@article{oai:repo.qst.go.jp:00043490,
 author = {Matsui, Yoshifumi and Gotou, Miyako and Iwakawa, Mayumi and Asano, Takehide and Kanmochi, Takashi and Imai, Takashi and Ochiai, Takenori and 松井 芳文 and 中渡 美也子 and 岩川 眞由美 and 浅野 武秀 and 今井 高志 and 落合 武徳},
 journal = {Oncology Reports},
 month = {},
 note = {We investigated the effects of the farnesyl transferase inhibitor (FTI) manumycin and the MEK inhibitor PD98059 on growth of human pancreatic cancer, with mutant (SUIT2) or wild-type (BxPC-3) K-ras, xenografted into nude mice. Tumor growth was not reduced by either of the agents at a dose of 3 mg/kg without irradiation. Growth of SUIT2 irradiated at 15 Gy or 30 Gy was reduced by manumycin and PD98059: at 15 Gy, tumor volume doubling time (TVDT) increased from 18.6+/-3.8 to 36.3+/-14.2 days with PD98059 (p<0.05); at 30 Gy, TVDT increased from 32.8+/-6.8 to 70.5+/-10.5 days and 70.7+/-1.5 days, respectively. Manumycin tended to reduce growth of BxPC-3, but the difference in TVDT was not statistically significant. PD98059 significantly increased the TVDT of BxPC-3 at 30 Gy from 34.4+/-18 to 62.6+/-9.8 at 30 Gy. The present results suggest that Ras signaling pathways are potential targets for manipulation of radiosensitivity, and that induction of an alternative pathway may enhance radiosensitivity of pancreatic cancer.},
 pages = {1525--1528},
 title = {Modified radiosensitivity of pancreatic cancer xenografts by farnesyl protein transferase inhibitor and MEK inhibitor},
 volume = {10},
 year = {2003}
}