2017 Fiscal Year Final Research Report
Identification of new molecular target associated with treatment-resistance of glioblastomas
| Project/Area Number |
15K10349
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurosurgery
|
|---|
| Research Institution | Chiba Cancer Center (Research Institute) |
|---|
Principal Investigator |
IUCHI TOSHIHIKO 千葉県がんセンター(研究所), 脳神経外科, 部長 (80370881)
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Keywords | glioblastoma / radiation / chemotherapy / resistance / molecular target / DNA repair |
|---|
| Outline of Final Research Achievements |
Copy number decrease of Rad51 (an essential factor of homologous recombination:HR) and XRCC6 (coding Ku70 which acts as the cornerstone of the non-homologous end joining: NHEJ) were associated with the survival of patients after chemo-radiotherapy, and were suspected to be a key molecule of tumor resistance to the treatment. However, from the comparative study of gene expression profiles between the samples from tumors pre- and just post-chemo-radiotherapy, genes involved in HR and NHEJ were down-regulated by the treatment, while CDKN1A and DDB2 expressions were up-regulated in the all cases. These data suggested the significant role of cell cycle arrest by CDKN1A and nucleotide excision repair, not HR nor NHEJ, plays a major role in tumor resistance to chemo-radiotherapy in glioblastomas.
|
| Free Research Field |
悪性脳腫瘍
|
