Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.3.5.5 (CPS)
1,262 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific activity of carbamoyl phosphate synthetase (glutamine-hydrolyzing), the first and rate-limiting enzyme of de novo uridine 5'-triphosphate biosynthesis, was increased in 13 transplantable hepatomas, particularly in the rapidly growing tumors (5.7- to 9.5-fold), and the rise was correlated with tumor growth rates. Thus, synthetase activity was linked with both hepatic neoplastic transformation and progression. Synthetase specific activity was so elevated in a transplantable sarcoma (18-fold) and a kidney adenocarcinoma (5-fold). The increased activity should enhance the capacity of the pathway and should confer selective advantages to cancer cells.
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PMID:Carbamoyl phosphate synthetase (glutamine-hydrolyzing): increased activity in cancer cells. 720 43

Two approaches are used to assess publication bias in the environmental tobacco smoke/coronary heart disease (ETS/CHD) literature: (1) Statistical tests applied to all sex-specific relative risk (rr) estimates from 14 previously published studies indicate that publication bias is likely. A funnel graph of the studies' log relative risks plotted against their standard errors is asymmetrical, and weighted regression of the studies' log relative risks on their standard errors is significant (P < 0.01). (2) Previously unpublished ETS/CHD relative risks from the American Cancer Society's Cancer Prevention Studies (CPS-I and CPS-II) and the National Mortality Followback Survey (NMFS) do not show an increased CHD risk associated with ETS exposure. CPS-I: men, rr = 0.97 (0.90-1.05); CPS-I: women, rr = 1.03 (0.98-1.08); CPS-II: men, rr = 0.97 (0.87-1.08); CPS-II: women, rr = 1.00, (0.88-1.14); NMFS: men, rr = 0.97 (0.73-1.28); women, rr = 0.99 (0.84-1.16). Comparison of pooled relative risk estimates from 14 previously published studies (rr = 1.29; 1.18-1.41) and unpublished results from three studies (rr = 1.00; 0.97-1.04) also indicates that published data overestimate the association of spousal smoking and CHD (chi 2 = 25.1; P < 0.0001).
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PMID:Publication bias in the environmental tobacco smoke/coronary heart disease epidemiologic literature. 778 30

To characterize demographic and regional variation in kidney stone prevalence in the U.S. we studied two nationwide cross-sectional surveys that included data on self-reported, physician-diagnosed kidney stones, supplementing published data on hospitalizations for stones. The larger study, Cancer Prevention Study II (CPS II), included 1,185,124 men and women, age > or = 30, recruited nationally in 1982, and provides state-specific prevalence estimates. The National Health and Nutrition Examination Survey (NHANES II) was a national probability sample of 25,286 U.S. adults interviewed between 1976 and 1980. Kidney stone prevalence increased with age until age 70, then declined and was higher in men than women and in whites than blacks. Prevalence among Hispanic and Asian men was intermediate between that of whites and blacks. There was a strong, statistically significant regional variability in stone prevalence among U.S. whites. The age-adjusted prevalence increased from north to south, and from west to east. The contrast in state-specific prevalence was greatest between men in North Carolina (prevalence = 14.9; 95% confidence interval = 14.2 to 15.7) and North Dakota (5.6; 4.7 to 6.4), and between women in South Carolina (6.4; 5.8 to 6.9) and South Dakota (2.4; 1.9 to 2.9). The marked variations in kidney stone prevalence by age, gender, race, and geographic location may provide clues to their etiology and prevention.
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PMID:Demographic and geographic variability of kidney stones in the United States. 799 11

Globally, oral cancer is one of the ten common cancers. In some parts of the world, including the Indian subcontinent, oral cancer is a major cancer problem. Tobacco use is the most important risk factor for oral cancer. The most common form of tobacco use, cigarette smoking, demonstrates a very high relative risk--in a recent cohort study (CPS II), even higher than lung cancer. In areas where tobacco is used in a smokeless form, oral cancer incidence is generally high. In the West, especially in the U.S. and Scandinavia, smokeless tobacco use consists of oral use of snuff. In Central, South, and Southeast Asia smokeless tobacco use encompasses nass, naswar, khaini, mawa, mishri, gudakhu, and betel quid. In India tobacco is smoked in many ways; the most common is bidi, others being chutta, including reverse smoking, hooka, and clay pipe. A voluminous body of research data implicating most of these forms of tobacco use emanates from the Indian subcontinent. These studies encompass case and case-series reports, and case-control, cohort, and intervention studies. Collectively, the evidence fulfills the epidemiological criteria of causality: strength, consistency, temporality, and coherence. The biological plausibility is provided by the identification of several carcinogens in tobacco, the most abundant and strongest being tobacco-specific N-nitrosamines such as N-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). These are formed by N-nitrosation of nicotine, the major alkaloid responsible for addiction to tobacco. The etiological relationship between tobacco use and oral cancer has provided us with a comprehensive model for understanding carcinogenesis.
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PMID:Epidemiology of cancer by tobacco products and the significance of TSNA. 868 60

