| Project/Area Number |
22790367
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Human pathology
|
|---|
| Research Institution | 地方独立行政法人神奈川県立病院機構 (2011)
Kanagawa Cancer Center Research Institute (2010) |
|---|
Principal Investigator |
SAKUMA Yuji 地方独立行政法人神奈川県立病院機構, 神奈川県立がんセンター(臨床研究所)・がん分子病態学部, 副技幹 (10364514)
|
|---|
| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | 肺腺癌 / 転移 / アポトーシス / EGFR / Src / EGFR遺伝子変異 / がん遺伝子Src / がん遺伝子 Src / EGFR 遺伝子変異 |
|---|
| Research Abstract |
EGFR-mutant lung adenocarcinoma cells in suspension culture system undergo massive apoptosis by treatment with EGFR tyrosine kinase inhibitors(TKIs). On the other hand, EGFR-mutant cells in monolayer culture system are much more resistant to EGFR TIKs-induced apoptosis than suspended tumor cells, although the phosphorylation of EGFR expressed in EGFR-mutant cells is completely suppressed in either culture condition. Also intrasinus floating tumor cells in metastasis-positive lymph nodes from EGFR-mutant lung adenocarcinoma patients expressed mutant specific EGFR in the same way as extracellular matrix adhesive tumor cells. These findings suggest that the tumor cells floating in vessels would be highly susceptible to EGFR TKIs.
|
