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Biomedical subjects

W D Thompson

Publications and source records attributed to W D Thompson.

At least 91 records · Page 5Linked to original sources
PubMed1991

Occupational exposure to electromagnetic fields and breast cancer in men.

Data from a population-based case-control study of breast cancer in men were used to examine the hypothesis that occupational exposure to electromagnetic fields increases the risk of breast cancer. Incident cases (n = 227) diagnosed between 1983 and 1987 were obtained from 10 population-based cancer registries of the Surveillance, Epidemiology, and End Results program of the National Cancer Institute. Controls (n = 300) were selected by random digit dialing and from Medicare eligibility lists. Exposure status, defined as ever having been employed in a job which has been classified as involving potential exposure to electromagnetic fields, was assigned without knowledge of case/control status. An elevated risk was found for any job with exposure (odds ratio (OR) = 1.8, 95 percent confidence interval (CI) 1.0-3.7), and risk was highest among electricians, telephone linemen, and electric power workers (OR = 6.0, 95 percent CI 1.7-21) and radio and communications workers (OR = 2.9, 95 percent CI 0.8-10). Risk did not vary with duration of exposed employment. The risk was highest among subjects who were first employed in jobs with exposure before the age of 30 years and who were initially exposed at least 30 years prior to diagnosis. These results lend support to the theory that electromagnetic fields may be related to breast cancer in men. The hypothesis warrants evaluation in women.

Adult↗
PubMed1991

Breast cancer in men: aspects of familial aggregation.

Familial aggregation of breast cancer in males was investigated in a population-based case-control study. Cases were ascertained from 10 Surveillance, Epidemiology, and End Results Program registries in the United States between 1983 and 1986. Controls were identified by random-digit dialing and from lists of Medicare recipients. The relative odds of developing breast cancer were similar in men with affected paternal and maternal relatives and in men with affected mothers and sisters. The risk increased with the number of affected relatives. The relative odds of developing breast cancer were greater in men with first-degree relatives who developed their mammary neoplasm before the age of 45 than in men with older first-degree affected relatives; the enhancement of risk in men with an affected sister was greater in those under age 60 than in older men. These results are similar to those observed by others in studies of breast cancer in women.

Breast Neoplasms↗
PubMed1991

Fibrinolysis and angiogenesis in wound healing.

The healing wound offers a clear example of the sequence of events in chronic inflammation leading to repair. Although angiogenesis has an obvious and essential role in this process, it has been little studied. For an angiogenic factor to seem relevant, it would have to be shown to precede the peak of increased vascularity. To define this peak, the vessel content of simple, incised mouse wounds was estimated using morphometry of histological sections, and found to rise to a maximum at days 5 and 6. Total angiogenic activity of aqueous extracts was found to reach a peak at day 3. The detection of such activity on the chick chorioallantoic membrane is very dependent on the preparation technique and the choice of proteinase inhibitors. Previous in vitro work by us using purified material has shown fibrin degradation products to be effective in stimulating angiogenesis. Fibrin degradation products are prominent on immunoblotting from day 3, when macrophages are plentiful, with a similar band pattern to human granulation tissue.

Animals↗
PubMed1991

Family history of gynaecological cancers: relationships to the incidence of breast cancer prior to age 55.

As part of a multi-centre epidemiological study of cancer in women between the ages of 20 and 54, data were collected concerning family history of gynaecological cancers in the female relatives of 4730 women with newly diagnosed breast cancer and the relatives of 4688 women from the general population. Women who were diagnosed with breast cancer prior to age 45 were more likely than controls to have a mother or sister with ovarian cancer (odds ratio (OR): 1.50), endometrial cancer (1.29), and cervical cancer (1.53), although none of these elevations achieved statistical significance. The corresponding odds ratios for women diagnosed with breast cancer between the ages of 45 and 54 were 1.88, 0.84 and 0.93. The association with ovarian cancer was statistically significant in this group (95% confidence interval (CI): 1.11-3.19). In this latter group, having a first degree relative with ovarian cancer was associated approximately as strongly with breast cancer as was having a first degree relative with breast cancer. The results suggest that there may be a shared genetic basis for some cancers of the breast and ovary. From a clinical perspective, the results indicate that in setting appropriate levels of screening for breast cancer and in establishing an appropriate age at which to begin such screening for a particular woman, her family history of ovarian cancer should be considered in addition to her family history of breast cancer.

