The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Aryl hydrocarbon receptor mediates sensitivity of MCF-7 breast cancer cells to antitumor agent 2-(4-amino-3-methylphenyl) benzothiazole.
Andrea I Loaiza-Pérez; Valentina Trapani; Curtis Hose; Sheo S Singh; Jane B Trepel; Malcolm F G Stevens; Tracey D Bradshaw; Edward A Sausville (Profiled Author: Edward A Sausville)
Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. email@example.com
Molecular pharmacology 2002;61(1):13-9.
2-(4-Amino-3-methylphenyl) benzothiazole (NSC 674495; DF 203) demonstrates drug uptake and metabolism by tumor cells sensitive to the antiproliferative activity of the drug [J Med Chem 1999;42:4172-4184]. In insensitive cells, little metabolism occurs. Because CYP1A1 can metabolize DF 203, the aryl hydrocarbon receptor (AhR) may mediate drug action. We demonstrate here that DF 203 increases CYP1A1 and CYP1B1 transcription in sensitive MCF-7 cells, accompanied by AhR translocation to the nucleus, increase in xenobiotic-responsive element (XRE)-driven luciferase activity, and induction of protein/DNA complexes on the XRE sequence of the CYP1A1 promoter. MDA-MB-435 and PC3 cells, resistant to DF 203, did not show drug-induced CYP1A1 and CYP1B1 gene expression. AhR was observed to be constitutively localized in the nucleus, with no induction of XRE-driven luciferase activity in transiently transfected cells and weak or no induction of protein/DNA complexes on the XRE sequence of CYP1A1. Taken together, these data elucidate a novel basis for antitumor drug action: induction in sensitive cells of a metabolizing system for the drug itself. These results suggest that clarification of the basis for differential engagement of AhR-related signaling in different tumor cell types may aid in further preclinical development and perhaps early clinical studies.
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V Trapani; V Patel; C-O Leong; H P Ciolino; G C Yeh; C Hose; J B Trepel; M F G Stevens; E A Sausville; A I Loaiza-PérezBritish journal of cancer 2003;88(4):599-605.
M S Chua; E Kashiyama; T D Bradshaw; S F Stinson; E Brantley; E A Sausville; M F StevensCancer research 2000;60(18):5196-203.
Andrea I Loaiza-Pérez; Susan Kenney; Jamie Boswell; Melinda Hollingshead; Michael C Alley; Curtis Hose; Henry P Ciolino; Grace C Yeh; Jane B Trepel; David T Vistica; et al.Molecular cancer therapeutics 2004;3(6):715-25.
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