Biomedical subjects

W Zheng

Publications and source records attributed to W Zheng.

At least 199 records · Page 11Linked to original sources

PubMed1997

Paternal cigarette smoking and the risk of childhood cancer among offspring of nonsmoking mothers.

BACKGROUND: Cigarette smoking has been shown to increase oxidative DNA damage in human sperm cells. Assessment of the role of cigarette smoking in the etiology of childhood cancer has focused primarily on the effect of maternal smoking. Similar studies in relation to paternal smoking, however, have been inconclusive. Few studies have evaluated the effect of paternal smoking in the preconception period, and most of these could not disentangle the effects of paternal from maternal smoking. PURPOSE: We investigated the relationship of paternal smoking, particularly in the preconception period, with childhood cancer among offspring of the nonsmoking mothers. METHODS: We conducted a population-based, case-control study in Shanghai, People's Republic of China, where the prevalence of smoking is high among men but extremely low among women. The study included 642 childhood cancer case patients (<15 years of age) and their individually matched control subjects. Information concerning parental smoking, alcohol drinking, and other exposures of the index child was obtained by direct interview of both parents of the study subjects. Odds ratios (ORs), derived from conditional logistic regression models, were used to measure the association between paternal smoking and risk of childhood cancers. RESULTS AND CONCLUSIONS: Paternal preconception smoking was related to a significantly elevated risk of childhood cancers, particularly acute leukemia and lymphoma. The risks rose with increasing pack-years of paternal preconception smoking for acute lymphocytic leukemia (ALL) (P for trend = .01), lymphoma (P for trend = .07), and total cancer (P for trend = .006). Compared with children whose fathers had never smoked cigarettes, children whose fathers smoked more than five pack-years prior to their conception had adjusted ORs of 3.8 (95% confidence interval [CI] = 1.3-12.3) for ALL, 4.5 (95% CI = 1.2-16.8) for lymphoma, 2.7 (95% CI = 0.8-9.9) for brain tumors, and 1.7 (95% CI = 1.2-2.5) for all cancers combined. Statistically significant increased risks of cancer were restricted to children under the age of 5 years at diagnosis or those whose fathers had smoked during all of the 5 years prior to conception. IMPLICATIONS: Further studies are needed to confirm the association of paternal smoking with increased risk of cancer in offspring, to clarify the pattern of risks in relation to the timing of cigarette smoking, and to elucidate the biologic mechanism involved in predisposing the offspring to cancer. For example, it may be that paternal smoking induces prezygotic genetic damage that, in turn, acts as the predisposing factor.

Adolescent↗

PubMed1997

Stabilization of cationic liposome-plasmid DNA complexes by polyamines and poly(ethylene glycol)-phospholipid conjugates for efficient in vivo gene delivery.

Stable complexes of cationic liposomes with plasmid DNA were prepared by (1) including a small amount of poly(ethylene glycol)-phospholipid conjugate or (2) condensing the DNA with polyamines prior to the formation of liposome-plasmid complexes. These preparations were stable for months at 4 degrees C and gave reproducible high transfection activity for in vivo gene delivery after intravenous injection in mice. Under these conditions, the expression of marker gene (luciferase) was primarily in the lungs (reaching values up to 3 ng expression per mg tissue protein), but also in other tissues to a lesser extent. Non-stabilized formulations lost all their transfection activity in 4 days. In these formulations cholesterol, not dioleoylphosphatidylethanolamine, was the helper lipid effective for sustaining high transfection activity in vivo. These new developments in formulation technology should enhance the potential for liposome-mediated gene therapy.

Animals↗

PubMed1997

Sinonasal cancer and occupation. Results from the reanalysis of twelve case-control studies.

