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K M Weiss

Publications and source records attributed to K M Weiss.

At least 91 records · Page 5Linked to original sources
PubMed1984

A method to detect excess risk of disease in structured data: cancer in relatives of retinoblastoma patients.

It is often of interest to know whether there is increased occurrence of a trait in a pedigree or other structured set of epidemiological data. In answering such questions most current methods use aggregate measures, such as relative risk, that may not relate the outcome for each individual to that individual's risk. In this paper we present a simple method, and its computational algorithm, to overcome this limitation. This new method also permits one to identify high-risk families or subsets of a collection of data, which is not always possible using other approaches. In a study of cancer risk among relatives of retinoblastoma patients, by applying this new method it was found that 11 of 33 families each obtained through a unilateral retinoblastoma patient are at statistically high risk of cancer at all sites combined, while there are 15 of 47 such families obtained through a bilaterally affected proband. These results are unlikely to have occurred by chance, indicating an overall excess risk in the ancestors of these retinoblastoma cases. The proposed test procedure does not specify the cause of elevated risk; however, a method is proposed that provides some indication regarding possible causal mechanisms under some circumstances.

Biometry↗
PubMed1984

Reconstruction of genealogies from vital records: the Laredo Epidemiology Project.

The Laredo Epidemiology Project is a study of the patterns of degenerative disease, particularly cancer, in the families of Laredo, Texas. The genealogical history of Laredo was reconstructed by the grouping of 350,000 individual church and civil vital event records into multigenerational families, with record linkage based on matching names. Mortality data from city death records are mapped onto these pedigrees for analysis. This paper describes the creation of the data base and evaluation of the links.

Computers↗
PubMed1984

Cancer mortality in relatives of retinoblastoma patients.

The risk of other cancers in relatives of retinoblastoma (RTB) patients was determined by a survey of the mortality experience of siblings, parents, parental siblings, and grandparents of all U.S. or Canadian RTB patients referred to The University of Texas M.D. Anderson Hospital and Tumor Institute between 1944 and 1980. Expected mortality was ascertained by the application of age-, sex-, race-, and calendar year-specific U.S. mortality rates to the observed person-years. Among 607 relatives of 33 unilateral-sporadic RTB probands, no excess in cancer deaths was observed (observed/expected = 18/22). Among 733 relatives of 47 bilateral-familial RTB probands, a slight excess in cancer deaths was observed (41/31). A significant excess in cancer deaths was occurred in relatives under age 55 years (18/9) and in fathers (7/1) of the bilateral RTB probands. To determine whether the cancer excess was related to some unique allele associated with second tumors in RTB survivors, the cancer mortality of 203 relatives of the 14 RTB patients with second tumors was examined, and no excess was observed (11/11). To determine whether the excess might be attributable to an unexpressed RTB gene or precursor, the mortality experience was examined in 6 kindreds in which parents, unaffected by RTB, had more than 1 child with RTB. Among these 72 relatives a significant excess in cancer deaths was observed (8/2). The findings demonstrate a modest overall cancer excess in relatives of hereditary RTB patients and suggest it may be attributable to an unexpressed RTB gene or precursor in a small number of kindreds. Mechanisms for an apparent "precursor" might involve a delayed mutation, genetic mosaicism, or a submicroscopic balanced chromosomal translocation.

Adolescent↗
PubMed1984

Multistage risk models and the age pattern in familial polyposis coli.

Multistage risk models provide a close fit to most age patterns of adult-onset cancers. Such models posit that a number of events must occur before some cell in a tissue is transformed from normal to neoplastic. When an approximate version of the models has been fitted to data, this number has been estimated to be about 4-6. In fitting the same approximate model to the age pattern of onset of colon cancer in bearers of the Familial Polyposis coli (FPC) gene, several authors have found that the number of stages estimated was about two to three fewer than those for colon cancer in the general population. However, when an exact multistage model is used rather than an approximation to it, this is no longer the case: the number of stages estimated from the general population becomes too large to be compatible with what is known about carcinogenesis from laboratory experiments, and the number estimated from FPC victims is larger than that for the general population. "Inherited-hit" models of the nature of the FPC gene may be correct at the cellular level, but multistage models as commonly formulated cannot be used on data on the age-onset patterns in populations of individuals to infer such mechanisms or estimate their parameters.

Age Factors↗
PubMed1984

[Not Available].

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Demography↗
PubMed1984

Genetics and epidemiology of gallbladder disease in New World native peoples.

Native peoples of the New World, including Amerindians and admixed Latin Americans such as Mexican-Americans, are highly susceptible to diseases of the gallbladder. These include cholesterol cholelithiasis (gallstones) and its complications, as well as cancer of the gallbladder. Although there is clearly some necessary dietary or other environmental risk factor involved, the pattern of disease prevalence is geographically associated with the distribution of genes of aboriginal Amerindian origin, and levels of risk generally correspond to the degree of Amerindian admixture. This pattern differs from that generally associated with Westernization, which suggests a gene-environment interaction, and that within an admixed population there is a subset whose risk is underestimated when admixture is ignored. The risk that an individual of a susceptible New World genotype will undergo a cholecystectomy by age 85 can approach 40% in Mexican-American females, and their risk of gallbladder cancer can reach several percent. These are heretofore unrecognized levels of risk, especially of the latter, because previous studies have not accounted for admixture or for the loss of at-risk individuals due to cholecystectomy. A genetic susceptibility may, thus, be as "carcinogenic" in New World peoples as any known major environmental exposure; yet, while the risk has a genetic basis, its expression as gallbladder cancer is so delayed as to lead only very rarely to multiply-affected families. Estimates in this paper are derived in part from two studies of Mexican-Americans in Starr County and Laredo, Texas.