Four of five cohort studies have shown an increase in cardio-vascular disease with increased parity, after control for a number of cardiovascular risk factors. The effect has been observed primarily in categories of four or more livebirths. To analyze this issue further, we conducted an analysis of 585,445 women from the American Cancer Society Cancer Prevention Survey II (CPS II). There were 4,787 deaths from coronary heart disease (International Classification of Diseases Codes 410-414) among these women during the follow-up period from 1981 to 1989. After controlling for a number of cardiovascular risk factors, we found no increased trend in heart disease with increased parity. Rare ratios for women with no live births or 1, 2, 3, 4, 5, and 6 or more livebirths were 1.00, 0.95, 0.89, 0.82, 0.94, 0.98, 0.94, respectively. Without control over confounders, however, we observed an increased risk for the highest party category (rate ratio = 1.18; 95% confidence interval = 1.04-1.34). Positive findings for parity to date have been found primarily in cohort studies representative of the general population, whereas our own data and another earlier negative study among nurses came from more select populations likely to be relatively homogeneous for socioeconomic variables. Positive findings in the literature may be due, at least in part, to confounding by unmeasured variables related to socioeconomic status.
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PMID:Parity and coronary heart disease among women in the American Cancer Society CPS II population. 889 93

Nonmalignant respiratory disease (NMRD) mortality was examined among woodworkers participating in the American Cancer Society's CPS-II cohort study. During the 6-year prospective follow-up there were 97 NMRD death's among 11,541 men reporting employment in wood-related occupations and 1,338 NMRD deaths among 317,424 men reporting no exposure to wood dust or wood-related jobs. Relative risks, adjusted for age and smoking, were calculated using Poisson regression. A small excess of NMRD was observed among woodworkers. However, the relative risk was higher among woodworkers who did not report exposure to wood dust (RR = 1.52, 95% CI = 1.18-1.97) than those who did (RR = 1.27, 95% CI = 0.91-1.77), and no clear trend with duration of exposure was observed. An excess of NMRD was observed among woodworkers reporting exposure to asbestos (RR = 1.59, 95% CI = 0.85-2.96), as well as the small number of woodworkers reporting exposure to formaldehyde (RR = 1.95, 95% CI = 0.63-6.06), but men not reporting exposure to these substances also had an excess risk. Although limited by a short follow-up period and crude indicators of exposure, the strengths of this analysis were the ability to compare woodworkers to a similar, healthy population and to adjust for the effects of smoking. Cohort studies with better exposure information are needed to examine the role of occupational exposures among woodworkers in the etiology of respiratory disease.
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PMID:Nonmalignant respiratory disease mortality among woodworkers participating in the American Cancer Society Cancer Prevention Study-II (CPS-II). 969 92

A plant polysaccharide, Aloe gel extract, was reported to have an inhibitory effect on benzo[a]pyrene (B[a]P)-DNA adduct formation in vitro and in vivo. Hence, chemopreventive effects of plant polysaccharides [Aloe barbadensis Miller (APS), Lentinus edodes (LPS), Ganoderma lucidum (GPS) and Coriolus versicolor (CPS)] were compared using in vitro short-term screening methods associated with both initiation and promotion processes in carcinogenesis. In B[a]P-DNA adduct formation, APS (180 micrograms/ml) was the most effective in inhibition of B[a]P binding to DNA in mouse liver cells. Oxidative DNA damage (by 8-hydroxydeoxyguanosine) was significantly decreased by APS (180 micrograms/ml) and CPS (180 micrograms/ml). In induction of glutathione S-transferase activity, GPS was found to be the most effective among plant polysaccharides. In screening anti-tumor promoting effects, APS (180 micrograms/ml) significantly inhibited phorbol myristic acetate (PMA)-induced ornithine decarboxylase activity in Balb/3T3 cells. In addition, APS significantly inhibited PMA-induced tyrosine kinase activity in human leukemic cells. APS and CPS significantly inhibited superoxide anion formation. These results suggest that some plant polysaccharides produced both anti-genotoxic and anti-tumor promoting activities in in vitro models and, therefore, might be considered as potential agents for cancer chemoprevention.
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PMID:In vitro chemopreventive effects of plant polysaccharides (Aloe barbadensis miller, Lentinus edodes, Ganoderma lucidum and Coriolus versicolor). 1042 20