A pooled reanalysis of twelve case-control studies on sinonasal cancer and occupation from seven countries was conducted in order to study associations with occupations other than wood- and leather-related occupations. The pooled data set included a total of 930 cases (680 men and 250 women) and 3,136 controls (2,349 men and 787 women). All the studies included a detailed occupational history for cases and controls. Each job was coded using the same classifications for occupation and industry. Two approaches were used in the analysis: systematic analysis of occupations; a priori analysis using a preestablished list of occupations and industries. The results confirmed associations observed in several studies not included in this analysis. For agricultural workers, significant excesses were observed for squamous cell carcinoma among women (OR = 1.69) and men (OR = 3.72 for ten years or more of employment as an orchard worker), and adenocarcinomas among men (OR = 2.98 for ten years or more of employment). Associations with textile occupations were observed for adenocarcinoma among women (OR = 2.60) and squamous cell carcinoma among men (OR = 5.09 for fiber preparers, 3.01 for bleachers). Elevated risks for both histologic types were observed among men employed in food manufacturing (OR = 3.25, adenocarcinoma), or as food preservers (OR = 13.9, squamous cell carcinoma), and among men employed as cooks (OR = 1.99, squamous cell carcinoma). A positive association with squamous cell carcinoma was observed for male transport equipment operators (OR = 1.21), and also with adenocarcinoma for male motor-vehicle drivers (OR = 2.50). A number of other associations were observed in the systematic analysis.

Adenocarcinoma↗

PubMed1997

Evaluation of potential sources of bias in a genetic epidemiologic study of breast cancer.

Systematic errors, or bias, can arise at several stages of a study, including selection of subjects, measurement of exposure and disease, and data analysis. Little attention appears to have been paid to potential sources of bias in genetic epidemiologic studies, despite the fact that the study of units (families) and members (relatives) within those units produces unique opportunities for bias to be introduced. The ability to evaluate whether selection bias has occurred is rare. In 1944, a case-control family study of breast cancer was initiated at the Dight Institute for Human Genetics at the University of Minnesota. A follow-up study of these 544 families is currently being conducted on sisters, daughters, nieces, and granddaughters of the probands, and a control group of women who are spouses of male first- and second-degree relatives. Updated data are collected on females who are 18 years or older through telephone interviews and questionnaires. The availability of detailed family history information on these families at baseline provided an opportunity to evaluate several potential sources of bias. Analyses were performed to determine if families lost to follow-up differed from those who were successfully located or excluded (ineligible), and whether participation rates within a family differed by relationship to proband, age, and family history of cancer. The latter participation rates for individuals were examined with respect to a telephone interview, a mailed questionnaire, and screening mammography. There were no statistically significant differences in the cancer histories of families that were excluded, those that were lost to follow-up, and those that participated. Within families, degree of relationship to the breast cancer proband was significantly associated with age-adjusted participation rates on mailed questionnaires (P < 0.005) and mammography (P < 0.005), but not telephone interviews (P = 0.29). After adjustment for age, marry-ins with a family history of breast cancer were not significantly more likely than marry-ins without a family history to undergo mammography (P = 0.11) or return mailed questionnaires (P = 0.74). Although non-participation is a potentially serious source of bias to a genetic epidemiologic study and the effect of variable participation rates should be explored when investigating the genetic component of a disease, it does not appear to be a problem for this particular study.

Adolescent↗

PubMed1997

A steroidal pheromone and spawning stimuli act via different neuroendocrine mechanisms to increase gonadotropin and milt volume in male goldfish Carassius auratus.

In goldfish (Carassius auratus), pheromonal 17alpha, 20beta-dihydroxy-4-pregnen-3-one (17,20beta-P) and spawning stimuli (interaction with a sexually active female releasing prostaglandin pheromone) both increase gonadotropin-II (GtH-II) and milt volume. In the goldfish pituitary, GtH-II release is stimulated by gonadotropin-releasing hormone (GnRH) and inhibited by dopamine (DA). In this study, we investigated the possibility that 17,20beta-P and spawning stimuli act via separate neuroendocrine mechanisms by determining whether their effects on GtH-II could be selectively disrupted by injection of DA type-2 receptor (D-2) agonists (bromocryptine and LY171555) or a goldfish GnRH antagonist, [Ac-Delta3-Pro1, 4FD-Phe2, d-Trp3,6]-mGnRH (analog E). D-2 agonists blocked 17,20beta-P-induced increases in GtH-II and milt volume but did not affect spawning-induced responses. GnRH antagonist blocked 17,20beta-P-induced increases in GtH-II and milt volume, and spawning-induced GtH-II increase, but did not affect spawning-induced increase in milt volume. These results suggest that (1) pheromonal 17,20beta-P and spawning stimuli increase GtH-II increase via distinct neuroendocrine mechanisms, (2) the effect of pheromonal 17,20beta-P on increasing milt volume is GtH-II-dependent, and (3) the effect of spawning stimuli on increasing milt volume is GtH-II-independent.

