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W D Thompson

Publications and source records attributed to W D Thompson.

At least 109 records · Page 6Linked to original sources
PubMed1989

Hypertension, pregnancy, and risk of breast cancer.

We investigated the relationship between hypertension and breast cancer using data from a large case-control study of women younger than 55 years. Among nulliparous women, there was little evidence of an association between hypertension and breast cancer. Among parous women, hypertension reduced the risk of breast cancer if it had been diagnosed at any time in their lives before the end of the most recent pregnancy (odds ratio = 0.73; 95% confidence interval = 0.59-0.92). Several earlier studies indicate that there is an association between hypertension during pregnancy and elevated levels of maternal serum alpha-fetoprotein. Thus, our results are consistent with the hypothesis that maternal exposure to alpha-fetoprotein during pregnancy protects women against the subsequent occurrence of breast cancer.

Adult↗
PubMed1989

Epidemiologic evidence of perinatal influence in the etiology of adult cancers.

Using data from 5489 cancer patients and 2647 patients without cancer we investigated whether parental age at the birth of the patient or the patient's rank within his sibship was related to the risk of cancer during adulthood. An increase of 10 years in maternal age was associated with an increase of 24% for the incidence of breast cancer (odds ratio = 1.24%; 95% CI = 1.09-1.41); the corresponding increase for paternal age was 19% (odds ratio = 1.19; 95% CI = 1.07-1.33). There was some evidence that the age of each parent may make an independent contribution to the risk of breast cancer. For certain types of genito-urinary cancers, the risk was higher when the parents were relatively young at the birth of the patient. These cancers included tumors arising in the prostate (odds ratios = 0.71 and 0.55 for maternal and paternal ages, respectively), testis (odds ratios = 0.57 and 0.52), penis (odds ratios = 0.37 and 0.45), kidney (odds ratios = 0.66 and 0.60), and bladder (odds ratio = 0.79 and 0.85). The associations for cancer of the prostate and bladder were stronger among patients who were diagnosed at a relatively young age. No statistically significant effects were found for birth order relative to adult cancers. The authors conclude that environmental factors that affect the parents or that operate in the perinatal period may have stronger influences on the incidence of adult cancers than have been previously recognized.

Adult↗
PubMed1989

Multiple births and maternal risk of breast cancer.

Data from the Cancer and Steroid Hormone Study, a large nationwide population-based case-control study conducted in the United States in 1980-1982, were analyzed to investigate whether pregnancies ending in a multiple birth affect the risk of subsequent breast cancer. The cases were 3,918 parous women who were aged 20-54 years and newly diagnosed with breast cancer; controls were 4,047 parous women selected randomly from the same geographic areas as the cases. Multiple births were reported by 118 cases and 161 controls. After adjustment for other reproductive variables, having a multiple last birth was found to be protective against breast cancer (odds ratio (OR) = 0.60, 95% confidence interval (CI) 0.43-0.85), whereas having a multiple birth prior to the last birth was not (OR = 1.11, 95% CI 0.79-1.57). To the authors' knowledge, this study is the first investigation to report such a protective effect, and thus the finding warrants replication. One mechanism that might account for the effect involves the increased output of alpha-fetoprotein by multiple fetal livers.

Adult↗
PubMed1989

Angiogenic stimulation compared with angiogenic reaction to injury: distinction by focal and general application of trypsin to the chick chorioallantoic membrane.

We have addressed the problem of distinguishing angiogenesis induced in the chick chorioallantoic membrane by injury and inflammation from angiogenesis induced by primary stimulation. Focal, slow-release application of trypsin stimulated a localized spoke-wheel pattern of vascularity. In comparison, a range of doses up to a sublethal amount of trypsin applied generally, in liquid form, resulted in no change in DNA synthesis or vessel content, despite a transient influx of inflammatory cells. This contrasts with previous work with fibrin degradation products, histamine and heparin which each produce characteristic patterns of increased DNA synthesis leading to angiogenesis in the entire 'dropped' area of the chorioallantoic membrane. Such general application, therefore, avoids the danger of misinterpretation of focal, toxic effects.

Allantois↗
PubMed1989

Evaluating genetic association among ovarian, breast, and endometrial cancer: evidence for a breast/ovarian cancer relationship.

