Elevated glutathione Stransferase P1 expression has been associated with resistance to cisplatin-based chemotherapy in several cancer cell lines. Our gene set comparison analyses demonstrate a significant overlap between the ES cell signatures and our chemotherapy resistance signatures. No prior studies have demonstrated the enrichment of ES cell signatures in clinical samples collected at the time of acquired resistance to cytotoxic chemotherapy. Accumulating evidence suggests an association between a stem cell phenotype and intrinsic chemoresistance. Animal studies have suggested that the cell population exhibiting cancer stem cell characteristics is enriched in xenograft Mechlorethamine hydrochloride tumors following chemotherapy. While ES cell signatures may not perfectly reflect the phenotype of gastric cancer stem cells, the enrichment of ES cell signatures in chemoresistant tumors may reflect the survival advantage of tumor cells expressing stem cell regulatory networks. This was validated by our finding that 72 genes shared by the acquired resistance and ES cell signatures were sufficient to predict the initial response to CF. This study has identified a molecular signature for acquired resistance to CF therapy in gastric cancer patients. This signature is able to identify patients likely to have a short or longer term response to CF suggesting it reflects the molecular profile of chemoresistant clones and not non-specific drug effects. Genes contained within this signature, such as Akt/mTOR pathway genes, TRAP1, RAD23A, and GSTP1, may be potentially useful targets for treating tumors resistant to CF therapy. Future studies will be required to confirm these results and to determine whether our novel approach to develop an acquired resistance signature that predicts the therapeutic response of patients to specific chemotherapies is applicable to other types of cancer. Mitochondria are eukaryotic Dexrazoxane hydrochloride organelles that are thought to have evolved from an alpha-proteobacterial endosymbiont about two billion years ago. The loss of bacterial autonomy and transition of the endosymbiont to a ”protomitochondrion” were associated with a reduction in the number of genes in the endosymbiont genome; these genes were either transferred to the nuclear genome or lost. While the genome of the extant alpha-proteobacterium Rickettsia prowazekii contains 834 protein-coding genes, the largest number of genes in a mitochondrial genome is found in Reclinomonas americana, with only three protein-coding genes present in the Plasmodium falciparum mitochondrial genome. Paradoxically, the reduction of the mitochondrial genome did not lead to a reduction of the organellar proteome. The acquisition of a mechanism for mitochondrial import at the earliest stage of the endosymbiont-toprotomitochondrion transition allowed the recruitment of the proteins of endosymbiotic origin that were now encoded in the nucleus, and the import of proteins of other origins. Contemporary mitochondrial proteomes contain hundreds of proteins, up to 1100 proteins in the mouse. Mitosomes are the most highly reduced forms of mitochondria, having completely lost their genomes and dramatically reduced their proteomes. Mitosomes have also lost many of the typical mitochondrial functions, such as respiration, the citric acid cycle, and ATP synthesis. Biosynthesis of FeS clusters is the only mitochondrial function seen to be retained by at least some mitosomes. Mitosomes have become established independently in diverse groups of unicellular eukaryotes; many of them once considered to be amitochondrial because they lack organelles with the expected mitochondrial morphology. Organisms with mitosomes live under oxygen-limiting conditions, like the human intestinal parasitesGiardia intestinalis and Entamoeba histolytica, or are intracellular parasites like the microsporidians Encephalitozoon cuniculi and Trachipleistophora hominis and the apicomplexan Cryptosporidium parvum. Mitosomes are tiny ovoid organelles enclosed by two membranes. Unlike mitochondria, the inner membrane of mitosomes does not form cristae.