Animals↗

PubMed1997

Early occurrence and prognostic significance of p53 alteration in primary carcinoma of the fallopian tube.

The pathogenesis of primary carcinoma of the fallopian tube (PCFT) is poorly understood. Tumor suppressor p53 gene alterations are common in human malignancies, but their role in the tumorigenesis and survival of PCFT is undefined. The objectives of this study were to define the occurrence and prognostic role of p53 alteration in PCFT and to examine the efficiency of immunohistochemistry (IHC) in detecting p53 alteration in PCFT. Fifty-two PCFT and 10 normal fallopian tubes were examined for p53 alteration by IHC and polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP). The Kaplan-Meier method was used to derive the survival function, while the log-rank test was used to compare curves for two or more groups. Other patients' characteristics were analyzed by two-tailed Fisher's exact tests. IHC correlated well with PCR-SSCP with 100% sensitivity and 83.3% specificity for detecting p53 alteration in this study. Thirty-one of 52 (57%) PCFT showed p53 alteration. Alteration of p53 occurred in all stages of PCFT with a similar incidence in carcinoma in situ and late-stage disease. Alteration of p53 was related to tumor histologic type. Significant survival difference was noted between advanced and early clinical stages but no such difference was identified among different tumor grades. Compared to the p53-nonaltered group, the presence of p53 alteration in PCFT was related to significantly decreased patient survival (RR = 6.8, 95% CI = 2.9-16.2) in multivariate analysis. In the subgroup of patients with residual tumor after surgery, those with p53-altered tumors had a significantly decreased survival compared to those with p53-nonaltered group (RR = 7.4, 95% CI = 1.9-28.2). Alteration of p53 is common and IHC is an efficient method to detect p53 alteration in PCFT. Shorter survival is associated with p53 alteration which is an independent marker for the disease in this study. Alteration of p53 may be an early event in tubal tumorigenesis and may play an important role in the development of PCFT. Whether detection of p53 alteration may serve as an indicator of high-risk patients for whom more aggressive adjuvant chemotherapy may be considered needs to be explored in the future.

Aged↗

PubMed1997

Multiple immunoreactive inhibin proteins in serum from postmenopausal women with epithelial ovarian cancer.

Inhibin is an ovarian protein previously shown, using a nonspecific assay, to be elevated in serum of women with ovarian cancer. However, inhibin is secreted in multiple biochemical forms, including dimeric inhibin A and B and alpha inhibin precursors (pro-alphaC), each of which can now be specifically measured. We have examined the secretion of inhibin B and pro-alphaC inhibin in serum from women with epithelial ovarian cancer (EOC) for the first time, and have compared these analytes to inhibin A and total inhibin (inhibin A + B + pro-alphaC) as potential serum markers for EOC in postmenopausal women. Of all the immunoreactive inhibin proteins studied, the best serum marker was pro-alphaC, with 22% of women with EOC having levels that exceeded the range of values in women without EOC. Since CA 125 and pro-alphaC levels were not significantly correlated, combination of these markers resulted in 87% of EOC cases having elevated preoperative serum levels, a 9% increase over CA 125 alone. These data suggest that alpha inhibin secretion, especially pro-alphaC, may be useful in addition to CA 125 as a serum marker for EOC in postmenopausal women.

Aged↗

PubMed1997

Effect of interleukin-8 on glomerular sulfated compounds and albuminuria.

