Biomedical subjects
Publications and source records attributed to E White.
Because there has been a recent trend toward delay of childbearing in the United States, women in the birth cohort of 1945-49 will have an estimated 5 per cent greater incidence of breast cancer, and those in the cohort of 1950-54 an estimated 9 per cent greater incidence compared with the cohort of 1935-39, which had the distribution of age at first birth most favorable for breast cancer risk.
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The prevalence of several known or suspected risk factors for breast cancer is changing among young women. The time trend in incidence of breast cancer among young women in western Washington was analyzed as a possible predictor of trends in future incidence rates. Data were from the Seattle-Puget Sound Surveillance, Epidemiology, and End Results cancer registry. For women age 25-44 years (n = 1,869 cases), the incidence of breast cancer increased by 22% (P less than .001) between the time periods 1974-77 and 1982-84. The estimated annual increase was 2.5% (P less than .001). The increase in incidence over time appeared to be greater among those residing in low-income census tracts of urban counties and among black women. Possible relationships between the observed increase in rates and trends of risk factors for breast cancer are discussed.
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For many diseases, a set of diagnostic criteria with perfect sensitivity and specificity does not exist. In the design of a follow-up study of such a disease, one often has a choice between using a set of narrow classification criteria for the disease outcome (i.e., a test with relatively high specificity and relatively low sensitivity) or a broader set of criteria (i.e., a more sensitive, less specific test). A model was investigated which simulated choices one may have between disease classification tests, to determine how the required sample size and bias in the estimates of the risk ratio and risk difference varied between tests. A two-sample study with nondifferential misclassification of disease outcome was assumed. Based on the model, the bias in the risk ratio increases as one increases the sensitivity of the diagnostic test at the expense of specificity. Conversely, the bias in the risk difference decreases with increasing sensitivity and declining specificity. The required sample size is minimized at relatively high sensitivity and relatively low specificity. Selection of the disease classification test as that at which the required sample size is minimized could reduce some of the large data collection costs of follow-up studies. The advantages and limitations of applying this technique to actual studies are discussed.
Adenovirus mutants carrying alterations in the gene encoding the E1B 19-kilodalton tumor antigen (19K protein) cause enhanced cytopathic effect (cyt phenotype) and the degradation of host-cell chromosomal DNA (deg phenotype) upon infection of human HeLa or KB cells. Furthermore, E1B 19K gene mutant viruses are defective for cellular transformation. We report that these mutant viruses possess a host-range phenotype for growth in human cells. In human HeLa cells the mutant viruses grew to the same levels as the wild-type virus, but they were severely defective for growth in KB cells. In human WI38 cells, the E1B 19K gene mutant viruses had a substantial growth advantage over the wild-type virus, yielding 500-fold-higher titers. Viral DNA synthesis was reduced 10- to 20-fold in WI38 cells infected with the wild-type virus relative to that synthesized by the E1B mutant viruses. Viral early and late protein synthesis was similarly reduced in wild type- relative to mutant-infected cells. These reduced levels of early gene expression in wild-type virus-infected cells were paralleled by comparably reduced levels of early cytoplasmic mRNA. The primary cause of this host-range phenotype appeared at the level of early gene transcription, since transcription of viral early genes in the mutant-infected cells was substantially greater than levels found in cells infected with the wild-type virus. These results implicate the E1B 19K tumor antigen in the regulation of adenovirus early gene expression. Specifically, the E1B 19K protein directly or indirectly exerts a negative effect on early gene transcription accounting for efficient gene expression from the E1B mutant viruses in WI38 cells. Based on these findings it is probable that the cyt and deg phenotypes observed in mutant-infected HeLa and KB cells are the result of the pleiotropic effect of this altered gene regulation.