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Science 2 April 1993:
Vol. 260. no. 5104, pp. 85 - 88
DOI: 10.1126/science.8465203
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Articles

Science, Vol 260, Issue 5104, 85-88
Copyright © 1993 by American Association for the Advancement of Science

articles

Altered growth of human colon cancer cell lines disrupted at activated Ki-ras

S Shirasawa, M Furuse, N Yokoyama, and T Sasazuki

Department of Genetics, Kyushu University, Fukuoka, Japan.

Point mutations that activate the Ki-ras proto-oncogene are presented in about 50 percent of human colorectal tumors. To study the functional significance of these mutations, the activated Ki-ras genes in two human colon carcinoma cell lines, DLD-1 and HCT 116, were disrupted by homologous recombination. Compared with parental cells, cells disrupted at the activated Ki-ras gene were morphologically altered, lost the capacity for anchorage-independent growth, grew more slowly both in vitro and in nude mice, and showed reduced expression of c-myc. Thus, the activated Ki-ras gene plays a key role in colorectal tumorigenesis through altered cell differentiation and cell growth.


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   Abstract »    Full Text »    PDF »
Oncogenes and Tumor Angiogenesis: Differential Modes of Vascular Endothelial Growth Factor Up-Regulation in ras-transformed Epithelial Cells and Fibroblasts.
J. Rak, Y. Mitsuhashi, C. Sheehan, A. Tamir, A. Viloria-Petit, J. Filmus, S. J. Mansour, N. G. Ahn, and R. S. Kerbel (2000)
Cancer Res. 60, 490-498
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Combination Therapy with the Farnesyl Protein Transferase Inhibitor SCH66336 and SCH58500 (p53 Adenovirus) in Preclinical Cancer Models.
L. L. Nielsen, B. Shi, G. Hajian, B. Yaremko, P. Lipari, E. Ferrari, M. Gurnani, M. Malkowski, J. Chen, W. R. Bishop, et al. (1999)
Cancer Res. 59, 5896-5901
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Ras Protein Farnesyltransferase: A Strategic Target for Anticancer Therapeutic Development.
E. K. Rowinsky, J. J. Windle, and D. D. Von Hoff (1999)
J. Clin. Oncol. 17, 3631-3652
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Requirement of the MAP kinase cascade for cell cycle progression and differentiation of human intestinal cells.
J. C. Aliaga, C. Deschenes, J.-F. Beaulieu, E. L. Calvo, and N. Rivard (1999)
Am J Physiol Gastrointest Liver Physiol 277, G631-G641
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Phase I Clinical/Pharmacokinetic and Pharmacodynamic Trial of the c-raf-1 Antisense Oligonucleotide ISIS 5132 (CGP 69846A).
J. P. Stevenson, K.-S. Yao, M. Gallagher, D. Friedland, E. P. Mitchell, A. Cassella, B. Monia, T. J. Kwoh, R. Yu, J. Holmlund, et al. (1999)
J. Clin. Oncol. 17, 2227
   Abstract »    Full Text »    PDF »
Activated Ki-Ras Suppresses 12-O-Tetradecanoylphorbol-13-acetate-induced Activation of the c-Jun NH2-Terminal Kinase Pathway in Human Colon Cancer Cells.
K. Okumura, S. Shirasawa, M. Nishioka, and T. Sasazuki (1999)
Cancer Res. 59, 2445-2450
   Abstract »    Full Text »    PDF »
T cell factor-activated transcription is not sufficient to induce anchorage-independent growth of epithelial cells expressing mutant beta -catenin.
A. I. M. Barth, D. B. Stewart, and W. J. Nelson (1999)
PNAS 96, 4947-4952
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Complementation of Defective Colony-Stimulating Factor 1 Receptor Signaling and Mitogenesis by Raf and v-Src.
N. Aziz, H. Cherwinski, and M. McMahon (1999)
Mol. Cell. Biol. 19, 1101-1115
   Abstract »    Full Text »    PDF »
p21WAF1/CIP1 Is Upregulated by the Geranylgeranyltransferase I Inhibitor GGTI-298 through a Transforming Growth Factor beta - and Sp1-Responsive Element: Involvement of the Small GTPase RhoA.
J. Adnane, F. A. Bizouarn, Y. Qian, A. D. Hamilton, and S. M. Sebti (1998)
Mol. Cell. Biol. 18, 6962-6970
   Abstract »    Full Text »
Regulation of Cell Death Protease Caspase-9 by Phosphorylation.
M. H. Cardone, N. Roy, H. R. Stennicke, G. S. Salvesen, T. F. Franke, E. Stanbridge, S. Frisch, and J. C. Reed (1998)
Science 282, 1318-1321
   Abstract »    Full Text »
Elevated Expression of Ets2 or Distinct Portions of Ets2 Can Reverse Ras-mediated Cellular Transformation.
G. Foos, J. J. Garcia-Ramirez, C. K. Galang, and C. A. Hauser (1998)
J. Biol. Chem. 273, 18871-18880
   Abstract »    Full Text »    PDF »
Impact of oncogenes in tumor angiogenesis: Mutant K-ras up-regulation of vascular endothelial growth factor/vascular permeability factor is necessary, but not sufficient for tumorigenicity of human colorectal carcinoma cells.
F. Okada, J. W. Rak, B. St. Croix, B. Lieubeau, M. Kaya, L. Roncari, S. Shirasawa, T. Sasazuki, and R. S. Kerbel (1998)
PNAS 95, 3609-3614
   Abstract »    Full Text »    PDF »
K- and N-Ras Are Geranylgeranylated in Cells Treated with Farnesyl Protein Transferase Inhibitors.
D. B. Whyte, P. Kirschmeier, T. N. Hockenberry, I. Nunez-Oliva, L. James, J. J. Catino, W. R. Bishop, and J.-K. Pai (1997)
J. Biol. Chem. 272, 14459-14464
   Abstract »    Full Text »    PDF »
Antisense Oligonucleotides Demonstrate a Dominant Role of c-Ki-RAS Proteins in Regulating the Proliferation of Diploid Human Fibroblasts.
G. Chen, S. Oh, B. P. Monia, and D. W. Stacey (1996)
J. Biol. Chem. 271, 28259-28265
   Abstract »    Full Text »    PDF »
K-ras Status Does Not Predict Successful Hepatic Resection of Colorectal Cancer Metastasis.
W. V. Kastrinakis, N. Ramchurren, M. Maggard, G. Steele Jr, and I. C. Summerhayes (1995)
Arch Surg 130, 9-14
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Ras Uses the Novel Tumor Suppressor RASSF1 as an Effector to Mediate Apoptosis.
M. D. Vos, C. A. Ellis, A. Bell, M. J. Birrer, and G. J. Clark (2000)
J. Biol. Chem. 275, 35669-35672
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Dual Growth Arrest Pathways in Astrocytes and Astrocytic Tumors in Response to Raf-1 Activation.
C. P. Fanton, M. McMahon, and R. O. Pieper (2001)
J. Biol. Chem. 276, 18871-18877
   Abstract »    Full Text »    PDF »
Bile Acid-induced Activation of Activator Protein-1 Requires Both Extracellular Signal-regulated Kinase and Protein Kinase C Signaling.
D. Qiao, W. Chen, E. D. Stratagoules, and J. D. Martinez (2000)
J. Biol. Chem. 275, 15090-15098
   Abstract »    Full Text »    PDF »


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