To evaluate the effect of interleukin-8 (IL8) on glomerular basement membrane (GBM) sulfated compounds and albuminuria, we infused IL8 in 1% bovine serum albumin (BSA) for 5 days into the left renal artery of Holtzman male rats at the rate of 10 microliters/h using an osmotic pump. Control rats received 1% BSA. A significant increase in urinary albumin/creatinine ratio was seen on the last day of IL8 infusion (0.38 +/- 0.11, mean +/- SEM) when compared with albumin/creatinine ratio prior to infusion (0.19 +/- 0.04, P = 0.04). No significant differences in urinary albumin excretion prior to and after infusion of 1% BSA were observed. On the last day of infusion, rats were injected with 35sulfate (1.0 mCi/200 g body weight) intraperitoneally and killed after 8 h. Glomeruli were isolated and GBM obtained. After 5 days of IL8 administration, there was a significant increase in 35sulfate uptake by GBM of the infused kidney (76 +/- 10 cpm/dry glomerular weight, mean +/- SEM) compared with the uptake seen in the contralateral kidney (53 +/- 9, P = 0.05). The in vivo infusion of IL8 increased the 35sulfate uptake by GBM and augmented the urinary albumin/creatinine ratio, suggesting that IL8 may induce albuminuria by altering the metabolism of the GBM sulfated compounds. This hypothesis needs to be confirmed by studies on glomerular charge selectivity and GBM anionic sites during the course of the infusion. Moreover, the persistence of the effect needs to be evaluated by prolonging the infusion for more than 5 days.

Albuminuria↗

PubMed1997

Morphologic changes induced by neoadjuvant androgen ablation may result in underdetection of positive surgical margins and capsular involvement by prostatic adenocarcinoma.

OBJECTIVE: Neoadjuvant androgen ablation (NAAA) causes significant cytoarchitectural changes in both benign and malignant prostatic epithelial cells that may contribute to underdetection of prostate cancer capsular involvement and positive surgical margins. METHODS: The aim of this study is to determine the ability of cytokeratin immunohistochemistry to enhance the determination of pathologic stage of prostate cancer following NAAA. RESULTS: Cytokeratin AE1/AE3 immunohistochemistry identified 6 (27.3%), 15 (68.2%), 5 (22.7%), and 5 (22.7%) cases of organ-confined disease, capsule penetration, positive surgical margin, and seminal vesicle involvement, respectively, as compared with 10 (45.5%), 10 (45.5%), 3 (13.6%), and 5 (22.7%) cases by hematoxylin-eosin (H&E) staining, respectively. Two cases without detectable tumor by H&E staining had demonstrable residual tumor by cytokeratin immunohistochemical staining. CONCLUSIONS: Cytokeratin immunohistochemistry revealed more extensive intracapsular, capsular, and extracapsular tumor involvement and higher rate of positive surgical margin than did conventional H&E staining. Therefore, the beneficial pathologic effects of NAAA observed may, in part, be attributable to the artifact of observation.

Adenocarcinoma↗

PubMed1997

Weight variability and incident disease in older women: the Iowa Women's Health Study.

OBJECTIVE: To evaluate the association between weight variability and disease incidence in women. DESIGN: Prospective cohort study, following women from 1986 through 1992. METHODS: A population-based sample of 33834 women aged 55-69 y, free of cancer and heart disease, completed a mail-based survey that included self-reported body weights at ages 18, 30, 40, 50 y, and currently. Weight variability was defined as (1) the root mean square error around the slope of weight on age (RMSE); and (2) categorical measures of weight change. Outcome measures were incidence of myocardial infarction (MI); stroke; diabetes; breast, endometrial, lung, or other cancer; total and hip fractures. RESULTS: Adjusted relative risks of MI, stroke, diabetes, and hip fracture increased with increasing weight variability. The age and body mass index-adjusted relative risks (RR) for highest vs lowest quartile of RMSE were: MI: 2.03; stroke: 1.61; diabetes: 1.42; breast cancer: 0.85; endometrial cancer: 0.88; lung cancer: 1.70; other cancer: 0.93; total fractures: 1.15; hip fractures: 1.45. The strongest associations between weight change categories and disease were for diabetes (RR compared to small gain/stable weight: large cycle, 1.72; small cycle, 1.55; large gain, 1.80; weight loss, 1.91; other pattern, 1.55). Large weight cycles were associated with higher risk of MI (RR = 1.89) and stroke (RR = 1.71). CONCLUSIONS: These findings are consistent with previous studies and suggest that weight variability is associated with higher risk of developing chronic diseases.

