Abstract

Abstract Background: In estrogen receptor positive (ER+) tumors, a low proliferative index (Ki-67) two weeks into endocrine therapy predicts response. FLT PET non-invasively measures tumor proliferation in vivo. The pre-operative window is an opportunity to assess impact of systemic therapies. We tested associations between FLT PET qualitative and quantitative measures and Ki-67 following two weeks of aromatase inhibitor (AI) therapy. Methods: Women with clinical stage I-II ER+ HER2– breast cancer underwent “run-in” of AI monotherapy prior to definitive surgery. Premenopausal women were given GNRH agonist treatment 2 W prior to AI therapy. FLT PET was performed before AI therapy, and 1-7 days before surgery. Ki-67 was measured in baseline core biopsy and surgical specimens. Results: Fourteen patients (8 postmenopausal, 6 premenopausal) have been enrolled. All have undergone baseline FLT PET imaging; 11 have completed imaging and surgery, including one premenopausal patient with no residual invasive carcinoma following 26 days of AI therapy. The majority harbored ductal carcinomas (n = 9, 5 with lobular histology) with the majority histologic grade ≥ 2 (n = 11). The median number of days exposed to AI was 19 (range, 9-42). Baseline SUVmax ranged from 1.2 to 3.9 (median 2.2), and post run-in SUV (6-64 days later) ranged from 1.2 to 2.8 (median 1.8). Baseline Ki-67 ranged from 6-26.2, median 11.6; surgical Ki-67 post AI therapy ranged from 0- 20.3 median 3.7, with seven below 5%. SUV and flux declined in most patients, as did Ki-67. Quantitative FLT flux correlated with tumor response assessed by proliferative index (Ki-67) before the “run-in” period, with a stronger correlation at surgery, Pearson correlation coefficients = 0.41 and 0.82, respectively. FLT SUV and qualitative changes were not strongly associated with Ki-67. Conclusions: Both pre and postmenopausal women with early stage breast cancer showed imaging and tissue response to endocrine therapy. Quantitative, but not qualitative FLT is a promising tool to assess tumor proliferation and response to therapy. Accrual is ongoing and updated results will be reported. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P4-01-02.

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