Associations Between Season of Birth and the Risk of Lung Cancer: Epidemiological Findings From Hungary

Lung cancer is the leading cause of cancer deaths worldwide. Both incidence and mortality of lung cancer are especially high in Hungary. Several investigations suggested recently that month of birth (MOB) is associated with the risks of several nonmalignant disorders as well as some malignant disorders. Only a few studies investigated previously the association between MOB and risk of lung cancer, but they provided inconsistent results. We, therefore, decided to investigate this issue in a large sample of individuals who died from lung cancer. Accordingly, we determined the MOB-associated risk of death by lung cancer between the years 1970 and 2009 among all individuals born in Hungary between 1925 and 1934. The final sample included about two million people. A total of 61,904 deaths by lung cancer occurred in this sample during the period investigated. Using analysis of variance (ANOVA), we did not find significant association between MOB and risk of lung cancer death, either in the whole population investigated (F?=?1.492; p?=?.145) or in the female subpopulation (F?=?1.535; p?=?.129). However, those males born in late spring (May–June) had a lower risk of lung cancer development (F?=?2.577; p?=?.006). Results of the Edwards test also did not suggest consistent association between MOB and risk of lung cancer death in the whole investigated period (1925–1934) in any populations (i.e., whole population or male and female subpopulations). In conclusion, we did not find significant association between MOB and risk of lung cancer in our total sample (although results alluded to a weak association between MOB and risk of lung cancer development among males). The possible associations between MOB and the risk of lung cancer development (or smoking) would require confirmation (or refutation) in large studies from other populations. (Author correspondence: dome_peter@yahoo.co.uk)     

Respiratory tract mortality in cement workers: a proportionate mortality study

Background

The evidence regarding the association between lung cancer and occupational exposure to cement is controversial. This study investigated causes of deaths from cancer of respiratory tract among cement workers.

Methods

The deaths of the Greek Cement Workers Compensation Scheme were analyzed covering the period 1969-1998. All respiratory, lung, laryngeal and urinary bladder cancer proportionate mortality were calculated for cement production, maintenance, and office workers in the cement industry. Mortality from urinary bladder cancer was used as an indirect indicator of the confounding effect of smoking.

Results

Mortality from all respiratory cancer was significantly increased in cement production workers (PMR?=?1.91; 95% CI 1.54 to 2.33). The proportionate mortality from lung cancer was significantly elevated (PMR?=?2.05; 95% CI 1.65 to 2.52). A statistically significant increase in proportionate mortality due to respiratory (PMR?=?1.7; 95% CI 1.2 to 2.34). and lung cancer (PMR?=?1.67;95% CI?=?1.15-2.34) among maintenance workers has been observed. The PMR among the three groups of workers (production, maintenance, office) did differ significantly for lung cancer (p?=?0.001), while the PMR for urinary bladder cancer found to be similar among the three groups of cement workers.

Conclusion

Cement production, and maintenance workers presented increased lung and respiratory cancer proportionate mortality, and this finding probably cannot be explained by the confounding effect of smoking alone. Further research including use of prospective cohort studies is needed in order to establish a causal association between occupational exposure to cement and risk of lung cancer.     

Professional exposure to goats increases the risk of pneumonic-type lung adenocarcinoma: results of the IFCT-0504-Epidemio study

