No abstract

No abstract

No abstract

Introduction: Approximately 25–30% of breast cancers are assumed to be HER-2/neu positive. It is well known that HER-2/neu-positive cancers after treatment with trastuzumab can become HER-2/neu negative. Change in HER-2/neu status from negative to positive following treatment has not been well studied. We describe a patient with inflammatory breast cancer who was initially HER-2/neu negative but became positive after treatment. A 59-year-old postmenopausal white female saw her surgeon for violaceous discoloration of the left breast for 4 months. The surgeon palpated a mass measuring 6 cm in the patient’s left breast. Additionally, there was violaceous discoloration involving two thirds of the breast. Biopsy of the breast mass and skin revealed inflammatory breast cancer. The tumor was estrogen receptor positive, progesterone receptor positive and HER-2/neu negative. The patient was given four cycles of chemotherapy with cyclophosphamide, doxorubicin and docetaxol. She subsequently underwent a mastectomy, excision of the skin over the chest wall and axillary node dissection. Of the axillary lymph nodes, 14/14 were involved. The tumor was still estrogen receptor positive and progesterone receptor positive, but HER-2/neu was 2+ by immunohistochemistry and amplified at 3.3 as detected by fluorescent in situhybridization. The patient received trastuzumab along with chemotherapy followed by radiation therapy and letrozole. She is currently receiving trastuzumab and letrozole in the adjuvant setting and appears to be doing well. Conclusion: A breast cancer which was initially HER-2/neu negative can become positive following treatment. Therefore, re-biopsy may be necessary during the course of treatment of breast cancer to re-assess the HER-2/neu status. This gives the clinician the opportunity to include drugs like trastuzumab and lapatinib in the treatment of patients with a transformation to HER-2/neu-positive cancer.

8044 Background: The eLung trial randomized chemotherapy naïve advanced NSCLC patients (pts) to 1 of 3 PD and concurrent CET followed by CET maintenance until progression, stratified by non-squamous (NSQ) and squamous (SQ) histology. Primary outcome results were reported (ESMO, Schwartzberg 2012). Pre-treatment tumor tissue and serum samples were prospectively collected. Methods: Tumor samples were analyzed for H-score (graded 0-300), calculated by the intensity and number of cells expressing EGFR by IHC; a score of >200 was considered high (Pirker 2011). Mutation analysis of EGFR and KRAS was performed by PCR. The VeriStrat multivariate serum protein test was performed on available serum samples assigning good and poor classifications (Taguchi 2007). Results: Of 601 pts enrolled on the trial, 378 consented to blood/tissue or both. The available tissue (N=210) and serum subsets (N=203) had similar demographics and survival outcome to the full trial set. Results for biomarkers/cohorts in the Table demonstrate that VeriStrat was highly significant for OS in all pts and NSQ, while H-score and EGFR mutations were significant only in NSQ. In adjusted Cox analysis VeriStrat was an independent predictor for OS, HR=.665, p=.026; H-score was not. Conclusions: VeriStrat classification significantly correlated with survival outcome in all pts treated with PD and CET and the NSQ subset; tissue biomarkers correlated in NSQ only. Further evaluation of these markers is warranted. [Table: see text]