The possibility of a genetic relationship between ovarian, breast, and endometrial cancer was investigated in data from a large multicenter, population-based, case-control study, the Cancer and Steroid Hormone Study conducted by the Centers for Disease Control (CDC). Age-adjusted relative risks (RRs) for mothers and sisters of 493 ovarian cancer cases, 895 breast cancer cases, and 143 endometrial cancer cases versus 4,754 controls were calculated. Significantly elevated age-adjusted RRs were found for ovarian cancer (RR = 2.8; 95% confidence interval [CI] = 1.6-4.9) and breast cancer (RR = 1.6; 95% CI = 1.1-2.1) among relatives of ovarian cancer probands and for breast cancer (RR = 2.1; 95% CI = 1.7-2.5) and ovarian cancer (RR = 1.7; 95% CI = 1.0-2.0) among relatives of breast cancer probands. Relatives of endometrial cancer probands had an elevated RR for endometrial cancer only (RR = 2.7; 95% CI = 1.6-4.8). The genetic relationship between ovarian, breast, and endometrial cancer was tested using a multivariate polygenic threshold model developed by Smith (1976), which was modified to accommodate three classes of probands. Estimates of heritability for ovarian, breast, and endometrial cancer were 40%, 56%, and 52%, respectively. There was a significant genetic correlation between ovarian and breast cancer (R12 = .484). Evidence for significant genetic overlap between endometrial cancer and either ovarian or breast cancer was not found. These results suggest the existence of a familial breast/ovarian cancer syndrome. Endometrial cancer, while heritable, appears to be genetically unrelated.

Adult↗
PubMed1989

Immunolocalisation of aspartic proteinases in the developing human stomach.

The distribution and time of appearance in the developing human stomach of the 4 aspartic proteinases, pepsinogen, progastricsin, slow-moving protease and cathepsin D, all present in gastric carcinoma, has been determined by the peroxidase-antiperoxidase method on formalin fixed paraffin embedded sections of fetal stomach. Slow-moving protease appears to be the dominant enzyme from 12 weeks gestation onward, although progastricsin is also present at this time. Pepsinogen and cathepsin D do not appear until 17-18 weeks.

Aspartic Acid Endopeptidases↗
PubMed1988

Risk of contralateral breast cancer. Associations with histologic, clinical, and therapeutic factors.

A case-control study was conducted to assess the risk factors associated with the development of a contralateral primary breast cancer among women who had had a first primary breast cancer. Hospital records were reviewed for 292 women with an incident contralateral breast cancer, diagnosed in one of eight hospitals between July 1, 1975 and December 31, 1983, and for a comparison group of 264 surviving unilateral breast cancer patients, previously diagnosed in the same hospitals. All subjects were identified through the records of the Connecticut Tumor Registry. Having an initial tumor containing lobular carcinoma was associated with an almost twofold increased risk of developing a contralateral cancer (aOR = 1.8; 95% CI: 1.0-3.5). Among those for whom a progesterone receptor assay was available, a positive assay was associated with an increased risk of a contralateral primary (aOR = 3.2; 95% CI: 1.0-9.5). AB blood type was also associated with an elevated risk, but this elevation was not statistically significant (aOR = 2.3; 95% CI: 0.7-7.7). Having received radiation treatment was not significantly associated with the risk of a contralateral primary (aOR = 0.9; 95% CI: 0.6-1.4), whereas chemotherapy treatment was associated with a significantly lowered risk (aOR = 0.3; 95% CI: 0.1-0.7). The association with chemotherapy appeared to be modified by body build (ROR = 1.5; 95% CI: 1.0-2.3 for a 2.5-unit differential in Quetelet's index).

Adult↗
PubMed1988

Relationship of epithelial ovarian cancer to other malignancies within families.

The relationship of family history of cancer of the breast, colon/rectum, cervix, endometrium, lung, and thyroid to the risk of epithelial ovarian cancer was investigated in a large population-based case-control study. The data consisted of family histories from 493 epithelial ovarian cancer cases and 2,465 controls aged 20-54 years. After controlling for potential confounders, risk for epithelial ovarian cancer was found to be significantly elevated among women reporting breast cancer and colo/rectal cancer in a first-degree relative. Adjusted odds ratios were 1.5 (95% CI = 1.1-2.1) and 1.9 (95% CI = 1.1-3.3), respectively. None of the remaining four types of cancer was found to be statistically associated with the risk of epithelial ovarian cancer. However, when histologic subtypes of epithelial ovarian cancer were considered, a family history of breast cancer was found to be associated with an elevated risk of endometrioid ovarian cancer (odds ratio = 2.3; 95% CI = 1.1-4.7), as was a family history of endometrial cancer (odds ratio = 2.7; 95% CI = 1.0-6.9). The results are considered in the context of other studies of familial patterns of cancer and are compared with published findings concerning the occurrence of multiple primary cancers in the same individual. The findings indicate that further study is warranted regarding possible genetic relationships between epithelial ovarian cancer and cancers arising in other organs.

Adult↗
PubMed1988

A reappraisal of the kappa coefficient.

Kappa is frequently used in epidemiology as an index of the quality of measurement for binary characteristics. The authors discuss the strong dependence of kappa on true prevalence, and they examine the relationship of the value of kappa to the degree of attenuation of the odds ratio that results from non-differential misclassification. It is concluded that under certain circumstances kappa can be interpreted as an indicator of validity, i.e. unbiasedness of the odds ratio, rather than simply as one of reliability. Cautions are stressed regarding (1) possible variation in the quality of measurement and (2) possible lack of independence of errors for the paired measurements from which kappa is calculated. An important implication for the design of reliability studies is that they should be conducted in populations where the distribution of the factor of interest is similar to that for the settings in which the measurement technique will ultimately be applied.

