scholarly journals Endogenous p21WAF1/CIP1 status predicts the response of human tumor cells to wild-type p53 and p21WAF1/CIP1 overexpression

2003 ◽  
Vol 10 (6) ◽  
pp. 457-467 ◽  
Author(s):  
Marijeta Kralj ◽  
Koraljka Husnjak ◽  
Tajana Körbler ◽  
Jasminka Pavelić
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Wild Type ◽  
Human Tumor Cells ◽  
Wild Type P53

scholarly journals Wild-type p53 triggers a rapid senescence program in human tumor cells lacking functional p53

1997 ◽  
Vol 94 (18) ◽  
pp. 9648-9653 ◽  
Author(s):  
M. M. Sugrue ◽  
D. Y. Shin ◽  
S. W. Lee ◽  
S. A. Aaronson
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Wild Type ◽  
Human Tumor Cells ◽  
Wild Type P53 ◽  
Senescence Program

scholarly journals Alterations in gene expression and sensitivity to genotoxic stress following HdmX or Hdm2 knockdown in human tumor cells harboring wild-type p53

Aging ◽  
2009 ◽  
Vol 1 (1) ◽  
pp. 89-108 ◽  
Author(s):  
Katherine Heminger ◽  
Michael Markey ◽  
Meldrick Mpagi ◽  
Steven J. Berberich
Keyword(s):  
Gene Expression ◽  
Tumor Cells ◽  
Human Tumor ◽  
Genotoxic Stress ◽  
Wild Type ◽  
Human Tumor Cells ◽  
Wild Type P53

scholarly journals Downregulation of telomerase reverse transcriptase mRNA expression by wild type p53 in human tumor cells

Oncogene ◽  
2000 ◽  
Vol 19 (45) ◽  
pp. 5123-5133 ◽  
Author(s):  
Dawei Xu ◽  
Qian Wang ◽  
Astrid Gruber ◽  
Magnus Björkholm ◽  
Zhiguo Chen ◽  
...  
Keyword(s):  
Reverse Transcriptase ◽  
Mrna Expression ◽  
Tumor Cells ◽  
Human Tumor ◽  
Telomerase Reverse Transcriptase ◽  
Wild Type ◽  
Human Tumor Cells ◽  
Wild Type P53

Phenoxodiol, a synthetic analog of genistein, generates ceramide and is equipotent in wild-type and multidrug-resistant human tumor cells

2005 ◽  
Vol 23 (16_suppl) ◽  
pp. 2075-2075 ◽  
Author(s):  
M. C. Cabot ◽  
J. Y. Yu ◽  
G. E. Kelly ◽  
D. M. Brown ◽  
K. M. Lucas ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Multidrug Resistant ◽  
Synthetic Analog ◽  
Wild Type ◽  
Human Tumor Cells

scholarly journals The Retinoblastoma Protein Is Required for Ras-Induced Oncogenic Transformation

2006 ◽  
Vol 26 (4) ◽  
pp. 1170-1182 ◽  
Author(s):  
Jonathan P. Williams ◽  
Timothy Stewart ◽  
Bihua Li ◽  
Roseann Mulloy ◽  
Dessislava Dimova ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Inhibitory Effect ◽  
Oncogenic Transformation ◽  
Wild Type ◽  
3T3 Cells ◽  
Human Tumor Cells ◽  
Ras Pathway ◽  
Retinoblastoma Tumor ◽  
Mutational Activation

ABSTRACT Most human cancers involve either mutational activation of the Ras oncogenic pathway and/or inactivation of the retinoblastoma tumor suppressor (RB) pathway. Paradoxically, tumors that harbor Ras mutations almost invariably retain expression of a wild-type pRB protein. We explain this phenomenon by demonstrating that Ras-induced oncogenic transformation surprisingly depends on functional pRB protein. Cells lacking pRB are less susceptible to the oncogenic actions of H-RasV12 than wild-type cells and activated Ras has an inhibitory effect on the proliferation of pRB-deficient human tumor cells. In addition, depletion of pRB from Ras-transformed murine cells or human tumor cells that harbor Ras pathway mutations inhibits their proliferation and anchorage-independent growth. In sharp contrast to pRB−/− 3T3 cells, fibroblasts deficient in other pRB family members (p107 and p130) are more susceptible to Ras-mediated transformation than wild-type 3T3 cells. Moreover, loss of pRB in tumor cells harboring a Ras mutation results in increased expression of p107, and overexpression of p107 but not pRB strongly inhibits proliferation of these tumor cells. Together, these findings suggest that pRB and p107 have distinct roles in Ras-mediated transformation and suggest a novel tumor-suppressive role for p107 in the context of activated Ras.

Creating human tumor cells

Nature ◽  
1999 ◽  
Author(s):  
Hannah Wunsch
Keyword(s):  
Tumor Cells ◽  
Human Tumor ◽  
Human Tumor Cells
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