| Item type |
☆紀要論文 / Departmental Bulletin Paper(1) |
| 公開日 |
2021-01-18 |
| タイトル |
|
|
タイトル |
<Original> NF1 and KRAS mutations in pancreatic cancer secondary to alcoholic chronic pancreatitis |
|
言語 |
en |
| 著者 |
Murase, Takaaki
Sakai, Kazuko
Satou, Takao
Nishio, Kazuto
Takeyama, Yoshifumi
|
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
主題 |
Pancreatic cancer, Chronic pancreatitis, Gene mutation, NF1, KRAS, Next-generation sequencing |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
departmental bulletin paper |
| ID登録 |
|
|
ID登録 |
10.15100/00021268 |
|
ID登録タイプ |
JaLC |
| 著者 所属 |
|
|
値 |
Department of Surgery, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Genome Biology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Division of Hosoital Pathology, Kindai University Hospital |
| 著者 所属 |
|
|
値 |
Department of Genome Biology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Surgery, Kindai University Faculty of Medicine |
| 版 |
|
|
出版タイプ |
NA |
|
出版タイプResource |
http://purl.org/coar/version/c_be7fb7dd8ff6fe43 |
| 出版者 名前 |
|
|
出版者 |
Kindai University Medical Association |
| 書誌情報 |
en : ACTA MEDICA KINDAI UNIVERSITY
巻 45,
号 2,
p. 31-37,
発行日 2020-12
|
| ISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
03866092 |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
[Abstract] The risk of developing pancreatic cancer is significantly higher in the patients with chronic pancreatitis than in those without chronic pancreatitis (CP). However, the genetic mechanisms for this increased risk remain unclear. We hypothesized that different genetic mechanisms may exist in the process of carcinogenesis secondary to CP.We included patients with pancreatic cancer who underwent pancreatectomy between 2012 and 2016 at Kindai University Hospital. Among them,3 patients had alcoholic CP for more than 2 years.We examined 3 types of tissue samples from each patient: cancerous, CP, and normal tissues. We extracted DNA from each tissue type and used next-generation sequencing (NGS) to detect mutations.We found genomic comutation of KRAS and NF1 in 1 patient. There were no mutations in normal tissues, but mutations occurred in CP tissues.The rate of dissection of pancreatic ductal adenocarcinoma (PDAC) from cancerous tissues was approximately 30%, and the variant frequency of NF1 and KRAS was 34% and 32%, respectively. The rate of dissection of pancreatic ductal tissue from CP tissues was approximately 20%, and the variant frequency of NF1 and KRAS was 19% and 21%, respectively. Comutation of NF1 and KRAS may be a carcinogenic mechanism of pancreatic cancer in patients with alcoholic CP. NF1 and KRAS mutations may be a therapeutic target in patients with pancreatic cancer secondary to CP. |
| フォーマット |
|
|
内容記述タイプ |
Other |
|
内容記述 |
application/pdf |
AA0050842X-20201200-0031.pdf (566.2 kB)
