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e11542 Background: BRCA1 mutation is associated with the TNBC phenotype. Loss of BRCA1, due to genetic mutation or post-genomic inactivation, should confer susceptibility to DNA-damaging agents, such as anthracyclines, but resistance to mitotic-spindle poisons such as taxanes. However, optimal adjuvant systemic therapy for TNBC is difficult to define because of a lack of prospective data in TNBC restricted populations. As our neo-adjuvant regimen changed in 2008 (A followed by D before 2008 then D followed by A from 2008); we were able to compare retrospectively A and D efficacy in matched cohorts of TNBC treated in neo-adjuvant setting. Methods: Group 1 includes 24 patients with TNBC treated between 2005 and 2008 with A followed by D (3x 5FU 500 mg/m², epirubicine 100 mg/m², cyclophosphamide 500 mg/m² followed by 3x docetaxel 100 mg/m²). Group 2 includes 24 patients with TNBC treated in NAS between 2008 and 2011 with D followed by A. Characteristics of group 1 and 2 (median age at diagnosis, tumor grade, Ki67, TNM) were similar. All patients had a core-biopsy before chemotherapy. Chemotherapy response was evaluated by CT scan before 1st cycle, between 3rd and 4th cycle then after the 6th cycle. Surgery was performed 4 weeks after the 6th cycle. Results: In group 1, objective response rate after 3 cycles was 58% (14/24) (RECIST criteria). There was no progression. Complete pathological response rate (no residual invasive and in-situ tumor in breast, no tumor in axillary nodes) was 25%. In group 2, objective response rate after 3 cycles was 25% (6/24). Progression rate was 13% (3/24). Complete pathological response rate was 29%. The objective response rate after the first three cycles was significantly different between group 1 and group 2 (two-sided p-value = 0,039, Fisher exact test). Conclusions: Our retrospective analysis showed that docetaxel was significantly less efficient than anthracycline-based chemotherapy in chemo-naïve TNBC patients. These data should be taken in consideration for clinical practice and further phase III trials design in TNBC.

Abstract #207 BACKGROUND. Pure tubular carcinoma (PTC) is a favourable histologic subtype of breast cancer with a low rate of lymph node involvement. This study was initiated to assess the sentinel lymph node (SLN) detection rate and the rate of axillary involvement. METHODS. Inclusion criteria were a PTC (tubular component >90%) core biopsy diagnosed breast cancer smaller than 20 mm, and a homolateral clinically axilla free of nodal involvement. Patients underwent a SLND alone or with an Axillary level I-II Lymphadenectomy (AL). An AL was performed in the case of the learning curve, or in the case of SLN involvement – macrometastases, micrometastases or isolated cells - or in the case of mapping failure. RESULTS. From January 1999 to December 2006, 234 patients were selected from 9 French Comprehensive Cancer Centers. Median tumour size was 9.59 mm (1-22) . The SLN detection rate was 97.9% (229/234). The median number of SLN harvested was 2.15 (range 0-8). Respectively the frequency of macrometastasis - >2mm - was 2.6% (6/229), micrometastasis was 6.5% (15/229) and isolated cells was 0.8% (2/229). There were no false negative cases among the 24 patients with a systematic complementary axillary lymphadenectomy performed in the case of a learning curve. Axillary macrometastasis were found in non sentinel lymph nodes after completed axillary lymphadenectomy in 3 / 6 patients with macrometastasis, in 1/15 patients with micrometastasis and in 0/2 patients with isolated cells. There was no lymph node involvement for tumour size < 10mm. Pathological tumor size >10 mm was statistically correlated to the risk of axillary involvement (p=0.0223). CONCLUSIONS. This study confirms that in the case of PTC ≤ 20mm SLN detection is feasible and the risk of lymph node involvement very low. In the case of PTC Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 207.

580 Background: BRCA1 being involved in DNA repair and apoptosis, its mutations may influence response to chemotherapy. In vitro studies demonstrated that loss of BRCA1 function increased sensitivity to platinum compounds and induced resistance to anthracyclines. BRCA1-related breast cancers tend to be ductal carcinomas with high tumor grade, absence of hormonal receptors and no HER2 overexpression, so called triple-negative. We retrospectively analyzed anthracycline-based neoadjuvant chemotherapy efficacy in triple- negative tumors according to BRCA1 status. Methods: 393 breast cancer pts were treated with FEC100 neoadjuvant chemotherapy (FU 500 mg/m2, epirubicine 100 mg/m2, cyclophosphamide 500 mg/m2) between 1/2000 and 12/2006. Out of them, 14% had a triple-negative phenotype (55 pts). Patients with young age at diagnosis or family history of breast cancer were offered genetic testing for BRCA1 and BRCA2 mutations. Twelve of these patients had a BRCA1 deleterious mutation with a triple-negative tumor. Characteristics of these 12 pts at diagnosis were: median age = 38, tumor stage = 7 T2N0, 2 T2N1, 2 T3N0, 1 T3N1. Results: Pathological complete response was defined as absence of invasive tumor in breast and axillary nodes. After 6 cycles of FEC100, 42% of patients with triple-negative tumors (23/55) had a pathological complete response, compared to 17% (2/12) with a BRCA1 mutation. Only one of the 12 BRCA1 patients had an axillary node involvement. Conclusions: In our series, BRCA1 deleterious mutations decreased anthracycline-based chemotherapy efficacy in triple- negative breast cancers. Platinum compounds should be evaluated in these BRCA1-related tumors. No significant financial relationships to disclose.

The authors report a cheap, simple, reliable and reproducible technique of breast specimen lumpectomy orientation.