Hormone replacement therapy and breast cancer risk.
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Breast Neoplasms↗
Biomedical subjects
K K Namboodiri
Publications and source records attributed to K K Namboodiri.
Nonsteroidal antiinflammatory drugs and breast cancer.
We examined the association of nonsteroidal antiinflammatory drugs and breast cancer risk in a case-control study of 511 breast cancer patients and 1,534 population control subjects. The relative risk of breast cancer was reduced in women using these compounds at least 3 times per week for > or = 1 year [odds ratio (OR) = 0.66; 95% confidence interval (CI) = 0.52-0.83]. Odds ratios were similar for use of ibuprofen (0.57) or aspirin per se (0.69). Breast cancer risk declined with increasing exposure, and the greatest risk reduction (40%; odds ratio = 0.60; 95% CI = 0.40-0.91) occurred at the highest level of use (daily intake for > or = 5 years). These results indicate that nonsteroidal antiinflammatory drugs may have chemopreventive potential against the development of breast cancer.
Adult↗
Breast cancer risk from diet, tobacco, and alcohol.
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Alcohol Drinking↗
The Ohio Cancer Information Service: technology transfer on clinical trials and other measures of cancer control.
We examined trends in caller queries on tobacco, mammography, Pap tests, and clinical trials to the NCI-sponsored Cancer Information Service (CIS) of Ohio via its toll free telephone number (1-800-4-CANCER) during 1986-1991. Calls on NCI-approved clinical trials and treatment protocols tripled during the study period (from 6% in 1986 to 20% in 1991, p < 0.01) primarily due to counselor-initiated (proactive) recommendations and actions. Calls on breast cancer showed a significant increase whereas calls on respiratory system cancers showed a decline over the time period. There was also a dramatic increase in calls on mammography, reflecting the impact of national and local promotion of breast screening. Queries on tobacco use and Pap tests declined, perhaps due to a perceived saturation effect of public education on these two topics. Our results support the use of CIS as a technology transfer system.
Breast Neoplasms↗
Breast cancer risk: effects of estrogen replacement therapy and body mass.
BACKGROUND: Epidemiologic studies have focused on the association between breast cancer risk and a variety of lifestyle and exogenous factors. PURPOSE: The purpose of this study was to clarify the effects of alcohol consumption, cigarette smoking, oral contraceptive (OC) use, estrogen replacement therapy (ERT), and body mass on risk of breast cancer. METHODS: These variables were examined in a case-control study of 604 patients with newly diagnosed breast cancer and 520 control subjects who did not have breast cancer and were frequency matched for age, hospital, and time of diagnosis. These case patients and control subjects were part of an ongoing study of breast cancer by the American Health Foundation and were selected for interview from hospitals in the New York City area from January 1987 through December 1989. The data were analyzed by computation of odds ratios (ORs) for potential risk factors, with adjustment for age at diagnosis and other potential confounding variables and with stratification by menopausal status. RESULTS: We observed positive effects of ERT and high body mass on the risk of postmenopausal breast cancer, particularly when each factor was examined in the absence of the other factor. In lean postmenopausal women, the adjusted summary OR associated with ERT was significantly elevated (OR = 2.0; 95% confidence interval [CI] = 1.1-3.5; P < .01), and there was a statistically significant dose response of breast cancer risk with ERT duration (adjusted ORs = 2.0 for < 5 years and 2.2 for > or = 5 years; positive trend, P < .02). Reciprocally, in women who did not receive ERT, high body mass (Quetelet index > 27) was a significant risk factor for postmenopausal breast cancer (OR = 2.1; 95% CI = 1.3-3.3; P < .02), and the linear trend in risk with increasing body mass was significant (positive trend, P < .02). The strongest effect of body mass occurred in women who were lean at age 18 and gained enough weight to place them in the upper tertile of body mass at the time of diagnosis (OR = 2.6; 95% CI = 1.5-4.6; P < .01). There was no evidence of significant positive associations between breast cancer risk and cigarette smoking, alcohol consumption, or OC use in any subgroup of these women. CONCLUSIONS: Our results support the hypothesis that excess adipose deposition heightens breast cancer risk in the postmenopausal years. Furthermore, they underscore the need for continuing investigation of the effects of exogenous estrogens on the development of this malignancy, particularly in lean postmenopausal women.
