| Project/Area Number |
26430174
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Tumor therapeutics
|
|---|
| Research Institution | Kindai University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
中川 和彦 近畿大学, 医学部, 教授 (40298964)
米阪 仁雄 近畿大学, 医学部附属病院, 講師 (30330260)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | HER2 / 乳癌 / 胃癌 / 化学療法 / 分子標的薬 / 薬剤耐性 / ヘレギュリン / 西日本がん研究機構 / WJOG7212G / cfDNA BC / N87 / SKBR-3 / 血漿検体 / heregulin / 分子標的治療 |
|---|
| Outline of Final Research Achievements |
Recombinant heregulin desensitized HER2 positive breast or gastric cancer cell lines to trastuzumab, lapatinib, but not to T-DM1. The SKBR3 and N87 cells were transfected with heregulin gene and sensitivities of those cell to each drug were evaluated. The transfectants were desensitized to trastuzumab and lapatinib, but not T-DM1. The resuls were likewise in the xenograft model innoculated with the heregulin-transfected N87 cells. In clinical specimens obtained from patinets with breast or gastric cancer who became resistant to trastuzumab, the expression levels of heregulin protein were upregulated compared to the pre-treatment samples, suggesting that heregulin is involved in the acquired resistance to anti-HER2 therapy, other than T-DM1.
|