Aged↗

PubMed1997

Increased expression of the cardiac L-type calcium channel in estrogen receptor-deficient mice.

Steroid hormones control the expression of many cellular regulators, and a role for estrogen in cardiovascular function and disease has been well documented. To address whether the activity of the L-type Ca2+ channel, a critical element in cardiac excitability and contractility, is altered by estrogen and its nuclear receptor, we examined cardiac myocytes from male mice in which the estrogen receptor gene had been disrupted (ERKO mice). Binding of dihydropyridine Ca2+ channel antagonist isradipine (PN200-110) was increased 45.6% in cardiac membranes from the ERKO mice compared to controls, suggesting that a lack of estrogen receptors in the heart increased the number of Ca2+ channels. Whole-cell patch clamp of acutely dissociated adult cardiac ventricular myocytes indicated that Ca2+ channel current was increased by 49% and action potential duration was increased by 75%. Examination of electrocardiogram parameters in ERKO mice showed a 70% increase in the QT interval without significant changes in PQ or QRS intervals. These results show that the membrane density of the cardiac L-type Ca2+ channel is regulated by the estrogen receptor and suggest that decreased estrogen may lead to an increase in the number of cardiac L-type Ca2+ channels, abnormalities in cardiac excitability, and increased risk of arrhythmia and cardiovascular disease.

Action Potentials↗

PubMed1997

Alpha and beta subunits of inhibin/activin as sex cord-stromal differentiation markers.

Inhibins (alpha and beta heterodimers) and activins (beta homodimers) are related peptides with opposing biologic action on gonadotropin regulation. They serve as components of the pituitary-gonadal feedback system. Although sex-cord stromal tumors can usually be distinguished from ovarian epithelial tumors or their metastases by morphology or by using antibodies against intermediate filaments, the diagnosis remains difficult in rare situations in such cases as sarcomatoid granulosa-theca cell tumors, ovarian small cell carcinomas, or soft-tissue sarcomas. A total of 28 sex cord-stromal tumors of the ovary and 43 non-sex cord-stromal tumors were immunohistochemically evaluated for the presence of alpha and beta subunits of inhibin and activin. For comparison, 10 normal adult gonads including seven ovaries with hilar regions and three testes also were examined. Immunoreactivity for both alpha and beta subunits of inhibin/activin was identified in both non-neoplastic and neoplastic granulosa, Sertoli, Leydig, hilar and luteinized theca cells, with the strongest immunoreactivity in Leydig and hilar cells. One of three Sertoli-Leydig cell tumors that showed a sarcomatoid growth pattern and one sex-cord tumor with annular tubules also were immunoreactive for both subunits. For non-sex cord stromal-derived ovarian tumors, alpha subunit immunoreactivity was negative in all but two of five ovarian mucinous tumors. Weak immunoreactivity for beta subunit was found in most ovarian surface epithelial carcinomas, two of four colonic, and one of three pancreatic carcinomas. No immunostaining was found in nonspecialized gonadal stromal or interstitial cells, thecal cells, germ cells, ovarian small cell carcinomas, carcinoid tumors, dysgerminomas, or leiomyosarcomas. Immunostaining of alpha subunit (inhibin alpha), but not of beta subunit could serve as a sex cord-stromal differentiation marker because alpha subunit alone is largely confined to sex cord-stromal lesions with the exception of some ovarian mucinous tumors. Further studies are needed to define the usefulness of this sex cord-stromal differentiation marker in the practice of surgical pathology. Coexpression of alpha and beta subunits in sex cord-stromal elements suggests that dimeric inhibin is expressed in these cells.

Activins↗

PubMed1997

Host-mediated modification of Sau3AI restriction in Listeria monocytogenes: prevalence in epidemic-associated strains.

