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ALDH1 expression was determined by immunohistochemistry. Results: The study enrolled 104 women. 52 (50%) were randomised to Arm A and 52 (50%) to Arm B. Most of the women (90%) had ductal carcinoma and 10% had lobular carcinoma. Of these 21 (20%) achieved a pathological complete response (pCR), 22 (21%) had residual node negative disease (pPR) and 61 (59%) had less significant response (NR). There was no correlation between baseline ALDH1 expression and tumour grade, stage, hormone receptor, HER2 status and Ki67 proliferation index. ALDH1 positivity at baseline was significantly associated with NR (p?=?0.012). Moreover, serial measurement in non-responders showed enrichment for ALDH1 expression in sequential tumour specimens (p?=?0.003). Overall there was no difference Obeticholic Acid solubility dmso according FARP1 to the sequence of chemotherapy used, however, women in Arm B showed a relatively higher ALDH1 enrichment after four cycles of taxane therapy. Conclusions: High ALDH1 expression is a predictor of poor pathological response to chemotherapy in breast cancer. Chemotherapy sequence has no effect on overall changes in ALDH1 expression; however, relative high resistance to taxane-based chemotherapy may require further investigation. P. Prithviraj, A. Jayachandran, M. Anaka, J. Cebon Cancer Immunobiology Laboratory, Ludwig Institute For Cancer Research, Melbourne, Australia Background: Melanoma is a common and highly aggressive form of skin cancer with a high propensity to metastasise. Insulin-like Growth Factor (IGF1) promotes melanoma metastasis and plays an important role in disease progression. Bioavailability of IGF1 is known to be regulated by IGF-binding proteins (IGFBPs). IGFBP4 forms a complex with IGF1 and inhibits release of active IGF1. IGFBP4 is cleaved by metalloproteinase Pregnancy-Associated Plasma Protein-A (PAPP-A) resulting in release of bioactive IGF1. Methods: PAPP-A mRNA expression was analysed by quantitative RT-PCR in forty-eight metastatic melanoma patient tumour samples, and in thirty-eight melanoma cell lines developed in our institute. PAPP-A secretion selleck inhibitor was quantified by commercial ELISA in twenty-one melanoma patient sera and eleven melanoma cell lines. Efficient knockdown of PAPP-A expression and secretion (down to