Adolescent↗
PubMed1982

Problems in the assessment of relative risk of chronic disease among biological relatives of affected individuals.

A question often asked in regard to a chronic disease is whether the risk to a biological relative of a case is evaluated, and if so by how much the risk is altered. To answer this question, data may be collected directly with genetic objectives in mind by ascertaining population of pedigrees. More often, the initial assessment of the question comes from family history data collected in an incidental manner in the course of a case-control or similar type of study. This paper discusses some limitations to the inferences which can be derived from such casual family history data. These include (i) poor statistical properties of standard relative risk measures, (ii) interpretational problems of observed relative risks when affected cases arise from genetic as well as nongenetic causes and when genes may not always be expressed in individuals in whom they are present, and (iii) confounding effects which may occur when a high risk allele alters the age of onset pattern of the disease. These problems result largely from a loss of design control over the degree of exposure of individuals ascertained and can lead to a small observed relative risk value even when genetic factors are important. Suggestions for handling such casual family history data are offered.

Age Factors↗
PubMed1981

A simple test for the aggregation of disease occurrence in genealogical data.

A simple test for the aggregation of occurrence of a trait in genealogical data is given; a test criterion is developed, and the power of the test to detect aggregation of risk is computed. The test utilizes pairs of individuals between whom transmission of risk factors may occur. As long as aggregation is reasonably strong and prevalence not too low, only modest amounts of data are required. It provides an easy and inexpensive first examination of data which can reveal whether the effort required to conduct more elaborate genealogical studies and analysis is warranted.

Genetic Diseases, Inborn↗
PubMed1980

A test for the radomness of the occurrence of a disease trait in familial or other similar ordered sequences of epidemiological data.

Through the construction of a probability distribution, a test is proposed for the randomness of the occurrence of an epidemiological event in a series of structured ordered sequences. Such sequences may be of persons admitted to hospital in some specified order, individuals seen in a large set of extended screening program, or individuals in a large set of extended genealogies. Modifications to account for the limited length of ascertained sequences are also given. The method will be particularly important in the first-stage evaluation of genealogical data to indicate the existence and degree of familial aggregation of diseases such as cancer and to justify more complex methods of analysis designed to evaluate the specific elements of causation that may be operating. The statistical power of this approach is also derived, considering the anticipated sample sizes in its application, to detect some forms of familial aggregation in a large genealogical data base from Laredo, Texas.

Age Factors↗
PubMed1980

Genetic epidemiology: four strategies.

Human genetics has long been preoccupied with the study of simple, single locus traits and, indeed, it is still asserted that "the primary goal of human genetic analysis should be the detection and estimation of single gene effects" (102). But there is increased recognition that the greater portion of the human burden of disease and disability stems not from such conditions but rather those in which the appearance of the disorder is only the last stage in a lifelong train of prodromal states. There is almost universal agreement that our living conditions and behavior are major contributory factors to their occurrence. It is equally true that there are inherent differences among us which also contribute. The assessment of the roles of these contributors, intrinsic and extrinsic, and the development of environmental manipulations which cure or prevent disease and disability of this nature have become the new frontiers of genetics and human medicine. We have described briefly four investigative, genetic strategies, two essentially concerned with analysis and two with sampling, which can contribute to the conquest of these frontiers. We have attempted to place these strategies in an epidemiologic context.

Epidemiologic Methods↗
PubMed1976

Archeology, population genetics and studies of human racial ancestry.

Using traditional classification, many people have tried to determine the place and time of origin of the major human races. Two basically conflicting views have prevailed, one asserting that races developed as local variations in a species evolving phyletically over much of the Old World for up to one million years, and the other view holding that present races are local variations on populations recently expanding into most areas and replacing the previous hominid inhabitants, this occurring since the time of the Neanderthals. Both views are based on the same archeological data. Gene frequency data and time-calibrated genetic distance measures have recently been applied to this problem. Here we show that the probable demographic nature of Pleistocene populations has obscured genetic distances to such an extent that they cannot be used to discriminate between the two viewpoints of racial origins. The racial classifications themselves are probably not useful in this context and obscure the question, so that we presently do not have a scientifically valid understanding of racial origins.

Archaeology↗
PubMed1975

The genetic structure of a tribal population, the Yanomama Indians. XII. Biodemographic studies.

The Yyanomama Indians of Southern Venezuela and Northern Brazil are one of the largest, relatively unacculturated tribes of the tropical rain forest. Over a period of eight years data have been collected from a considerable portion of their territory on estimated age, sex ratio, fertility rates (as determined by physical examination and urine tests), and infant death rates. Although it has been impossible to collect direct data on infanticide, this subject can be approached indirectly through distortions of the sex ratio and anecdotal information. Some historical data are also available as a basis for estimating tribal expansion in the past 100 years. With this material it has been possible to construct Life Tables for the anomama,, and to explore the results of various perturbations of the input parameters. Data are also presented on patterns of mating and reproduction: number of spouses, mean and variance in number of surviving children, frequency of "extra-marital conceptions" based on the results of extensive blood group typings, and consanguinity rates as determined by observation and computer simulation. Although we do not present the Yanomama as typical, these data are seen as providing a basis for more realistic population models than have existed in the past. In addition, the data provide a basis for relatively precise estimates of such demographic measures as Fisher's Reproductive Value, Crow's Index of Total Selection, and Weiss' Index of Growth Regulation.

Adolescent↗