Most major food-related outbreaks of listeriosis have been traced to a cluster of genetically related strains of serovar 4b (epidemic clone). In spite of numerous searches, distinct bacteriologic or virulence-related features unique to these strains have eluded identification, although a restriction fragment length polymorphism (RFLP) characteristic of the epidemic clone has previously been described (W. Zheng and S. Kathariou, Appl. Environ. Microbiol. 61:4310-4314, 1995). We found that DNAs from 75 strains which were derived from three separate outbreaks and which had the epidemic clone-specific RFLP were also invariably resistant to digestion by Sau3AI and other restriction endonucleases sensitive to cytosine methylation at 5' GATC 3' sites. This modification of Sau3AI restriction was host mediated, as it did not persist when DNA was cloned and propagated in Escherichia coli, and was uncommon among other Listeria strains. Epidemic-associated strains with this modification were resistant to infection by phage propagated in a serotype 4b strain which was not known to be involved in an epidemic and which lacked the epidemic clone-specific RFLP. Screening for susceptibility to MboI digestion revealed that these epidemic strains lacked methylation of adenines at GATC sites. This type of modification was rare among Listeria strains and was found in only three (of eight screened) strains of serovar 1/2b, possibly representing one clonal lineage.

Adenine↗

PubMed1997

Presence of activin, inhibin, and follistatin in epithelial ovarian carcinoma.

Activin induces proliferation in epithelial ovarian carcinoma cell lines, whereas follistatin (FS), an activin binding protein, inhibits this action. To test the hypothesis that activin production, in excess of inhibin and FS, results in cell proliferation in epithelial ovarian tumors, messenger RNA (mRNA) expression of the activin family of proteins, FS, and activin type I and II receptors was examined in 25 primary epithelial ovarian tumors and tumor epithelium in culture (n = 7) using RT-PCR. Activin A was measured in the serum of ovarian cancer patients, and activin A, total inhibin, and FS protein secretion was measured from primary epithelial tumors in vitro. The effect of activin and FS on cell proliferation was assessed by measuring [3H]thymidine incorporation. All results were compared with normal ovarian epithelium. All epithelial ovarian tumors expressed mRNA for the alpha, beta A, and beta B subunits; FS 288 and 315; and the activin type IA, IB, II, and IIB receptors. beta A mRNA expression, as assessed using semiquantitative RT-PCR, was 3-fold greater in cultured tumor epithelium than in primary tumors (band density 0.86 +/- 0.17 vs. 0.28 +/- 0.09; P < 0.01). In addition, beta A mRNA was abundantly expressed in normal epithelium in culture (n = 2), whereas only trace amounts were seen in 2/9 primary epithelial samples. Activin protein was secreted by 24/25 primary epithelial ovarian tumors (range 0.2-155.8 ng/mL). In contrast, total inhibin was secreted by only 2/25 (range 0.01-0.92 ng/mL), whereas free FS was not detectable in the medium of any tumor (< 0.5 ng/mL). Treatment with activin or FS did not consistently affect cell growth. Measurement of serum activin A in a subset of subjects and in 27 additional subjects with epithelial ovarian carcinoma (n = 33) revealed preoperative activin A levels > 3 SD above the mean for pre- and postmenopausal women in 13/33 (39%) subjects. We conclude that in epithelial ovarian cancer: 1) beta A subunit mRNA is expressed, 2) activin protein is secreted more frequently than inhibin and in greater quantities than FS, 3) beta A subunit mRNA expression is greater in neoplastic and normal epithelium in culture than in the primary tissue, 4) the majority of tumors in culture do not respond to activin or FS treatment with proliferation, and 5) serum activin levels may reflect tumor secretion in some patients. Thus, activin A appears to be available as an autocrine/paracrine factor in epithelial ovarian tumors and may contribute to circulating levels, but its role in tumorigenesis has yet to be defined.

Activins↗

PubMed1997

The steroid pheromone 4-pregnen-17,20ss-diol-3-one increases fertility and paternity in goldfish.