Adult↗
Hematopoietic and lymphoproliferative cancer among male veterans using the Veterans Administration Medical System.
Hematopoietic and lymphoproliferative cancer risk among the 3.7 million United States male veterans who use the Veterans Administration (VA) medical system annually was assessed using age-specific incidence curves and cumulative incidence rates. Relative risk comparing the VA with general population risk estimates from the Surveillance, Epidemiology, and End Results (SEER) data were increased significantly for all malignancies examined. The VA sample showed risk increases of 93% for Hodgkin's disease, 20% for non-Hodgkin's lymphomas, 51% for multiple myelomas, and 40% for all leukemias. Among the leukemia subtypes, the observed risk increases were 54%, 23%, 80%, and 46% for lymphocytic, granulocytic, monocytic, and other forms of leukemia, respectively. The large size of the sample and the consistency of risk estimates with two different methods confer validity and strength to these findings. The possible relevance of the high prevalence of tobacco and alcohol use in this population sample to the current findings is discussed and the need for further analytic investigations to explain the increases in risk is emphasized.
Adult↗
Ohio Cancer Information Service: a decade of experience.
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Consumer Behavior↗
Biological and cultural sources of familial resemblance in plasma lipids: a comparison between North America and Israel--the Lipid Research Clinics Program.
Heterogeneity in determinants of familial resemblance of lipid and lipoprotein levels between populations in North America and Israel was investigated using path analysis. A common protocol, identical measurement techniques, and the same statistical procedures were used in the two samples. Both genetic (h2) and cultural (c2) determinants of inheritance were significant for all lipid variables in the two studies. Genetic and cultural heritability of total cholesterol (h2 = 0.61, c2 = 0.02), low-density lipoprotein cholesterol (h2 = 0.59, c2 = 0.02), and high-density lipoprotein cholesterol (h2 = 0.55, c2 = 0.06) did not differ significantly between North America and Israel, while there was a significant difference for triglyceride (h2 = 0.41, c2 = 0.07 in North America; h2 = 0.61, c2 = 0.05 in Israel). Secondary parameters of the path model describing intrafamilial environmental relationships differed between the two countries. In particular, there was a higher correlation between marital environments in Israel for all traits except triglyceride, and a larger effect of father's environment on offspring's environment in Israel for all traits. Within both populations, variation of plasma lipids and lipoproteins was mostly explained by genetic factors and random unmeasured environmental factors. The contribution of common family environment was found to be small, though statistically significant. This is probably due to homogeneity of the distribution of familial environmental determinants within both countries.
Cholesterol↗
Genetic analysis of serum lipid levels and blood pressure in a large kindred.
A 267-member Caucasian kindred with a high incidence of cardiovascular disease, originally from Evans County, Georgia, was chosen for genetic analysis of serum lipid levels and blood pressure. Total serum cholesterol, triglycerides, high density lipoprotein cholesterol (HDL), and systolic and diastolic blood pressures were natural logarithm transformed and then adjusted for significant age, sex, and behavioral trait effects. Major gene pedigree analysis was used to estimate genetic parameters and to test hypotheses about the mode of transmission of each trait. Multivariate methods were also used to estimate linear combinations of the variables that best fit genetic models. The data were consistent with a major gene segregating for high levels of triglycerides in this kindred. However, dominant and recessive hypotheses could not be distinguished. Although diastolic blood pressure fit a mixture of two distributions significantly better than a single normal, major gene hypotheses could be rejected while the no-transmission hypothesis could not. There was no evidence of a major gene effect on cholesterol, HDL, systolic blood pressure, or any of the hypothetical traits represented by linear functions of the physical-lipid traits.
Adult↗
Parent-offspring aggregation of plasma lipids in selected populations in North America and Israel. The Lipid Research Clinics Prevalence Study.
Parent-offspring associations of total cholesterol and triglycerides were compared between family dyads in six North American populations examined between 1972 and 1976 as part of the North American Lipid Research Clinics Prevalence Study and those from families examined between 1976 and 1979 at the Lipid Research Clinic located in Jerusalem. Common study design, protocol, and laboratory techniques were used by all Lipid Research Clinics. The authors first examined homogeneity of familial correlations across clinics in the North American population and across origin groups in the Israeli sample. In general, correlations were homogeneous across clinics and origin groups, except for parent-daughter pairs for triglycerides in North America. The pooled familial correlations were similar in the two study populations. There was no asymmetry in parent-offspring correlations by the sex of the offspring. The pooled mother-child correlations were significantly higher than father-child values in the North American sample only. The strength of parent-offspring similarity showed no consistent pattern of change with level of education of parents in either study group. Patterns of familial similarity are discussed in relation to genetic, cultural, and environmental differences between the two study populations.