Adult↗
PubMed1991

Genetic analysis of breast cancer in the cancer and steroid hormone study.

The familial risk of breast cancer is investigated in a large population-based, case-control study conducted by the Centers for Disease Control. The data set is based on 4,730 histologically confirmed breast cancer cases aged 20 to 54 years and on 4,688 controls who were frequency matched to cases on the basis of both geographic region and 5-year categories of age, and it includes family histories, obtained through interviews of cases and controls, of breast cancer in mothers and sisters. Segregation analysis and goodness-of-fit tests of genetic models provide evidence for the existence of a rare autosomal dominant allele (q = .0033) leading to increased susceptibility to breast cancer. The effect of genotype on the risk of breast cancer is shown to be a function of a woman's age. Although, compared with noncarriers, carriers of the allele appear to be at greater risk at all ages, the ratio of age-specific risks is greatest at young ages and declines steadily thereafter. The proportion of cases predicted to carry the allele is highest (36%) among cases aged 20-29 years. This proportion gradually decreases to 1% among cases aged 80 years or older. The cumulative lifetime risk of breast cancer for women who carry the susceptibility allele is predicted to be high, approximately 92%, while the cumulative lifetime risk for noncarriers is estimated to be approximately 10%.

Adult↗
PubMed1990

Lung cancer and exposure to tobacco smoke in the household.

BACKGROUND: The relation between passive smoking and lung cancer is of great public health importance. Some previous studies have suggested that exposure to environmental tobacco smoke in the household can cause lung cancer, but others have found no effect. Smoking by the spouse has been the most commonly used measure of this exposure. METHODS: In order to determine whether lung cancer is associated with exposure to tobacco smoke within the household, we conducted a population-based case--control study of 191 patients with histologically confirmed primary lung cancer who had never smoked and an equal number of persons without lung cancer who had never smoked. Lifetime residential histories including information on exposure to environmental tobacco smoke were compiled and analyzed. Exposure was measured in terms of "smoker-years," determined by multiplying the number of years in each residence by the number of smokers in the household. RESULTS: Household exposure to 25 or more smoker-years during childhood and adolescence doubled the risk of lung cancer (odds ratio, 2.07; 95 percent confidence interval, 1.16 to 3.68). Approximately 15 percent of the control subjects who had never smoked reported this level of exposure. Household exposure of less than 25 smoker-years during childhood and adolescence did not increase the risk of lung cancer. Exposure to a spouse's smoking, which constituted less than one third of total household exposure on average, was not associated with an increase in risk. CONCLUSIONS: The possibility of recall bias and other methodologic problems may influence the results of case-control studies of environmental tobacco smoke. Nonetheless, our findings regarding exposure during early life suggest that approximately 17 percent of lung cancers among nonsmokers can be attributed to high levels of exposure to cigarette smoke during childhood and adolescence.

Adolescent↗
PubMed1990

Familial clustering of neural tube defects and gastric cancer.

A retrospective cohort study was conducted to determine whether producing an offspring with a neural tube defect (NTD) is associated with the development of unusual patterns of cancer among the parents in subsequent years. Mothers and fathers who had a child with an NTD in Upstate New York from 1945 to 1955 were followed through 1979 and compared to a control group of parents with normal offspring. Overall mortality and site-specific cancer incidence were not significantly different for case parents versus control parents, with the exception of gastric cancer, which occurred significantly more frequently in case parents. The finding of a familial association between NTDs and gastric cancer, coupled with a parallel decline in rates of these two diseases, suggests a common aetiology, perhaps related to dietary factors.

Adult↗
PubMed1990

Age at onset as an indicator of familial risk of breast cancer.