Pneumonic-type lung adenocarcinoma (P-ADC) represents a distinct subset of lung cancer with specific clinical, radiological, and pathological features. Given the weak association with tobacco-smoking and the striking similarities with jaagsiekte sheep retrovirus (JSRV)-induced ovine pulmonary adenocarcinoma, it has been suggested that a zoonotic viral agent infecting pulmonary cells may predispose to P-ADC in humans. Our objective was to explore whether exposure to domestic small ruminants may represent a risk factor for P-ADC. We performed a multicenter case-control study recruiting patients with P-ADC as cases and patients with non-P-ADC non-small cell lung cancer as controls. A dedicated 356-item questionnaire was built to evaluate exposure to livestock. A total of 44 cases and 132 controls were included. At multivariate analysis, P-ADC was significantly more associated with female gender (Odds-ratio (OR)?=?3.23, 95% confidence interval (CI): 1.32-7.87, p?=?0.010), never-smoker status (OR?=?3.57, 95% CI: 1.27-10.00, p?=?0.015), personal history of extra-thoracic cancer before P-ADC diagnosis (OR?=?3.43, 95% CI: 1.10-10.72, p?=?0.034), and professional exposure to goats (OR?=?5.09, 95% CI: 1.05-24.69, p?=?0.043), as compared to other subtypes of lung cancer. This case-control suggests a link between professional exposure to goats and P-ADC, and prompts for further epidemiological evaluation of potential environmental risk factors for P-ADC.     

Association between the OGG1 Ser326Cys and APEX1 Asp148Glu polymorphisms and lung cancer risk: a meta-analysis

The previous published data on the association between the 8-oxo-guanine glycosylase-1 (OGG1) and apurinic/apyrimidinic-endonuclease-1 (APEX1/APE1) polymorphisms and lung cancer risk remained controversial. Several polymorphisms in the OGG1 and APEX1 gene have been described, including the commonly occurring Ser326Cys in OGG1 and Asp148Glu in APEX1. This meta-analysis of literatures was performed to derive a more precise estimation of the relationship. A total of 37 studies were identified to the meta-analysis, including 9,203 cases and 10,994 controls for OGG1 Ser326Cys (from 25 studies) and 3,491 cases and 4,708 controls for APEX1 Asp148Glu (from 12 studies). When all the eligible studies were pooled into the meta-analysis of OGG1 Ser326Cys polymorphism, significantly increased lung cancer risk was observed in recessive model (OR?=?1.17, 95?% CI?=?1.03–1.33) and in additive model (OR?=?1.21, 95?% CI?=?1.03–1.42). In the stratified analysis, significantly increased risk of lung cancer was also observed on the population-based studies (recessive model: OR?=?1.26, 95?% CI?=?1.08–1.46, additive model: OR?=?1.42, 95?% CI?=?1.06–1.73) and non-smokers (dominant model: OR?=?1.20, 95?% CI?=?1.02–1.42, recessive model: OR?=?1.20, 95?% CI?=?1.02–1.40, additive model: OR?=?1.35, 95?% CI?=?1.08–1.68). Additionally, when one study was deleted in the sensitive analysis, the results of OGG1 Ser326Cys were changed in Asians (recessive model: OR?=?1.16, 95?% CI?=?1.06–1.27, additive model: OR?=?1.23, 95?% CI?=?1.09–1.38). When all the eligible studies were pooled into the meta-analysis of APEX1 Asp148Glu polymorphism, there was no evidence of significant association between lung cancer risk and APEX1 Asp148Glu polymorphism in any genetic model. In the stratified analysis, significantly decreased lung adenocarcinoma risk was observed in recessive model (OR?=?0.68, 95?% CI?=?0.48–0.97, P _h?=?0.475, I²?=?0.0?%). Additionally, when one study was deleted in the sensitive analysis, the results of APEX1 Asp148Glu were changed in Asians (recessive model: OR?=?1.21, 95?% CI?=?1.03–1.43) and smokers (dominant model: OR?=?1.62, 95?% CI?=?1.08–2.44, additive model: OR?=?1.37, 95?% CI?=?1.02–1.84). In summary, this meta-analysis indicates that OGG1 Ser326Cys show an increased lung cancer risk in Asians and non-smokers, APEX1 Asp148Glu polymorphism may be associated with decreased lung adenocarcinoma risk, and APEX1 Asp148Glu polymorphism show an increased lung cancer risk in Asians and smokers. However, a study with the larger sample size is needed to further evaluated gene-environment interaction on OGG1 Ser326Cys and APEX1 Asp148Glu polymorphisms and lung cancer risk.     

