Ann C. Preisinger

TL;DR: It is found that ras-gene mutations occurred in 58 percent of adenomas larger than 1 cm and in 47 percent of carcinomas, which are consistent with a model of colorectal tumorigenesis in which the steps required for the development of cancer often involve the mutational activation of an oncogene coupled with the loss of several genes that normally suppress tumors.

TL;DR: The data suggest that p53 gene mutations may be involved in colorectal neoplasia, perhaps through inactivation of a tumor suppressor function of the wild-type p53 genes.

TL;DR: In addition to its implications concerning the genetic events underlying tumorigenesis, tumor allelotype may provide a molecular tool for improved estimation of prognosis in patients with colorectal cancer.

TL;DR: A number of bladder tumors can arise from the uncontrolled spread of a single transformed cell, which can then grow independently with variable subsequent genetic alterations.

TL;DR: Several X-chromosome probes derived from the hypoxanthine phosphoribosyltransferase gene and the phosphoglycerate kinase gene could be used for clonal analysis in over 50% of American females and were found to accurately reflect clonality in more than 95% of 92 tumors tested.