The familial risk of breast cancer was investigated in a large population-based, case-control study conducted by the Centers for Disease Control. The data set included 4,730 histologically confirmed breast cancer cases aged 20-54 years and 4,688 controls who were frequency matched to cases by geographic region and 5-year categories of age. Family history of breast cancer among first-degree female relatives of cases and controls was utilized. To identify factors associated with familial risk of breast cancer, a Cox proportional hazards model was used, modeling time to onset of breast cancer among mothers and sisters. Case relatives were at greater risk than control relatives. Among relatives of cases, a significant increase in the risk of breast cancer was associated with decreasing age at onset of the case and with having an additional relative affected with breast cancer. The hazard ratio for the mother of a case with breast cancer diagnosed at 50 years of age was 1.7 (95% confidence interval (Cl) 1.4-2.0), compared with 2.7 (95% Cl 2.2-3.2) and 4.3 (95% Cl 3.3-5.6) for the mother of a case whose diagnosis occurred at 40 and 30 years of age, respectively. The hazard ratio for the sister of a case with an unaffected mother and at least one affected sister in addition to the case was 3.6 (95% Cl 2.1-6.1) when the case was diagnosed at age 50, compared with 5.8 (95% Cl 3.4-10.0) and 9.4 (95% Cl 5.3-16.7) when the case was diagnosed at 40 and 30 years of age, respectively. The hazard ratio for the sister of a case with an affected mother and no additional affected sisters was 5.9 (95% Cl 3.9-8.9) when the case was diagnosed at age 50, compared with 9.4 (95% Cl 6.2-14.4) and 15.1 (95% Cl 9.4-24.3) when the case was diagnosed at 40 and 30 years of age, respectively. The hazard ratio for the sister of a case with both an affected mother and at least one affected sister aside from the case was 17.1 (95% Cl 9.4-31.3) when the case was diagnosed at age 50, compared with 27.5 (95% Cl 15.0-50.3) and 44.2 (95% Cl 23.5-83.2) when the case was diagnosed at 40 and 30 years of age, respectively. No effect of case's menopausal status and bilaterality was found, indicating that in addition to a positive family history, age at onset is the strongest indicator of a possible genetic subtype of breast cancer in these data.

Adult↗
PubMed1990

Infertility and breast cancer: a population-based case-control study.

To investigate whether a history of infertility affects a woman's risk of developing breast cancer, the authors analyzed case-control data collected between 1980 and 1982 as part of the Cancer and Steroid Hormone Study. The 4,730 cases were women aged 20-54 years with a first diagnosis of breast cancer ascertained from eight population-based cancer registries; the 4,688 controls were women randomly selected from the general population of these same eight areas. After controlling for age, age at first birth, and parity, the odds ratio (OR) for breast cancer associated with infertility was 1.01 (95% confidence interval (CI) 0.89-1.15) among gravid women. Controlling for age, the odds ratio was 0.82 (95% CI 0.59-1.14) among nulligravid women. Women who reported that the reason for their infertility was a problem with their ovaries had a risk similar to that for women without a history of infertility (OR = 0.75, 95% CI 0.48-1.24). Women whose physicians reported that the reason for their infertility was anovulation or Stein-Leventhal syndrome also had risks similar to those for women without a history of infertility (OR = 1.26 (95% CI 0.67-2.34) and OR = 1.13 (95% CI 0.46-2.78), respectively). Menopausal status, age at menarche, history of spontaneous abortions, drinking or smoking behavior, use of exogenous hormones, or family history of breast cancer did not appreciably alter the observed odds ratios. If infertility has an effect on breast cancer that is independent of age at first birth, then the effect is small.

Adult↗
PubMed1990

Maternal age at birth and risk of breast cancer in daughters.

Data from a large case-control study of breast cancer were examined to test the hypothesis that maternal age at the birth of female offspring is related to the incidence of breast cancer in daughters. Participants were between the ages of 20 and 54 at the time of the study. Based on results for 2,492 parous women who were newly diagnosed with breast cancer and 2,687 parous controls from the general population, a 15-year increase in maternal age was found to be associated with a 29% increase in the risk of breast cancer in daughters. Adjustment for the daughter's age, her own reproductive history, and other potential confounding factors yielded an estimate of 25% for this increase in risk (95% CI, 8% to 46%). The corresponding increase among 499 nulliparous cases and 457 nulliparous controls was 7%, which was not statistically significantly different in magnitude from the increase among parous women. These findings provide evidence for perinatal influences on the subsequent incidence of breast cancer during adulthood. Although specific mechanisms cannot be inferred directly, the results are consistent with the hypothesis that mutations in the genes of the human egg or sperm play a role in the etiology of breast cancer in female offspring.