Adolescent↗
Segregation analysis of low levels of high-density lipoprotein cholesterol in the collaborative Lipid Research Clinics Program Family Study.
Complex segregation analysis with the unified mixed model in white families from nine lipid research clinics was carried out to delineate the mode of familial transmission of plasma high-density-lipoprotein cholesterol (HDL-C). Three groups of families from the collaborative Lipid Research Clinics Program Family Study were assessed: 1,146 selected at random, 483 obtained through hypercholesterolemic probands, and 177 selected from the random sample because a number had low HDL-C, the sample sizes being 4,279, 1,807 and 735, respectively. The data were first transformed and adjusted for effects of covariates. Analyses were performed within clinic and selection strata and also pooled across clinics within strata. The results were consistent across strata and identified two major HDL-C clusters with means separated by approximately 3 SD. There was significant evidence of transmission of a major factor for low HDL-C, but transmission did not conform to Mendelian segregation expectations. There was also evidence of significant multifactorial transmission. Since low HDL-C levels are a major independent risk factor for coronary heart disease, the association of a major factor with familial aggregation of low HDL-C emphasizes the importance of detailed within-family sampling for low HDL-C after identifying a proband whose predominant dyslipoproteinemia is low HDL-C.
Cholesterol, HDL↗
Cancer mortality rates and trends for whites and non-whites in Ohio: 1956-1983.
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Adult↗
Segregation and linkage analysis of alpha-N-acetyl-D-glucosaminidase (NAG) levels in a black family.
Alpha-N-acetyl-D-glucosaminidase (NAG) activities were evaluated on serum samples from 67 persons in a large black family. These data were analyzed in conjunction with those from 126 previously tested unrelated blacks [Vance et al, 1980]. After loge transformation, admixture analysis indicated a significantly better fit (P less than .01) of a mixture of 2 normal distributions for NAG activity versus a single normal distribution. Segregation analysis using the transmission probability model of Elston and Stewart [1971] demonstrated that a genetic model fits the data better than the random "environmental" model. Thus, the existence of a major gene is suggested in the family, although the possibility of polygenic or other familial effects cannot be ruled out. These results confirm the existence of a polymorphism for NAG reported earlier in a series of White half-sib twin families [Vance et al, 1980]. However, the estimates of the means of the three genotypes (AA, AA', A'A') appear to differ in the two racial groups. Thus, the data suggest either a racial polygenic effect and/or different alleles segregating in the two populations. In fact, thermal stability data [Vance et al, 1981a] suggest that at least two alleles are structurally distinct. Linkage analysis of the pedigree with 20 marker loci gave no clear indication of linkage. A lod score of 1.44 was found at 0 recombination with orosomucoid (ORM).
Acetylglucosaminidase↗
The Collaborative Lipid Research Clinics Family Study: biological and cultural determinants of familial resemblance for plasma lipids and lipoproteins.
This paper reports on the biological and cultural determinants of total, LDL, and HDL cholesterol, and triglyceride (TC, LDL-C, HDL-C, TG) levels using a general linear model on randomly selected family data collected during 1975-1978 at nine North American Lipid Research Clinics. Initially, the analyses were clinic-specific to assess the importance of genetic and cultural transmission, marital resemblance, and other determinants of these traits and then were made jointly to identify the nature and sources of any heterogeneity between clinics. There was evidence of significant genetic and cultural factors for all traits in most clinics. Clinic heterogeneity was also significant, but excluding one clinic reduced the heterogeneity considerably. The genetic (h2) and cultural (c2) heritabilities for the remaining eight clinics were homogeneous with pooled estimates of h2 of .556 +/- .028, .539 +/- .028, .485 +/- .029, and .358 +/- .028, and of c2 of .029 +/- .006, .033 +/- .006, .075 +/- .008, and .089 +/- .009 for TC, LDL-C, HDL-C, and TG, respectively. Among the traits, HDL-C exhibited the most difference among clinics, and both HDL-C and TG showed the largest cultural heritability. The relevance of these and similar studies in a broader understanding of the determinants of plasma lipids and lipoproteins is discussed.
