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Biomedical subjects

D Dix

Publications and source records attributed to D Dix.

45 records · Page 3Linked to original sources
PubMedDate not supplied

On the role of aging in carcinogenesis.

BACKGROUND: Previously we identified the age at half-total incidence (Age 1/2) for a variety of tumors. In this paper, we compare the Age 1/2 with the age- standardized incidence rate (ASR) in populations that differ a) genetically and environmentally and b) genetically but not environmentally. MATERIALS AND METHODS: From 1990-era data, we calculated 95% confidence limits about mean values for Age 1/2 and ASR for cancers of the stomach, colon, rectum, lung, female breast, corpus uterus, ovary, testis and prostate. RESULTS: In populations that differed genetically and environmentally as well as those that differed genetically but not environmentally, we observed large variations in ASR, with little or no variation in Age 1/2. CONCLUSION: The determinants of ASR are distinct from the determinants of Age 1/2 and likely to be genes that can vary between tissues of tumor origin but are common to all people.

Age Factors↗
PubMedDate not supplied

On the role of aging in cancer incidence: analysis of the skin cancer data.

Worldwide age-incidence patterns for melanoma, non-melanoma skin cancer, and the group of all cancers except non-melanoma skin cancer from 1971 to 1976 were normalized for differences in frequency of occurrence and compared. The percentage of total cancer incidence that occurred in young subjects was greater for melanoma and less for non-melanoma skin cancer than for the group of all cancers. The risk for melanoma was apparent by age 15, much earlier than for non-melanoma skin cancer and the group of all cancers. While the risk for non-melanoma skin cancer and the group of all cancers increased continuously with advancing age, the risk for melanoma was constant beyond age 35. We conclude that risk for melanoma is unusually concentrated among the young, and, therefore, that protection from sun exposure is particularly important for this group.

Age Factors↗
PubMedDate not supplied

On the role of aging in cancer incidence: cohort analyses of the lung cancer data.

Lung cancer age-specific mortality rates for male and female cohorts born in the United States between 1903 and 1928 increase from age 32 to 52 according to an equation of the form log (mortality rate) = m(age) + b, where m and b are constants. Variation exists among the cohorts in the magnitudes of m and b, but correlation coefficients between age-mortality patterns among all cohorts are highly positive (r greater than 0.98, p less than 0.01), indicating that the form of the equation is similarly appropriate for each cohort. Because cigarette smoking behavior has varied among cohorts and between sexes, we conclude that the form of the equation, i.e., the exponential nature of the lung cancer age-mortality pattern, is independent of environmental carcinogenicity and is best attributed to some aspect of the intrinsic aging process.

Adult↗
PubMedDate not supplied

On the role of aging in cancer incidence: analysis of the lung cancer data.

Age-specific lung cancer mortality rates for U.S. males and females from 1935 to 1978 were normalized to describe the percentage of total mortality in a given era which occurred at a given age interval. Correlation coefficients between age-mortality patterns for various eras were calculated and found to be highly positive. We conclude that the shape of the lung cancer age-mortality pattern has remained remarkably constant despite dramatic changes in the carcinogenicity of the lung environment, and suggest that shape is determined by an invariant influence which is best attributed to some aspect of the aging process.

Adult↗
PubMedDate not supplied

The incidence of female cancers: correlations with etiologic implications.

Correlation coefficients were calculated between incidence rates for the most frequent female cancers in populations throughout the world. Positive correlations were generally weak, and we conclude that most female cancers do not share a dominant etiologic factor which is inherent in cancer incidence rates. However, most cancers do exhibit similar age-incidence patterns. We also conclude that the determinant of shape in cancer age-incidence patterns is common to most female cancers, internationally invariant, and independent of the determinants of cancer incidence rates. Breast cancer exhibits an unusual age-incidence pattern with a peculiar dependence on the frequency of breast cancer occurrence.

Age Factors↗
PubMedDate not supplied

The incidence of female breast and genital cancer: analysis of the age-dependence.

Worldwide age-incidence patterns for female breast and genital cancers were normalized for differences in frequency of tumor occurrence and compared. The percentage of total cancer incidence which occurred in elderly subjects differed between populations but was similar for cancer of the breast, ovary, and corpus uteri within a given population. In addition, cancers of the breast, ovary, and corpus uteri exhibited similar ranges of distribution about the worldwide median incidence at all age intervals and strong positive correlations between crude incidence rates in the populations studied. Despite these and other similarities, breast cancer exhibited a correlation between crude incidence rate and percentage of total incidence which occurred in elderly subjects which was not apparent in the genital cancers. We cannot exclude the possibility that this correlation is coincidental. However the possibility of identifying factors predisposing to or protecting against breast cancer is attractive. The results of this study suggest that such factors would apply to breast but not to genital tissue.

Adult↗
PubMedDate not supplied

The incidence of breast cancer: analysis of the age dependence.

The incidence of female breast cancer was studied as a function of age in 71 different populations throughout the world. Incidence data was normalized for differences in frequency of occurrence. Median normalized incidence increased exponentially from age 20 to 45. After age 45 the rate of incidence decreased, and we suggest that menopause may be responsible for the rate reduction. Populations were not randomly distributed about the total population median normalized incidence at the various age intervals. Populations were classified according to their age-incidence patterns in 3 groups: Group 1 (with median % incidence after age 69=50): Group 2 (with median % incidence after age 69=47), and Group 3 (with median % incidence after age 69=31). At most age intervals, the normalized incidence in Group 1 populations was less than the total median, while the normalized incidence in Group 3 populations was greater than the total median. Although we cannot exclude the possibility that the variation in age-incidence patterns among the population groups is an artifact of tumor registration errors, evidence suggests that such an artifact is unlikely. Breast cancer occurs more frequently in Group I populations than it does in Group 3 populations. We suggest that Group 3 populations may share an element of protection from, or that Group I populations may share an element of risk for, breast cancer.

Adult↗
PubMedDate not supplied

The incidence of male genital tumors: a cellular model for the age dependence.

Most human tumors, including most male genital tumors, exhibit an exponential increase in incidence with advancing age of the host. This exponential age-incidence pattern can be explained by the accumulation of mutations in the stem cells of the tissues of tumor origin. The age-incidence pattern for testicular tumors, however, is unique with a large linear increase in incidence from age 14 to 30 and a linear decline in incidence from age 30 to 60. After age 60, the incidence of testicular tumors remains low and constant. The probability of testicular tumorigenesis is determined by the susceptibility of male germ cells to neoplastic mutation and/or the neoplastic mutagenicity of the male germ cell environment. Since there is no evidence for an environmental mutagen which is specific for male germ cells, and since male germ cells are unusually susceptible to mutation, we interpret the variation in testicular tumor incidence with age as a reflection of the susceptibility of male germ cells to neoplastic mutation. Cell are most susceptible to mutation during genome replication and we propose a model for testicular tumorigenesis which is consistent with the available data on male germ cell proliferation and with the data on testicular tumor incidence.

Adolescent↗