Adult↗
PubMed1990

Kappa and attenuation of the odds ratio.

This paper explores the relation between reliability and validity for binary variables. An equation is first derived for expressing the kappa coefficient of reliability as a function of true prevalence, sensitivity, specificity, and the degree of correlation of errors within true positives and within true negatives. It is then shown that under certain circumstances kappa is closely related to an index of the validity of the odds ratio as a means for quantifying an association between an imperfectly classified binary factor and membership in two subpopulations. This index is defined as the ratio of the observed odds ratio minus one to the true odds ratio minus one. Numerical results indicate that, when error rates are high, kappa can be of smaller magnitude than this index of validity. When the value of kappa reflects substantial correlation of errors, however, the value of kappa typically exceeds that of the index of validity. Correlated errors among the true negatives are found to affect the correspondence between kappa and the index of validity rather differently than do correlated errors among the true positives. Although kappa often exceeds the index of validity, use of kappa to correct the odds ratio for attenuation owing to nondifferential misclassification generally leads to undercorrection rather than overcorrection. Consequently, the relation between kappa and the index of the validity of the odds ratio may have practical value for reducing bias in the estimation of exposure-disease associations in epidemiologic research.

Case-Control Studies↗
PubMed1990

Factors relevant to stimulatory activity of fibrin degradation products in vivo.

Extracts of atherosclerotic lesions contain a range of fibrin degradation products (FbDP), similar fragments have been detected in extracts from human and mouse healing skin wounds and from the invasive edge of human breast carcinomas, which are all proliferating systems. We have previously shown that FbDP stimulate cell proliferation including angiogenesis in the chick chorioallantoic membrane (CAM), and sought to characterize further the active components. Fibrin prepared from platelet-rich and platelet-free plasma, and purified Kabi fibrinogen, was treated with plasmin, and the digests were all active. FbDP from platelet-rich plasma clots also increased vascularity of the CAM. Prior removal of fibronectin from plasma by gelatin-Sepharose affinity chromatography did not affect proliferative activity. Current studies showed that long digests of fibrin, in which the only major band detectable is fibrin fragment E are active. Commercial fibrinogen derived fragment E, itself inactive on the CAM, becomes active after exposure to thrombin cleavage of fibrinopeptides. Recently fragment E has been isolated from shorter digests, by simple filtration through a Millipore 0.2 microns centrifuge filter. It displayed similar activity to the fragment E obtained from long digests. Fragment E in plaque extracts has been shown consistently to lack fibrinopeptide A indicating it is of fibrin origin.

Allantois↗
PubMed1990

Using age of onset to distinguish between subforms of breast cancer.

Information on family history and age of onset of breast cancer is examined in an attempt to distinguish between postulated early and late onset forms of breast cancer and to estimate the familial correlation between any subforms that may exist. Data are taken from the Cancer and Steroid Hormone Study, a multicentre, population-based, case-control study conducted by the Centers for Disease Control (CDC). The data set includes 4730 histologically confirmed breast cancer cases aged 20-54 and 4688 controls who were frequency-matched to cases by geographic region and five-year categories of age. Data regarding family history of breast cancer for mothers and sisters of cases and controls are used in this analysis. The methods of Smith (1976) are modified to obtain maximum likelihood estimates of heritability and familial correlation using 35, 40, 45, and 50 years of age as the dividing point between early and late onset. The heritabilities for both the early and late onset forms decrease and approach one another in size with increasing age cutpoint, although the heritability for the early group is always greater than that for the late group. Irrespective of cutpoint, the familial correlation between the two groups does not differ significantly from one, providing evidence for a single genetic form of breast cancer with familial cases increasingly represented among cases with earlier onset.

