Abstract

Every year worldwide approximately 3 million cancer patients receive chemotherapy. Unfortunately in many cases the treatment does not prolong patient’s survival time. Chemotherapy and radiation therapy still remain the major strategies with or without surgery. One of the main obstacles in chemoand radiation therapy is the rapid development of resistance by the cancer cells. In recent years, the Heat Shock Protein HSP27 has been identified as one of the key players driving resistance development. HSP27 is overexpressed in many kinds of cancer and influences cellular processes like apoptosis (programmed cell death), DNA repair, recombination, and metastasis. As a result, cancer cells are able to suppress apoptosis and develop resistance towards cytostatic drugs such as Gemcitabine which is used as standard therapy in pancreatic cancer. To address this problem the HSP27-inhibitor BVDU ((E)-5-(2-Bromovinyl)-2′-deoxyuridine, RP101) was administered in combination with Gemcitabine to prevent resistance development. In the study design, the human pancreatic adenocarcinoma cell line Capan-2 was exposed to Gemcitabine alone and in combination with BVDU. Differential gene expression was displayed using DNA microarrays. This paper presents the resulting dataset, with pairwise comparison of control (untreated), Gemcitabine-, BVDU-, and Gemcitabine+BVDU treated probes. The five spreadsheet files are openly accessible for validation, re-use and aggregation in future research. Creative Commons BY-NC-SA 4.0 © 2015 Hosting by Procon Ltd. All rights reserved. Heinrich J-C & Fahrig F. Biomed Data J. 2015; 1(2): 7-9

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