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Abstract B08: ER chaperone GRP78 increases chemoresistance in pancreatic ductal adenocarcinoma
Conclusions: Collectively, our data show that GRP78 expression promotes chemoresistance in PDAC and therapeutic strategies blocking the activity of GRP78 increase the efficacy of currently available therapies.Citation Format: Jenifer B. Gifford, Wei Huang, Ann E. Zeleniak, Antreas Hindoyan, Hong Wu, Timothy R. Donahue, Reginald Hill.{Authors}. ER chaperone GRP78 increases chemoresistance in pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 Suppl):Abstract nr B08.
Source: Cancer Research - December 13, 2016 Category: Cancer & Oncology Authors: Jenifer B. Gifford, Wei Huang, Ann E. Zeleniak, Antreas Hindoyan, Hong Wu, Timothy R. Donahue, Reginald Hill Tags: Molecular Drivers of Pancreatic Cancer Biology and Metastasis Source Type: research

Abstract 2225: c-Myc and Frizzled 8 play a major role in the regulation of cancer stem cells and drug resistance in triple-negative breast cancer
In this study, we have found that c-Myc overexpression increased FZD8 expression, and its downstream signaling and together protect the cells from drug mediated cell death compared to vector transfected cells. c-Myc over-expressing cells do not show increased mammosphere formation; the numbers of CSCs per mammosphere are much higher compared to vector transfected controls. CDK inhibitor (dinaciclib) enhanced the cell death in c-Myc over expressing non-CSCs with minimal effect on CSCs. Inhibition of c-Myc using siRNA reduced c-Myc, FZD-8 and CSCs and enhanced sensitivity of cells to cisplatin plus TRAIL. Taken together, our...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yin, S., Cheriyan, V. T., Rishi, A. K., Reddy, K. B. Tags: Tumor Biology Source Type: research

Abstract 737: Clonal evolution of the HER2 L755S mutation as a mechanism of acquired HER-targeted therapy resistance
Conclusion: Acquired L/LT resistance in the two BT474 R lines is due to selection of HER2 L755S subclones present in parental cells. The higher HER2 L755S levels in BT474 parentals compared with other parentals, and detection of its subclonal presence in a pre-treatment HER2+ BC patient, suggest that sensitive mutation detection methods will be needed to identify patients with potentially actionable HER family mutations in primary tumor. Treating this patient group with an irreversible TKI like Afa may prevent resistance and improve clinical outcome of this subset of HER2+ BC.Citation Format: Xiaowei Xu, Agostina Nardone, ...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Xu, X., Nardone, A., Hu, H., Qin, L., Nanda, S., Heiser, L., Wang, N., Covington, K., Chen, E., Renwick, A., Mitchell, T., Shea, M., Wang, T., De Angelis, C., Contreras, A., Gutierrez, C., Fuqua, S., Chamness, G., Shaw, C., Li, M., Wheeler, D., Hilsenbeck Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 920: Secreted frizzled related protein 1 (SFRP1) as potential regulator of chemotherapy response for patients with triple negative breast cancer (TNBC)
Conclusion: We suggest SFRP1 as a novel predictive marker of chemotherapy sensitivity to taxane, anthracycline and platinum-containing chemotherapy independent of Ki67 expression. Further on, we have shown the influence of SFRP1 on cancerous characteristics thus, suggesting SFRP1 as potential prognostic marker. Molecular role of SFRP1 may be the influence on enrichment of cancer stem cell population which are known to be resistant against chemotherapeutics and radiation and are usually slow proliferating. Interestingly, the mTOR/PI3K signaling might be activated via loss of SFRP1 which could display an opportunity for pati...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Huelsewig, C., Bernemann, C., Ruckert, C., Kiesel, L., Goette, M., Rody, A., Pusztai, L., Hempel, G., Liedtke, C. Tags: Clinical Research (Excluding Clinical Trials) Source Type: research