Adult↗
PubMed1990

A clinical application of iodine quantitation using digital fluorography.

A preliminary clinical study of 20 patients is described in which a method of iodine quantitation in vitro using digital fluoroscopy was applied to the intravenous urogram. It was possible to quantitate iodine levels, in terms of mass thickness, in both the renal parenchyma and collecting system in 38 of 40 kidneys studied (20 patients). In the two kidneys on which measurements could not be made, the cause of failure was subtraction artefact due to movement of bowel gas, compounded in one case by poor renal opacification. The variations of iodine mass thickness against time were plotted and their forms were similar to dynamic computed tomography and magnetic resonance imaging studies of transplanted kidneys. Potential clinical applications of this method, in particular the functional assessment of the dilated upper urinary tract, are suggested based on its ability to offer quantitative information in addition to anatomical images.

Adult↗
PubMed1990

Atherosclerotic plaque growth: presence of stimulatory fibrin degradation products.

Focal smooth muscle cell proliferation is widely perceived as a key event in the formation of stenosing atherosclerotic lesions, but the stimuli for this remain uncertain. Soluble extracts of human aortic intima from proliferative gelatinous and transitional lesions, as well as surface encrusted thrombi, have been shown by us to be mitogenic for the chick chorioallantoic membrane (CAM). They have also been shown to stimulate increase in vascularity of the CAM. When active samples were passed through anti-albumin and anti-whole-serum affinity columns, mitogenic activity in the unabsorbed, fibrin related antigen fraction remained close to the original whole extract level. In contrast, when the unabsorbed fractions from anti-whole-serum columns were passed through an antifibrinogen affinity columns, the activity was reduced to insignificant levels. Similarly, whole extracts lost activity after passing through an antifibrinogen column. This has been taken one stage further by dividing the unabsorbed fraction from an anti-whole-serum column into two equal volumes and passing one half through an antifibrinogen fragment D affinity column, and the other through an antifibrinogen fragment E affinity column. The activity of the unabsorbed fraction from the fragment D column remained the same, but that from the fragment E column was significantly reduced. Most of the fibrin degradation products (FbDP) in lesion extracts are derived from fibrin, not fibrinogen, and clotting out fibrinogen and fragment X with thrombin did not remove the activity. Whole extracts of atherosclerotic lesions clotted on the CAM surface as has previously been shown with plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Allantois↗
PubMed1990

Artificial exudate: stimulation of cell proliferation by plasma not serum is associated with fibrinolysis.

Despite its abundance of cell culture growth factors, serum does not enhance growth of the in vivo test system, the chick chorioallantoic membrane (CAM). Previously we have also shown that fibrinogen (Kabi) and its degradation products do not display mitogenic activity on the CAM, but have now been surprised to find stimulation of DNA synthesis (up to 2.5-fold) 18 h after application of human plasma [incorporation of [3H]thymidine control mean +/- SEM 8442 +/- 1338 dpm/CAM (n = 8); test--20 199 = 3491 (n = 6); t-test P less than 0.01)]. Plasma (platelet-rich and platelet-poor) was freshly prepared by minicolumn removal of citrate at 16 degrees C; 0.3 ml aliquots of 10% human plasma were applied to the CAM and groups were fixed at various time intervals. Cross-sections were examined histologically, including immunoperoxidase studies with antihuman fibrinogen which does not cross react with chick fibrinogen, and autoradiography with [3H]thymidine. Initially, a layer of plasma was observed on the surface of the CAM. After 1 h a condensed fibrillar layer of fibrin was formed and was still present at 6 h. This was associated with increased [3H]thymidine labelling of the surface layer of the CAM. By 18 h the fibrin had disappeared, indicating that it had been lysed by the CAM, and widespread [3H]thymidine labelling was observed. No inflammatory cell infiltrate was apparent, but marked oedema developed. Oedema alone was observed in controls receiving serum or Dulbecco buffer. Both platelet-rich and platelet-free plasma gave stimulation of mitogenic activity, implying that platelet-derived growth factor is not involved in the stimulation of the CAM.(ABSTRACT TRUNCATED AT 250 WORDS)

Allantois↗