T Mashima

Summary

Affiliation: Cancer Institute Hospital
Country: Japan

Publications

  1. pmc De novo fatty-acid synthesis and related pathways as molecular targets for cancer therapy
    T 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
  2. ncbi request reprint Selective activation of apoptosis program by S-p-bromobenzylglutathione cyclopentyl diester in glyoxalase I-overexpressing human lung cancer cells
    H Sakamoto
    Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo 170 8455, Japan
    Clin Cancer Res 7:2513-8. 2001
  3. doi request reprint Promotion of glioma cell survival by acyl-CoA synthetase 5 under extracellular acidosis conditions
    T Mashima
    Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan
    Oncogene 28:9-19. 2009
  4. ncbi request reprint Involvement of transcriptional repressor ATF3 in acceleration of caspase protease activation during DNA damaging agent-induced apoptosis
    T Mashima
    Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Kami-Ikebukuro, Toshima-ku, Tokyo, Japan
    J Cell Physiol 188:352-8. 2001
  5. ncbi request reprint Glyoxalase I is involved in resistance of human leukemia cells to antitumor agent-induced apoptosis
    H Sakamoto
    Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan
    Blood 95:3214-8. 2000

Collaborators

Detail Information

Publications5

  1. pmc De novo fatty-acid synthesis and related pathways as molecular targets for cancer therapy
    T 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...
  2. ncbi request reprint Selective activation of apoptosis program by S-p-bromobenzylglutathione cyclopentyl diester in glyoxalase I-overexpressing human lung cancer cells
    H 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...
  3. doi request reprint Promotion of glioma cell survival by acyl-CoA synthetase 5 under extracellular acidosis conditions
    T 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...
  4. ncbi request reprint Involvement of transcriptional repressor ATF3 in acceleration of caspase protease activation during DNA damaging agent-induced apoptosis
    T 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...
  5. ncbi request reprint Glyoxalase I is involved in resistance of human leukemia cells to antitumor agent-induced apoptosis
    H 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...