Associations of Spexin and cardiometabolic parameters among women with and without gestational diabetes mellitus

Spexin (SPX) is a novel biomarker abundantly expressed in several animal and human tissues implicated in food intake and glucose control, respectively. As new roles for SPX are emerging, the present study explored for the first time, the associations of SPX to several cardiometabolic indices and inflammatory markers in pregnant women, a demographic not yet investigated with respect to SPX. A total of 117 Saudi women subdivided to those with gestational diabetes mellitus (GDM) (N?=?63) and those without (N?=?54) were included in this cross-sectional study. Anthropometry, glycemic, lipid, vitamin D, adipocytokines and inflammatory markers were measured consecutively at baseline and after the 2nd and 3rd trimesters. Age- and BMI adjusted comparisons revealed that levels of SPX were not significantly different in pregnant women with and without GDM. In all subjects, circulating levels of SPX showed modest associations with glucose (R?=?0.18; p?=?.08) and HOMA β (R?=??0.19; p?=?.09) as well as significant positive associations with total cholesterol (R?=?0.25; p?=?.02), LDL-cholesterol (R?=?0.25; p?=?.02), 25(OH)D (R?=?0.22; p?=?.04), albumin (R?=?0.30; p?<?.01) and IL1β (R?=?0.41; p?<?.01). Stepwise regression analysis also suggested that IL1β, leptin and albumin were the significant predictors of SPX. In summary, SPX levels modestly affect glucose and insulin sensitivity in pregnant women but is not associated with GDM and obesity. The significant association of SPX to ILβ warrants further investigation as to the role of SPX in immune modulation.     

NFKB1 insertion/deletion promoter polymorphism increases the risk of advanced ovarian cancer in a Chinese population

Ovarian cancer is the leading cause of death among all gynecological cancers. This is mainly attributed to its frequent presentation at an advanced stage (International Federation of Gynecology and Obstetrics stage III-IV). Nuclear factor-kappaB (NF-κB) is critically involved in the carcinogenesis and development of ovarian cancer. A functional insertion/deletion polymorphism (-94 ins/del ATTG) in the promoter region of the NFKB1 gene, which encodes the p50 subunit of the NF-κB protein, has been recently identified and shown to increase the susceptibility to many diseases. The purpose of this study was to explore the association between this polymorphism and the risk of advanced ovarian cancer in a Chinese population. A total of 179 advanced ovarian cancer patients and 223 healthy controls were recruited into this study. Genotypes were determined using polymerase chain reaction-capillary electrophoresis method. The insertion increased the risk of advanced ovarian cancer (odds ratio?=?2.111, 95% confidence intervals?=?1.125-3.961, p?=?0.019 for heterozygote insertion, and odds ratio?=?2.656, 95% confidence intervals?=?1.397-5.051, p?=?0.002 for homozygote insertion) compared with homozygote deletion. Similar results were seen in age-adjusted analyses (p?相似文献   

Association of glutathione S-transferase P1 gene polymorphism with the susceptibility of lung cancer

The conclusions of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) gene polymorphism and the risk of lung cancer are still debated. GSTP1 is one of the important mutant sites reported at present. This meta-analysis was performed to evaluate the association between GSTP1 and the risk of lung cancer. The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. Forty-four reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and lung cancer susceptibility, consisting of 12,363 patients with lung cancer and 13,948 controls. The association between GSTPI G allele and lung cancer risk was found in this meta-analysis (OR 1.08, 95?% CI 1.02–1.15, P?=?0.01). However, the GG genotype and AA genotype were not associated with the susceptibility of lung cancer. Furthermore, there was no association between GSTP1 A/G gene polymorphism and the risk of lung cancer in Caucasians, and East-Asians. In conclusion, GSTP1 G allele is associated with the lung cancer susceptibility. However, more studies on the relationship between GSTP1 A/G gene polymorphism and the risk of lung cancer should be performed in the future.     

