Affiliation: Cancer Institute Hospital
- De novo fatty-acid synthesis and related pathways as molecular targets for cancer therapyT Mashima
Division of Molecular Biotherapy, Cancer Chemotherapy Centre, Japanese Foundation for Cancer Research, 3 10 6 Ariake, Koto ku, Tokyo 135 8550, Japan
Br J Cancer 100:1369-72. 2009..These observations suggest that enzymes in the lipid synthesis pathway would be rational therapeutic targets for cancer. To this end, we review the enzymes in de novo fatty-acid synthesis and related pathways...
- Selective activation of apoptosis program by S-p-bromobenzylglutathione cyclopentyl diester in glyoxalase I-overexpressing human lung cancer cellsH Sakamoto
Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo 170 8455, Japan
Clin Cancer Res 7:2513-8. 2001..In this study, we quantitatively measured GLO1 enzyme activity in various human solid tumor cells, and the antiproliferative effect of the GLO1 inhibitor was examined...
- Promotion of glioma cell survival by acyl-CoA synthetase 5 under extracellular acidosis conditionsT Mashima
Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan
Oncogene 28:9-19. 2009..These results indicate that ACSL5 is a critical factor for survival of glioma cells under acidic tumor microenvironment, thus providing novel molecular basis for cancer therapy...
- Involvement of transcriptional repressor ATF3 in acceleration of caspase protease activation during DNA damaging agent-induced apoptosisT Mashima
Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Kami-Ikebukuro, Toshima-ku, Tokyo, Japan
J Cell Physiol 188:352-8. 2001..Since CRE-dependent transcription functions as cell survival signaling, ATF3 could control the upstream signaling of apoptosis by repressing CRE-dependent gene expression of cell survival factors...
- Glyoxalase I is involved in resistance of human leukemia cells to antitumor agent-induced apoptosisH Sakamoto
Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan
Blood 95:3214-8. 2000..Taken together, these results indicate that GLO1 is a resistant factor to antitumor agent-induced apoptosis in human leukemia cells and that the GLO1 inhibitor could be a drug resistance-reversing agent...