scholarly journals SAR studies of 4-pyridyl heterocyclic anilines that selectively induce autophagic cell death in von Hippel-Lindau-deficient renal cell carcinoma cells

2011 ◽  
Vol 19 (11) ◽  
pp. 3347-3356 ◽  
Author(s):  
Muriel Bonnet ◽  
Jack U. Flanagan ◽  
Denise A. Chan ◽  
Edwin W. Lai ◽  
Phuong Nguyen ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Death ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Autophagic Cell Death ◽  
Von Hippel Lindau ◽  
Sar Studies

scholarly journals 4-Pyridylanilinothiazoles That Selectively Target von Hippel−Lindau Deficient Renal Cell Carcinoma Cells by Inducing Autophagic Cell Death

2010 ◽  
Vol 53 (2) ◽  
pp. 787-797 ◽  
Author(s):  
Michael P. Hay ◽  
Sandra Turcotte ◽  
Jack U. Flanagan ◽  
Muriel Bonnet ◽  
Denise A. Chan ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Death ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Autophagic Cell Death ◽  
Von Hippel Lindau

scholarly journals Ubenimex enhances the radiosensitivity of renal cell carcinoma cells by inducing autophagic cell death

2016 ◽  
Vol 12 (5) ◽  
pp. 3403-3410 ◽  
Author(s):  
Shuai Liu ◽  
Xiaoqing Wang ◽  
Jiaju Lu ◽  
Liping Han ◽  
Yongfei Zhang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Death ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Autophagic Cell Death

Targeting the Loss of the von Hippel-Lindau Tumor Suppressor Gene in Renal Cell Carcinoma Cells

2007 ◽  
Vol 67 (12) ◽  
pp. 5896-5905 ◽  
Author(s):  
Patrick D. Sutphin ◽  
Denise A. Chan ◽  
James M. Li ◽  
Sandra Turcotte ◽  
Adam J. Krieg ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Tumor Suppressor ◽  
Cell Carcinoma ◽  
Tumor Suppressor Gene ◽  
Renal Cell ◽  
Suppressor Gene ◽  
Carcinoma Cells ◽  
Von Hippel Lindau

scholarly journals Novel oncolytic adenovirus sensitizes renal cell carcinoma cells to radiotherapy via mitochondrial apoptotic cell death

2014 ◽  
Vol 11 (3) ◽  
pp. 2141-2146 ◽  
Author(s):  
REN-FU CHEN ◽  
YUE-YAN LI ◽  
LIAN-TAO LI ◽  
QIAN CHENG ◽  
GUAN JIANG ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Death ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Apoptotic Cell ◽  
Oncolytic Adenovirus ◽  
Apoptotic Cell Death ◽  
Carcinoma Cells

scholarly journals Autophagic cell death associated to Sorafenib in renal cell carcinoma is mediated through Akt inhibition in an ERK1/2 independent fashion

PLoS ONE ◽  
2018 ◽  
Vol 13 (7) ◽  
pp. e0200878 ◽  
Author(s):  
Leticia Serrano-Oviedo ◽  
Marta Ortega-Muelas ◽  
Jesús García-Cano ◽  
María Ll. Valero ◽  
Francisco J. Cimas ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Death ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Autophagic Cell Death

scholarly journals A Precision Strategy to Cure Renal Cell Carcinoma by Targeting Transglutaminase 2

2020 ◽  
Vol 21 (7) ◽  
pp. 2493 ◽  
Author(s):  
Soo-Youl Kim ◽  
Jeffrey W. Keillor
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Death ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Hypoxia Inducible Factor ◽  
Physiological Role ◽  
Transglutaminase 2 ◽  
Cell Renal Cell Carcinoma ◽  
Von Hippel Lindau ◽  
High Level

In a recent report, no significance of transglutaminase 2 (TGase 2) was noted in the analyses of expression differences between normal and clear cell renal cell carcinoma (ccRCC), although we found that knock down of TGase 2 induced significant p53-mediated cell death in ccRCC. Generally, to find effective therapeutic targets, we need to identify targets that belong specifically to a cancer phenotype that can be differentiated from a normal phenotype. Here, we offer precise reasons why TGase 2 may be the first therapeutic target for ccRCC, according to several lines of evidence. TGase 2 is negatively regulated by von Hippel-Lindau tumor suppressor protein (pVHL) and positively regulated by hypoxia-inducible factor 1-α (HIF-1α) in renal cell carcinoma (RCC). Therefore, most of ccRCC presents high level expression of TGase 2 because over 90% of ccRCC showed VHL inactivity through mutation and methylation. Cell death, angiogenesis and drug resistance were specifically regulated by TGase 2 through p53 depletion in ccRCC because over 90% of ccRCC express wild type p53, which is a cell death inducer as well as a HIF-1α suppressor. Although there have been no detailed studies of the physiological role of TGase 2 in multi-omics analyses of ccRCC, a life-long study of the physiological roles of TGase 2 led to the discovery of the first target as well as the first therapeutic treatment for ccRCC in the clinical field.

Proximal 3p deletion in renal cell carcinoma cells from a patient with von Hippel-Lindau disease

1987 ◽  
Vol 27 (2) ◽  
pp. 345-348 ◽  
Author(s):  
Charles R. King ◽  
R.Neil Schimke ◽  
Terry Arthur ◽  
Barbara Davoren ◽  
Debra Collins
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Carcinoma Cells ◽  
Von Hippel Lindau ◽  
Von Hippel Lindau Disease
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