Long non-coding RNA POLR2E gene polymorphisms increased the risk of prostate cancer in a sample of the Iranian population

The current study aimed to examine the impact of POLR2E rs1046040 and rs3787016 polymorphisms on prostate cancer (PCa) risk in a sample of southeast Iranian population. The present case-control study was performed on 178 patients with PCa and 180 benign prostatic hyperplasia (BPH). Genotyping of the variants was done by mismatch PCR-RFLP. The findings showed that the rs3787016 C?>?T variant significantly increased the risk of PCa in codominant (OR?=?1.84, 95% CI?=?1.12-3.03, P?=?0.018, CT vs CC), dominant (OR?=?1.88, 95% CI?=?1.63-3.05, P?=?0.011, CT?+?TT vas CC) and allele (OR?=?1.77, 95% CI?=?1.52-2.72, P?=?0.010, T vs C) inheritance model. Regarding rs1046040 C?>?T polymorphism, the findings revealed that the CT genotype significantly increased the risk of PCa compared to the CC genotype (OR?=?1.60, 95% CI?=?1.03-2.49, P?=?0.043). Furthermore, rs3787016 CT/rs1046040?CC as well as rs3787016 CT/rs1046040 CT increased the risk of PCa compared to the CC/CC genotype (p?=?0.029 and p?=?0.014, respectively). Haplotype analysis proposed that rs3787016 T/rs1046040 C significantly increased the risk of PCa compared to C/C (p?=?0.037). No significant association was observed between POLR2E variants and clinicopathological characteristics of PCa patients. In conclusion, the findings propose that POLR2E variants may be a risk factor for susceptibility to PCa in a sample of Iranian population.     

Association between p53 codon 72 genetic polymorphisms and tobacco use and lung cancer risk in a Chinese population

Genetic polymorphisms of p53 codon 72 are thought to have significant effects on the metabolism of environmental carcinogens and thus on lung cancer risk, but the reported results are not always consistent. The aim of this study is to investigate the relationship between p53 codon 72 genetic polymorphisms and tobacco use and lung cancer risk in a Chinese population. A population-based control study was conducted in 360 lung cancer patients and 360 cancer-free controls. The genotype of the p53 codon 72 was determined by using a polymerase chain reaction?Crestriction fragment length polymorphism assay. Patients with lung cancer had a significantly lower frequency of Pro/Pro genotype [odds ratio (OR)?=?0.58, 95?% confidence interval (CI)?=?0.40, 0.84; P?=?0.004] and Pro allele (OR?=?0.72, 95?% CI?=?0.59, 0.89; P?=?0.002) than controls. Patients with squamous cell carcinoma had also a significantly lower frequency of Pro/Pro genotype (OR?=?0.45, 95?% CI?=?0.25, 0.82; P?=?0.009). In the analysis combining p53 codon 72 polymorphisms and smoking, smokers who had smoked for more than 30 pack-years had a significantly lower frequency of Pro/Pro genotype (OR?=?0.52, 95?% CI?=?0.30, 0.92; P?=?0.03) compared with non-smokers. This study suggests that p53 codon 72 polymorphisms play a role in the development of lung cancer and modifies the risk for smoking-related lung cancer in a Chinese population.     

