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Tamoxifen improved survival for ER-positive patients with high levels of ER-alpha S118-P

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Patients whose ER-positive breast tumors had high levels of phosphorylation of ER-alpha serine-118-P had a significant recurrence-free survival while assigned to adjuvant tamoxifen.

Approximately 50% of breast carcinomas are resistant to tamoxifen. Preclinical studies have shown that ER-alpha S118-P is required for response to tamoxifen.

A group of European researchers evaluated the predictive and prognostic capacity of ER-alpha S118-P in a randomized, phase-2 trial. Premenopausal patients with stage II breast cancer (n=239) were treated from January 1986 through September 1991 at two clinics in Sweden. Patients were randomly assigned to two years of adjuvant tamoxifen or no systemic treatment.

Compared with patients in the untreated group, researchers observed that patients assigned to tamoxifen whose tumors had high ER-alpha S118-P expression had improved recurrence-free survival, 23.7 recurrences per 1,000 person-years vs. 72.2 recurrences per 1,000 person-years, (HR for recurrence=0.36; 95% CI, 0.20-0.65). They did not find the same trend in patients with low ER-alpha S118-P expression, 51.0 recurrences per 1,000 person-years vs. 57.0 recurrences per 1,000 person-years (HR=0.87; 95% CI, 0.51-1.48).

ER-alpha S118-P expression was not associated with recurrence-free survival in the untreated group (HR=1.23; 95% CI, 0.76-1.99).

The researchers concluded that, if these observations are confirmed by further study, the use of ER-alpha S118-P expression as a biomarker could have a significant impact on patients with breast cancer. Offering tamoxifen to the 52% of patients with high ER-alpha S118-P expression could result in a 10-year recurrence-free survival of 64% for those patients.

“Consequently, treatment guided by ER-alpha S118-P status may save unnecessary treatment for half of the premenopausal breast cancer patients with ER-positive tumors while maintaining approximately the same 10-year recurrence-free survival,” they wrote.

Kok M. J Natl Cancer Inst. 2009;doi:10.1093/jnci/djp412.

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