@article{oai:shiga-med.repo.nii.ac.jp:00003471,
 author = {新田, 直樹 and 中洲, 敏 and 野﨑, 和彦 and NITTA, Naoki and NAKASU, Satoshi and SHIMA, Ayako and NOZAKI, Kazuhiko},
 issue = {Suppl 17},
 journal = {Surgical neurology international},
 month = {Jul},
 note = {BACKGROUND:
Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) acts as a downstream effector of phosphatidyl-inositol-3 kinase, which is frequently hyperactivated in glioblastoma multiforme and links to cell signaling in cellular proliferation, differentiation, metabolism, and survival. Although many studies have suggested the importance of mTORC1 in tumorigenesis, its role remains unclear in brain tumors other than glioblastoma.
METHODS:
In the present study, we evaluated the activation of mTORC1 in 24 cases of primary central nervous system lymphoma (PCNSL).
RESULTS:
Immunohistochemical analysis showed overexpression of Rheb, which is immediately upstream of mTORC1, in 20 cases of PCNSL. Immunohistochemical analysis also showed overexpression of phospho-4E-BP1 (Thr37/46) and phospho-S6 (Ser235/236), which are increased after mTORC1 activation as mTORC1 downstream effectors in 17 and 21 cases, respectively.
CONCLUSION:
Our data suggest that abnormal activation of the mTORC1 signaling pathway may cause tumor growth in patients with PCNSL., Journal Article},
 pages = {S475--80},
 title = {mTORC1 signaling in primary central nervous system lymphoma.},
 volume = {7},
 year = {2016}
}