EphB2 SNPs and sporadic prostate cancer risk in African American men

The EphB2 gene has been implicated as a tumor suppressor gene somatically altered in both prostate cancer (PC) and colorectal cancer. We have previously shown an association between an EphB2 germline nonsense variant and risk of familial prostate cancer among African American Men (AAM). Here we set out to test the hypothesis that common variation within the EphB2 locus is associated with increased risk of sporadic PC in AAM. We genotyped a set of 341 single nucleotide polymorphisms (SNPs) encompassing the EphB2 locus, including known and novel coding and noncoding variants, in 490 AA sporadic PC cases and 567 matched controls. Single marker-based logistical regression analyses revealed seven EphB2 SNPs showing statistically significant association with prostate cancer risk in our population. The most significant association was achieved for a novel synonymous coding SNP, TGen-624, (Odds Ratio (OR) =?0.22; 95% Confidence Interval (CI) 0.08-0.66, p?=?1×10(-5)). Two other SNPs also show significant associations toward a protective effect rs10465543 and rs12090415 (p?=?1×10(-4)), OR?=?0.49 and 0.7, respectively. Two additional SNPs revealed trends towards an increase in risk of prostate cancer, rs4612601 and rs4263970 (p?=?0.001), OR?=?1.35 and 1.31, respectively. Furthermore, haplotype analysis revealed low levels of linkage disequilibrium within the region, with two blocks being associated with prostate cancer risk among our population. These data suggest that genetic variation at the EphB2 locus may increase risk of sporadic PC among AAM.     

Evening preference is related to the incidence of depressive states independent of sleep-wake conditions

Although evening preference has recently been identified as a risk factor for depression, it has not been substantiated whether evening preference is a direct risk factor for depressive states, or if it is associated secondarily through other factors, such as delayed sleep timing and shortened sleep duration. The objective of this study is to investigate associations in Japanese adult subjects between evening preference and incidence of depressive states, adjusting for various sleep parameters related to depressive states. The Morningness-Eveningness Questionnaire (MEQ), the Pittsburgh Sleep Quality Index (PSQI), and the Center for Epidemiologic Studies Depression Scale (CES-D) were administered to 1170 individuals (493 males/677 females; mean and range 38.5 and 20-59 yrs) to assess their diurnal preferences, sleeping states, and presence of depression symptoms. Subjects were classified into five chronotypes based on MEQ scores. Evening preference was associated with delayed sleep timing, shortened sleep duration, deteriorated subjective sleep quality, and worsened daytime sleepiness. Logistic regression analysis demonstrated that the extreme evening type (odds ratio [OR]?=?1.926, p?=?.018) was associated with increased incidence of depressive states and that the extreme morning type (OR?=?0.342, p?=?.038) was associated with the decreased incidence of depressive states, independent of sleep parameters, such as nocturnal awakening (OR?=?1.844, p?相似文献   

Mortality in relation to smoking: 20 years' observations on male British doctors.

In 1951 the British Medical Association forwarded to all British doctors a questionnaire about their smoking habits, and 34440 men replied. With few exceptions, all men who replied in 1951 have been followed for 20 years. The certified causes of all 10 072 deaths and subsequent changes in smoking habits were recorded. The ratio of the death rate among cigarette smokers to that among lifelong non-smokers of comparable age was, for men under 70 years, about 2:1, while for men over 70 years it was about 1-5:1. These ratios suggest that between a half and a third of all cigarette smokers will die because of their smoking, if the excess death rates are actually caused by smoking. To investigate whether this is the case, the relation of many different causes of death to age and tobacco consumption were examined, as were the effects of giving up smoking. Smoking caused death chiefly by heart disease among middle-aged men (and, with a less extreme relative risk, among old men,) lung cancer, chronic obstructive lung disease, and various vascular diseases. The distinctive features of this study were the completeness of follow-up, the accuracy of death certification, and the fact that the study population as a whole reduced its cigarette consumption substantially during the period of observation. As a result lung cancer grew relatively less common as the study progressed, but other cancers did not, thus illustrating in an unusual way the causal nature of the association between smoking and lung cancer.     

Month of birth is associated with mortality among older people in Japan: Findings from the JAGES cohort

Month of birth (MOB) has been linked to a variety of health conditions in adulthood. This study examined the association between MOB and mortality among the healthy elderly in Japan, where a practice of traditional age reckoning was employed up until the late 1940s. The results showed male participants born in December were more likely to die earlier while those born in January had lower mortality. It is possible that social factors in early life, such as the time period when a birth is officially registered, may have implications for health that stretch across the life course.     