The authors explored two methodological issues in the estimation of smoking-attributable mortality for the United States. First, age-specific and age-adjusted relative risk, attributable fraction, and smoking-attributable mortality estimates obtained using data from the American Cancer Society's second Cancer Prevention Study (CPS II), a cohort study of 1.2 million participants (1982-1988), were compared with those obtained using a combination of data from the National Mortality Follow-back Survey (NMFS), a representative sample of US decedents in which information was collected from informants (1986), and the National Health Interview Survey (NHIS), a nationally representative household survey (1987). Second, the potential for residual confounding of the disease-specific age-adjusted smoking-attributable mortality estimates was addressed with a model-based approach. The estimated smoking-attributable mortality based on the CPS II for the four most common smoking-related diseases-lung cancer, chronic obstructive pulmonary disease, coronary heart disease, and cerebrovascular disease-was 19% larger than the estimated smoking-attributable mortality based on the NMFS/NHIS, yet the two data sources yielded essentially the same smoking-attributable mortality estimate for lung cancer alone. Further adjustment of smoking-attributable mortality for disease-appropriate confounding factors (education, alcohol intake, hypertension status, and diabetes status) indicated little residual confounding once age was taken into account.
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PMID:Methodological issues in estimating smoking-attributable mortality in the United States. 1099 48

Body weight and height have both been associated consistently with postmenopausal breast cancer but less consistently with prostate cancer. The present study examined the relationship between body mass index (BMI), height, and death from prostate cancer in two large American Cancer Society cohorts. Men in the study were selected from the male participants in Cancer Prevention Study I (CPS-I; enrolled in 1959 and followed through 1972) and Cancer Prevention Study II (CPS-II; enrolled in 1982 and followed through 1996). After exclusions, 1,590 prostate cancer deaths remained among 381,638 men in CPS-I and 3,622 deaths among 434,630 men in CPS-II. Cox proportional hazards modeling was used to compute rate ratios (RR) and to adjust for confounders. Prostate cancer mortality rates were significantly higher among obese (BMI, > or =30) than nonobese (BMI, <25) men in both cohorts [adjusted RR, 1.27; 95% confidence interval (CI), 1.04-1.56 in CPS-I; RR, 1.21; 95% CI, 1.07-1.37 in CPS-II]. Prostate cancer mortality rates in the CPS-I cohort were lowest for the shortest men (RR, 0.80; 95% CI, 0.63-1.03 for men <65 inches versus 65-66 inches) and highest for the tallest men (RR, 1.39; 95% CI, 1.11-1.74 for men > or =73 inches tall versus 65-66 inches). Rates remained constant among men 65-72 inches tall. No association between height and prostate cancer mortality was observed in the CPS-II cohort (RR, 1.03; 95% CI, 0.82-1.29 for men > or =75 versus 65-66 inches). These results support the hypothesis that obesity increases risk of prostate cancer mortality. Decreased survival among obese men may be a likely explanation for this association.
Cancer Epidemiol Biomarkers Prev 2001 Apr
PMID:Body mass index, height, and prostate cancer mortality in two large cohorts of adult men in the United States. 1131 75

Supplementation with antioxidant vitamins has been associated with decreased risk of stomach cancer or regression of precancerous lesions in high-risk areas of China and Colombia. We examined the association between stomach cancer mortality and regular use (> or =15 times per month) of individual vitamin C supplements, individual vitamin E supplements, and multivitamins among 1,045,923 United States adults in the Cancer Prevention Study II (CPS-II) cohort. CPS-II participants completed a questionnaire at enrollment in 1982 and were followed for mortality through 1998. During follow-up, there were 1,725 stomach cancer deaths (1,127 in men and 598 in women). After adjustment for multiple potential stomach cancer risk factors, vitamin C use at enrollment was associated with reduced risk of stomach cancer mortality [rate ratio (RR), 0.83; 95% confidence interval (CI), 0.68-1.01]. However, this reduction in risk was observed only among participants with short duration use at enrollment (RR, 0.68; 95% CI, 0.51-0.91 for <10 years of use; RR, 1.00; 95% CI, 0.73-1.38 for > or =10 years of use). There was no association between stomach cancer mortality and regular use of vitamin E (RR, 1.02; 95% CI, 0.82-1.27) or multivitamins (RR, 0.89; 95% CI, 0.77-1.03), regardless of duration of use. Our results suggest that the use of vitamin C, vitamin E, or multivitamin supplements may not substantially reduce risk of stomach cancer mortality in North American populations in which stomach cancer rates are relatively low. Our results do not rule out effects of vitamin supplementation in areas in which stomach cancer rates are high and stomach cancer etiology may differ.
Cancer Epidemiol Biomarkers Prev 2002 Jan
PMID:Vitamin C, vitamin E, and multivitamin supplement use and stomach cancer mortality in the Cancer Prevention Study II cohort. 1181 99


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