Influence on survival rate of epigenetic inactivation in RUNX3 gene at 1p36 in human pancreatic cancer

Pancreatology ◽  
2013 ◽  
Vol 13 (2) ◽  
pp. e62
Author(s):  
S. Nomoto ◽  
Y. Inokawa ◽  
H. Sugimoto ◽  
T. Fujii ◽  
S. Yamada ◽  
...  
2008 ◽  
Vol 98 (10) ◽  
pp. 1690-1695 ◽  
Author(s):  
S Nomoto ◽  
T Kinoshita ◽  
T Mori ◽  
K Kato ◽  
H Sugimoto ◽  
...  

2020 ◽  
Vol 111 (12) ◽  
pp. 4594-4604
Author(s):  
Kanchan Chakma ◽  
Zhaodi Gu ◽  
Yakefujiang Abudurexiti ◽  
Tatsuo Hata ◽  
Fuyuhiko Motoi ◽  
...  

2010 ◽  
Vol 999 (999) ◽  
pp. 1-11
Author(s):  
P. Ulivi ◽  
C. Arienti ◽  
W. Zoli ◽  
M. Scarsella ◽  
S. Carloni ◽  
...  

Epigenomes ◽  
2020 ◽  
Vol 4 (3) ◽  
pp. 18
Author(s):  
Murat Toruner ◽  
Martin E. Fernandez-Zapico ◽  
Christopher L. Pin

Pancreatic cancer remains among the deadliest forms of cancer with a 5 year survival rate less than 10%. With increasing numbers being observed, there is an urgent need to elucidate the pathogenesis of pancreatic cancer. While both contribute to disease progression, neither genetic nor environmental factors completely explain susceptibility or pathogenesis. Defining the links between genetic and environmental events represents an opportunity to understand the pathogenesis of pancreatic cancer. Epigenetics, the study of mitotically heritable changes in genome function without a change in nucleotide sequence, is an emerging field of research in pancreatic cancer. The main epigenetic mechanisms include DNA methylation, histone modifications and RNA interference, all of which are altered by changes to the environment. Epigenetic mechanisms are being investigated to clarify the underlying pathogenesis of pancreatic cancer including an increasing number of studies examining the role as possible diagnostic and prognostic biomarkers. These mechanisms also provide targets for promising new therapeutic approaches for this devastating malignancy.


2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Jiewei Lin ◽  
Zhiwei Xu ◽  
Junjie Xie ◽  
Xiaxing Deng ◽  
Lingxi Jiang ◽  
...  

AbstractAPOL1 encodes a secreted high-density lipoprotein, which has been considered as an aberrantly expressed gene in multiple cancers. Nevertheless, the role of APOL1 in the regulatory mechanisms of pancreatic cancer remains unknown and should be explored. We identified APOL1 was abnormally elevated in human pancreatic cancer tissues compared with that in adjacent tissues and was associated with poor prognosis. The effects of APOL1 in PC cell proliferation, cell cycle, and apoptosis was verified via functional in vitro and in vivo experiments. The results showed that knockdown of APOL1 significantly inhibited the proliferation and promoted apoptosis of pancreatic cancer. In addition, we identified APOL1 could be a regulator of NOTCH1 signaling pathway using bioinformatics tools, qRT-PCR, dual-luciferase reporter assay, and western blotting. In summary, APOL1 could function as an oncogene to promote proliferation and inhibit apoptosis through activating NOTCH1 signaling pathway expression in pancreatic cancer; therefore, it may act as a novel therapeutic target for pancreatic cancer.


Oncogene ◽  
2021 ◽  
Author(s):  
Qun Chen ◽  
Peng Shen ◽  
Wan-Li Ge ◽  
Tao-Yue Yang ◽  
Wu-Jun Wang ◽  
...  

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