article Open AccessTop 1% cited

Mechanisms of Tamoxifen Resistance: Increased Estrogen Receptor-HER2/neu Cross-Talk in ER/HER2-Positive Breast Cancer

JNCI Journal of the National Cancer Institute · 2004 · Vol. 96(12) · pp. 926–935

Jianzhong Shou✉(Baylor College of Medicine)Suleiman MassarwehC. K. OsborneA. E. WakelingSimak AliHelen A. WeissRachel Schiff

View via DOI Full-text PDF

Abstract

Tamoxifen behaves as an estrogen agonist in breast cancer cells that express high levels of AIB1 and HER2, resulting in de novo resistance. Gefitinib's ability to eliminate this cross-talk and to restore tamoxifen's antitumor effects should be tested in the clinic.

Estrogen and related hormone effects HER2/EGFR in Cancer Research Cytokine Signaling Pathways and InteractionsTamoxifenCancer researchEstrogen receptorCoactivatorBiologyChromatin immunoprecipitationEstrogen receptor alphaEndocrinologyInternal medicineBreast cancer

MeSH terms

GefitinibAnimalsBreast NeoplasmsEnzyme InhibitorsEpidermal Growth FactorFemaleHumansMice, Inbred BALB CMice, NudePhosphorylationProtein-Tyrosine KinasesQuinazolinesReceptors, EstrogenTamoxifenTransplantation, Heterologous

Citations

1,165

FWCI

44.01

field-weighted impact

References

Percentile

100%

vs. same field & year

Citations per year

Cited by

Drug Resistance in Cancer: An Overview