Antonette C. Preisinger

TL;DR: It is suggested that most tumours with allelic deletions of chromosome 17p contain p53 point mutations resulting in amino-acid substitutions, and p53 gene mutations are clustered in four 'hot-spots' which exactly coincide with the four most highly conserved regions of the gene.

TL;DR: The APC gene was identified in a contig initiated from the MCC gene and was found to encode an unusually large protein, and these two closely spaced genes encode proteins predicted to contain coiled-coil regions, which were also expressed in a wide variety of tissues.

TL;DR: The data suggest that more than one gene on chromosome 5q21 may contribute to colorectal neoplasia, and that mutations of the APC gene can cause both FAP and GS.

TL;DR: A contiguous stretch of DNA comprising 370 kilobase pairs has now been cloned from a region of chromosome 18q suspected to reside near the DCC gene, which may play a role in the pathogenesis of human colorectal neoplasia, perhaps through alteration of the normal cell-cell interactions controlling growth.

TL;DR: Data suggest that the rate limiting step in p53 inactivation is point mutation and that once a mutation occurs, loss of the remaining wild-type allele rapidly follows, and the p53 gene may play a causal role in this progression.