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Science 4 September 1998:
Vol. 281. no. 5382, pp. 1438 - 1441
DOI: 10.1126/science.281.5382.1438
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News Focus

CELL BIOLOGY:
How a Growth Control Path Takes a Wrong Turn to Cancer

Elizabeth Pennisi

As researchers uncover the internal workings of one of the cell's key developmental and growth regulatory pathways--called the Wnt pathway after the protein that sets it in motion--they are getting a better grasp on the causes of cancer. Because activation of the Wnt pathway stimulates cell growth, researchers had long suspected that too much Wnt signaling could cause problems. The new work, described on page 1509 of this issue, provides further support for that idea, and also helps explain how the pathway malfunctioning might lead to cancer. It shows that damage to a well-known tumor suppressor gene--the adenomatous polyposis coli gene (APC), which is lost or inactivated in some 85% of colorectal cancers--can result in activation of an equally prominent oncogene--the c-MYC gene--via the Wnt pathway. Such abnormal MYC activation may in turn lead to excessive cell proliferation. Researchers are becoming optimistic that they can put these results to work developing new anticancer drugs that act by blocking c-MYC activation.

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Cancer Res. 61, 5619-5629
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c-myc/p53 Interaction Determines Sensitivity of Human Colon Carcinoma Cells to 5-Fluorouracil in Vitro and in Vivo.
D. Arango, G. A. Corner, S. Wadler, P. J. Catalano, and L. H. Augenlicht (2001)
Cancer Res. 61, 4910-4915
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Increased {beta}-Catenin Expression and Nuclear Translocation Accompany Cellular Hyperproliferation in Vivo.
J. H. Sellin, S. Umar, J. Xiao, and A. P. Morris (2001)
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Prostacyclin-mediated activation of peroxisome proliferator-activated receptor delta in colorectal cancer.
R. A. Gupta, J. Tan, W. F. Krause, M. W. Geraci, T. M. Willson, S. K. Dey, and R. N. DuBois (2000)
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Secreted Frizzled-related Protein-1 Binds Directly to Wingless and Is a Biphasic Modulator of Wnt Signaling.
A. Uren, F. Reichsman, V. Anest, W. G. Taylor, K. Muraiso, D. P. Bottaro, S. Cumberledge, and J. S. Rubin (2000)
J. Biol. Chem. 275, 4374-4382
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Axin Forms a Complex with MEKK1 and Activates c-Jun NH2-terminal Kinase/Stress-activated Protein Kinase through Domains Distinct from Wnt Signaling.
Y. Zhang, S. Y. Neo, X. Wang, J. Han, and S.-C. Lin (1999)
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H-Ras Activation Promotes Cytoplasmic Accumulation and Phosphoinositide 3-OH Kinase Association of {beta}-Catenin in Epidermal Keratinocytes.
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J. Cell Biol. 146, 967-980
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Topical Review: Molecular Heterogeneity in Medulloblastoma With Implications for Differing Tumor Biology.
A. M. Adesma (1999)
J Child Neurol 14, 411-417
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Quantitation of MYC Gene Expression in Sporadic Breast Tumors with a Real-Time Reverse Transcription-PCR Assay.
I. Bieche, I. Laurendeau, S. Tozlu, M. Olivi, D. Vidaud, R. Lidereau, and M. Vidaud (1999)
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Overexpression of Protein Kinase C beta II Induces Colonic Hyperproliferation and Increased Sensitivity to Colon Carcinogenesis.
N. R. Murray, L. A. Davidson, R. S. Chapkin, W. Clay Gustafson, D. G. Schattenberg, and A. P. Fields (1999)
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K. Ogawa, Y. Yamada, K. Kishibe, K. Ishizaki, and Y. Tokusashi (1999)
Cancer Res. 59, 1830-1833
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Nuclear beta-catenin and the development of bilateral symmetry in normal and LiCl-exposed chick embryos.
T Roeser, S Stein, and M Kessel (1999)
Development 126, 2955-2965
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