summary, a) the molecular mechanism(s) contributing to Tzb resistance in our SKBR3/Tzb100 model appear to be clearly different to those previously reported as we found important transcriptional up-regulatory transcriptional changes in HER2 gene expression levels relative to parental cells; b) since FASN inhibition acts on HER2 gene expression via reduction of its transcription rate, Tzb-conditioned HER2-overexpressing breast cancer cells not only retain but further gain sensitivity to FASN inhibition; and c) transcriptional suppression of HER2 expression using FASN blockers may represent a new molecular strategy in the management of Tzb-resistant breast cancer disease.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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