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C Coles

Publications and source records attributed to C Coles.

9 recordsLinked to original sources
PubMed1992

p53 mutations in breast cancer.

We have identified and analyzed 41 mutations in p53 in sporadic breast tumors from 136 unselected breast cancer patients and estimate that approximately 40% of such tumors contain p53 mutations. The frequency of G-T transversions and the incidence of guanosine mutations in the nontranscribed strand of the p53 gene were found to be higher than expected, and we suggest, therefore, that exogenous carcinogens have an etiological role in sporadic breast cancers. Mutations were recorded in 44 codons of the p53 gene, with no obvious mutational hot-spots, although mutations at codons 175, 194, 273, and 280 accounted for 25% of the changes. One germ-line mutation was found in 136 patients and so we conclude that constitutional mutation of p53 may be an uncommon etiological factor in breast cancer.

Base Composition↗
PubMed1990

Evidence implicating at least two genes on chromosome 17p in breast carcinogenesis.

The DNA of paired tumour and blood leucocyte samples from a large series of breast cancer patients was analysed to map regions of loss of heterozygosity on chromosome 17. The high frequency of loss of heterozygosity on 17p was confirmed, and a third of informative tumours had also lost an allele at the long arm locus THH59. On the short arm two distinct regions of loss of heterozygosity were identified, in bands p13-3 and p13-1. The latter probably involves the structural gene p53, which has been implicated as an oncogene or as a tumour suppressor in various human cancers. 17p 13-3, however, showed a significantly higher frequency of loss of heterozygosity, and there was no correlation between allele losses at the two sites. Nevertheless, loss of heterozygosity at 17p 13-3 is associated with overexpression of p53 mRNA, suggesting the existence of a gene some 20 megabases telomeric of p53 that regulates its expression. Lesions of this regulatory gene seem to be involved in the majority of breast cancers.

Alleles↗
PubMed1988

Late-onset schizophrenia. Studying clinical validity.

The authors compared clinical characteristics of 36 late-onset schizophrenic patients from four centers (hospitals in San Diego, Baltimore, Los Angeles, and Montreal). There was a preponderance of the paranoid type with bizarre delusions and auditory hallucinations, chronic course of illness, and response to relatively low doses of neuroleptics. A comparison of late-onset and younger schizophrenic patients revealed both similarities and differences between the two groups. The authors reviewed the relevant literature and discussed the implications for assessing the validity of the concept of late-onset schizophrenia. They believe that, although less common, late-onset schizophrenia is probably as valid an entity (or group of entities) as schizophrenia with onset before age 45.

Adult↗