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[Cancer Research 54, 5523-5526, November 1, 1994]
© 1994 American Association for Cancer Research
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Molecular Determinants of Dysplasia in Colorectal Lesions1

Jin Jen2, Steve M. Powell2, Nickolas Papadopoulos, Kelly J. Smith, Stanley R. Hamilton, Bert Vogelstein and Kenneth W. Kinzler3

The Johns Hopkins Oncology Center, Baltimore, Maryland 21231 [J. J., S. M. P., N. P., K. J. S., B. V., K. W. K.], and Department of Pathology, The Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205-2196 [S. R. H.]

One hallmark of malignant potential is dysplasia, the disruption of normal morphology. While it is generally recognized that cancer is the result of a series of genetic changes, the relationship of these alterations and their timing to the advent of dysplasia remains obscure. To address this issue, 54 small benign colorectal lesions of various malignant potential were analyzed for APC and K-RAS mutations, two alterations which have been implicated in the early stages of colorectal tumorigenesis. APC mutations were closely associated with dysplasia. In contrast, K-RAS mutations were found to be remarkably common in small nondysplastic lesions which apparently have a limited potential to progress to larger tumors. These results provide evidence that the nature and order of genetic changes can have a specific impact on both tumor morphology (e.g., dysplasia) and the likelihood of tumor progression.

1 This work was supported in part by grants from the Clayton Fund and NIH Grants GM-07184 and CA-57345. B. V. is an American Cancer Society Research Professor.

2 These authors contributed equally to this work.

3 To whom correspondence should be addressed at The Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231.

Received 7/28/94. Accepted 9/20/94.




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