2017 Fiscal Year Final Research Report
Analysis of JAK-STAT pathway in diffuse large B-cell lymphoma
| Project/Area Number |
15K08371
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Human pathology
|
|---|
| Research Institution | University of the Ryukyus |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
大島 孝一 久留米大学, 医学部, 教授 (50203766)
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Keywords | 遺伝子変異 / JAK-STAT / 悪性リンパ腫 / 次世代シークエンス / STAT3 / びまん性大細胞型B細胞リンパ腫 |
|---|
| Outline of Final Research Achievements |
STAT3 associated genes are often mutated in diffuse large B-cell lymphoma (DLBCL) and their roles as prognostic markers and therapeutic targets were analyzed.
Immunohistochemistry and mutation analysis focusing STAT3 associated genes were performed with FFPE samples from 279 DLBCL patients. Cell of origin was determined with Hans algorithm. Phosphorylated STAT3 (pSTAT3) was detected in 122 cases (44%) and biased toward non-GCB type (P<0.001). MYD88 L265P and EBV positivity were significantly associated with non-GCB type and pSTAT3 expression (P<0.001). STAT3 and non-L265P MYD88 mutations were relatively enriched in GCB type and only the former was significantly associated with pSTAT3 expression (P=0.02). Clinically, pSTAT3 expression and COO was not associated with overall survival. EBV positivity and STAT3 mutations were correlated with poorer and better prognosis, respectively. Our data clarified clinicopathological diversity of STAT3 activation in DLBCL.
|
| Free Research Field |
血液病理学
|