Data Interpretation, Statistical↗
PubMed1988

Risk of contralateral breast cancer: associations with factors related to initial breast cancer.

A case-control study was conducted to assess the risk factors associated with the development of a contralateral primary breast cancer among women who had had a first primary breast cancer. Hospital records were reviewed for 292 women who had an incident contralateral breast cancer, diagnosed in one of eight Connecticut hospitals between July 1, 1975 and December 31, 1983, and for a comparison group of 264 surviving unilateral breast cancer patients previously diagnosed in the same hospitals. All subjects were identified through the records of the Connecticut Tumor Registry. A family history of breast cancer in any first- or second-degree relative was associated with an almost threefold increased risk of developing a contralateral cancer (adjusted odds ratio (OR) = 2.8, 95% confidence interval (CI) = 1.6-4.9). Further, this relation was modified by the time elapsed since the initial cancer diagnosis (ratio of OR = 1.9, 95% CI = 1.2-3.0 for a five-year differential in time since initial diagnosis). A delay of 10 years in first full-term pregnancy was associated with a 36% decrease in risk (adjusted OR = 0.6, 95% CI = 0.3-1.2); this estimate excluded the magnitude of increased risk usually observed in studies of initial breast cancer. A conceptual framework is presented for assessing the study findings in the context of previous studies that have examined the corresponding associations for initial primary breast cancers.

Adult↗
PubMed1988

Familial ovarian cancer: a population-based case-control study.

Data from a multicenter population-based case-control study were analyzed to assess the degree of aggregation of ovarian cancer in families. Included as cases were 493 women aged 20-54 who had been newly diagnosed with epithelial ovarian cancer. The frequency with which cases reported a family history of ovarian cancer was compared with the frequency for a group of 2,465 controls selected by random digit dialing. The odds ratios for ovarian cancer in first- and second-degree relatives were 3.6 (95% confidence interval (Cl) 1.8-7.1) and 2.9 (95% Cl 1.6-5.3), respectively, compared with women with no family history of ovarian cancer. The null hypothesis of no association was excluded on both the maternal and paternal sides of the families studied. Ovarian cancer in relatives was reported by women with malignant lesions but not by women with borderline lesions. These results did not seem to be attributable to the possible confounding effects of any of several covariates or to errors in reporting family history of ovarian cancer.

Adult↗
PubMed1988

Effect of the mast cell activator compound 48/80 and heparin on angiogenesis in the chick chorioallantoic membrane.

The mast cell activator, compound 48/80, produced increased vascularity and tortuosity of blood vessels in the chorioallantoic membrane (CAM) of ten day old embryonic chicks. Application of 400 micrograms/ml resulted in rapid mast cell granule release, observed after 1 min at both light and electron microscopy level, and resulted in the greatest increase (69%) in CAM mesenchymal vessels. The half-maximal dose was 38.6 micrograms/ml, computer-derived from the dose-response data. It is apparent that a single episode of mast cell degranulation is sufficient to induce vessel growth over several days, but the fact that a sublethal dose is required for maximum stimulation casts doubt on its biological significance. This pattern of response resembles that previously found by us with histamine and has not been found so far with commercial heparins and chemically modified derivatives. In contrast, a sublethal dose of porcine intestinal sodium heparin results in an antiangiogenic effect on the ectodermal capillary plexus.

Allantois↗
PubMed1987

Tumours acquire their vasculature by vessel incorporation, not vessel ingrowth.

This study was designed to investigate the early development of tumour circulation using a transplantable mouse mammary adenocarcinoma. Tumour cells (10(6] were injected subcutaneously into the flank and groups of treated mice were killed at 24 h intervals up to 12 days; the tumours and surrounding tissues being processed by standard histological methods. Sections of tumour were sub-divided into neoplastic tissue, vessels and connective tissue using computer-assisted morphometric techniques: the host tissue around the tumour was similarly quantified for vessels and connective tissue. With increasing tumour size, the proportion of vessels within tumours rapidly increased to reach a plateau of approximately 1.5 per cent of tumour volume, a 400 per cent increase on the vascular density of normal subcutaneous tissue. Within tumours, vascular density was always higher at the periphery than the centre. The most pronounced increase in vascular density affected the host tissue around the tumour. It is not clear why vascular development is most prominent outwith the tumour when postulated angiogenic factors, such as tumour angiogenesis factor, are presumably released within. Our results imply, however, that tumours acquire their vasculature by infiltration into, and expansion between, a network of newly formed vessels in the surrounding connective tissue.

Adenocarcinoma↗