Previous studies in goldfish (Carassius auratus) showed that the oocyte maturation-inducing steroid 4-pregnen-17,20ss-diol-3-one (17,20ssP) functions after release as a pheromone that increases male serum gonadotropin II (GtH II) concentration, milt (sperm and seminal fluid) volume and sexual activity, effects hypothesized to increase male reproductive success in the sperm competition of multi-male spawnings. The present study tested this hypothesis by determining whether overnight exposure to 17,20ssP increases fertility. In pair spawnings, 17,20ssP-exposed males fertilized a greater percentage of eggs than did control males, apparently because 17,20ssP-exposed males had more releasable sperm at the onset of spawning. Microsatellite DNA paternity analysis showed that 17,20ssP-exposed males also fertilized more eggs in competitive spawnings involving one control male and one 17,20ssP-exposed male. This effect of 17,20ssP on competitive fertility could be due to demonstrated increases in spawning activity, milt volume, duration of sperm motility and proportion of motile sperm. However, it appears that a change in sperm quality is a major component of the pheromonal effect because, in competitive in vitro fertilizations, sperm from 17,20ssP-exposed males fertilized more eggs than did sperm from control males. The results indicate that the response to pheromonal 17,20ssP is a major determinant of reproductive success in male goldfish.

Journal Article↗

PubMed1997

The association of drinking water source and chlorination by-products with cancer incidence among postmenopausal women in Iowa: a prospective cohort study.

OBJECTIVES: This study assessed the association of drinking water source and chlorination by-product exposure with cancer incidence. METHODS: A cohort of 28,237 Iowa women reported their drinking water source. Exposure to chlorination by-products was determined from statewide water quality data. RESULTS: In comparison with women who used municipal ground-water sources, women with municipal surface water sources were at an increased risk of colon cancer and all cancers combined. A clear dose-response relation was observed between four categories of increasing chloroform levels in finished drinking water and the risk of colon cancer and all cancers combined. The relative risks were 1.00, 1.06, 1.39, and 1.68 for colon cancer and 1.00, 1.04, 1.24, and 1.25 for total cancers. No consistent association with either water source or chloroform concentration was observed for other cancer sites. CONCLUSIONS: These results suggest that exposure to chlorination by-products in drinking water is associated with increased risk of colon cancer.

Chlorine↗

PubMed1997

[Fluorescence lifetimes of squamous carcinoma, adenocarcinoma and normal human lung tissues in vitro by time-resolved fluorescence].

Using pulsed dye laser 632.8nm, lifetimes of adenocarcinoma, squamous carcinoma and normal human lung tissues in vitro have been measured by time-resolved fluorescence as 5.1, 5.6 and 6.3 ns respectively. Time-resolved fluorescence shows that the decay time of tumor tissues is faster than that of normal tissues. The results may offer new diagnostic method to determine cancer.

Adenocarcinoma↗

PubMed1997

Association of family history of cervical, ovarian, and uterine cancer with histological categories of lung cancer: the Iowa Women's Health Study.

A family history of cervical, ovarian, or uterine cancer has been shown to be associated with increased lung cancer risk among postmenopausal women. The present report examines the hypotheses that a family history of cervical cancer is positively associated with histological subtypes of lung cancer most strongly associated with smoking and that a family history of ovarian or uterine cancer are positively associated with risk of adenocarcinoma of the lung. Data are from the Iowa Women's Health Study, a prospective cohort study of 34,480 women ages 55-69 in 1986. Personal smoking histories, use of alcohol, and family history of selected cancers in first- and second-degree relatives were collected at baseline. Follow-up for cancer occurrence was achieved through the State Health Registry of Iowa. After baseline exclusions, a total of 343 incident lung cancers were identified in the cohort at risk through 1994. Women with a family history of cervical cancer in a first-degree relative had a multivariate-adjusted relative risk of lung cancer of 1.6 [95% confidence interval (CI): 0.98-2.6] compared to women without a family history. The risk was particularly high for malignancies most strongly associated with smoking (squamous, small cell, and large cell tumors; relative risk, 2.0; 95% CI, 1.1-3.7). Consistent with our hypotheses, a family history of ovarian cancer was associated with an approximately 2-fold increased risk (multivariate adjusted) of adenocarcinoma of the lung; the association with malignancies more strongly associated with smoking was inverse (relative risk, 0.6; 95% CI, 0.2-2.4). A family history of uterine cancer was not associated with adenocarcinoma, but there was a positive association observed for the most strongly smoking-associated histological types. These results suggest that a family history of cervical cancer is a modest independent risk factor for lung cancers most strongly associated with smoking, and a family history of ovarian cancer is a risk factor for adenocarcinoma of the lung.

Adenocarcinoma↗