Cholesterol↗
A multivariate analysis of familial associations of lipoprotein levels in the Lipid Research Clinics Collaborative Family Study: I. Familial correlation and regression analyses.
In view of the complex, intraindividual relationships among different lipoprotein levels (LDL-C, HDL-C, and VLDL-C), multivariate methods aimed at assessing joint familial associations and their possible determinants were performed in the white, random sample component of the Collaborative Lipid Research Clinics Family Study data (1,336 families with 5,097 subjects). After appropriate transformations and covariate adjustments of the data, several kinds of correlation and regression analyses were performed, taking into consideration variable family size and possible age and clinic differences. The association patterns across clinics and age strata were found to be homogeneous for the vast majority of comparisons. The results of multivariate analyses (especially the significant association of each lipoprotein among biological relatives), the persistence of parental levels as the best predictors for the same lipoprotein levels among the offspring, and the essentially unchanged partial correlation estimates as compared to ordinary correlations suggest strong influence of factors specific to each lipoprotein in the familial associations. But the highly significant intraindividual correlations and the nonnegligible cross-correlations among relatives also suggest the additional presence of common underlying factors for the familial associations, especially between HDL-C and VLDL-C and to a lesser extent between LDL-C and VLDL-C. The issues stemming from these analyses and the directions for further analyses are discussed.
Cholesterol↗
Genetic Analysis Workshop II: segregation and linkage analysis.
Familial segregation and linkage analyses were performed on two sets of the Genetic Analyses Workshop II data. The salient features of the mode of inheritance of the disease trait and its linkage/association with polymorphic markers and also marker-marker linkages were delineated using statistical-genetic techniques.
Adult↗
Coagulation factor XIII: a useful polymorphic genetic marker.
The plasmas of two groups of subjects were examined for blood coagulation Factor XIII-A (FXIII-A, F13A) by electrophoresis in agarose using a Tris-EDTA-borate buffer to separate the common variants, F13A*1, F13A*2, and F13A*3. Dimeric subunits were visualized in UV light as monodansyl cadaverine bound to casein at the position of the transglutaminase activity representing F13A. One test group consisted of 307 members of three large Caucasian families. The other consisted of 148 consecutive patients whose plasmas had been sent to the clinical laboratory for determination of prothrombin time. Segregation analysis and father-to-son transmission confirmed that F13A is inherited as an autosomal co-dominant trait. The allelic frequencies in the random sample were F13A*1 = 0.82 and F13A*2 = 0.18. This sample included both blacks and whites, and the gene frequencies were not significantly different in the two races. The gene frequencies among the unrelated spouses of the three white families were A*1 = 0.75, A*2 = 0.24, A*3 = 0.01. Genetic equilibrium was present in both groups. The degree of polymorphism, the availability of blood, the ease of assessment, the absence of selective pressure, and the uniformity of gene frequencies in two major American ethnic groups make F13A a very useful marker for linkage studies and paternity testing. F13A has been provisionally assigned to chromosome 6. Linkage analysis of our family data did not provide evidence of linkage to two chromosome 6 markers, properdin factor B (BF) and glyoxalase 1 (GLO). The highest lod score (Z) was between F13A and the Kidd (Jk) blood group (theta = 0.68 at = 0.24).
Alleles↗
The Collaborative Lipid Research Clinics Program Family Study. II. Response rates, representativeness of the sample, and stability of lipid and lipoprotein levels.
The Collaborative Family Study (1975-1978), the third phase of the Lipid Research Clinics Program Population Studies, covers 2405 probands and 15,693 of their relatives from nine North American communities. This sample was examined for participation differences across race, sex, locality, educational level, and reason for selection. The participation rates were somewhat lower for blacks, younger age groups, and subjects with lower educational levels. The probands' reason for selection into the study had little impact on the participation of probands or relatives. Moreover, based on information gathered at earlier examinations on eligible Family Study probands, the cornary risk factor profile appeared to be similar among participants and nonparticipants . The available longitudinal lipid data on probands indicated general consistency in lipid levels within subjects over short periods of time, in cholesterol even more so than in triglycerides. Among age strata, the younger subjects showed the least intrapersonal stability, especially for triglycerides.
Adolescent↗