Tumor necrosis factor alpha and beta and interferon gamma gene polymorphisms in Turkish breast cancer patients

Cytokine genes are important for researching cancer predisposition to cancers that elicit anti-tumor immune response. In this study, we investigated the association between breast cancer and tumor necrosis factor alpha (TNF-α) -308 (G>A), TNF-β +252 (A>G), and interferon gamma (IFN-γ) +874 (T>A) gene polymorphisms in a Turkish population. This study involved 204 female breast cancer patients and 204 healthy female controls. Genomic DNA was extracted from EDTA-preserved peripheral venous blood of patients and controls by a salting-out method and analyzed by polymerase chain reaction, allele-specific oligonucleotide polymerase chain reaction, and restriction fragment length polymorphism. TNF-α -308 genotype was found to have no effect on breast cancer susceptibility. However, there were statistically significant differences between the genotype frequencies of patients and controls for TNF-β polymorphism (p?=?0.016) and the allele and genotype frequencies for the IFN-γ polymorphism (p?=?0.0312 and p?=?0.001, respectively). In the composite genotype analysis, the TNF-α/β GAAG composite genotype (p?=?0.0424), the TNF-α/IFN-γ GGTT and GATT composite genotypes (p?=?0.0296 and p?=?0.0129, respectively), the TNF-β/IFN-γ AGTT composite genotype (p?=?0.0003), and the TNF-α/β/IFN-γ GGAGTT and GAAGTT composite genotypes (p?=?0.0437 and p?=?0.0038, respectively) were estimated to have a protective effect against breast cancer. However, the TNF-α/IFN-γ GGTA composite genotype is a risk factor for breast cancer (p?=?0.0156). In conclusion, TNF-β +252GG genotype was found more frequent in Turkish breast cancer patients than controls and IFN-γ TA+AA genotypes were estimated to increase breast cancer risk significantly in Turkish population.     

Analysis of trends in cancer mortality in England and Wales during 1951-80 separating changes associated with period of birth and period of death.

Cancer mortality rates in England and Wales were analysed so to describe simultaneously changes affecting successive generations--that is, associated with period of birth--as well as changes associated with the period of which the deaths took place. When mortality from all cancers was considered the analysis implied that, contrary to a widely held view, the rate of death from cancer had been declining in each sex in successive generations. For men the decline had occurred in generations born since 1900, whereas for women the peak came in the 1925 birth group. On the other hand, there had been little decline in the rates associated with period of death. Five examples of cancers of specific organs for which the trends contrasted are shown.     

Waist circumference as compared with body-mass index in predicting mortality from specific causes

Background

Whether waist circumference provides clinically meaningful information not delivered by body-mass index regarding prediction of cause-specific death is uncertain.

Methods

We prospectively examined waist circumference (WC) and body-mass index (BMI) in relation to cause-specific death in 225,712 U.S. women and men. Cox regression was used to estimate relative risks and 95% confidence intervals (CI). Statistical analyses were conducted using SAS version 9.1.

Results

During follow-up from 1996 through 2005, we documented 20,977 deaths. Increased WC consistently predicted risk of death due to any cause as well as major causes of death, including deaths from cancer, cardiovascular disease, and non-cancer/non-cardiovascular diseases, independent of BMI, age, sex, race/ethnicity, smoking status, and alcohol intake. When WC and BMI were mutually adjusted in a model, WC was related to 1.37 fold increased risk of death from any cancer and 1.82 fold increase risk of death from cardiovascular disease, comparing the highest versus lowest WC categories. Importantly, WC, but not BMI showed statistically significant positive associations with deaths from lung cancer and chronic respiratory disease. Participants in the highest versus lowest WC category had a relative risk of death from lung cancer of 1.77 (95% CI, 1.41 to 2.23) and of death from chronic respiratory disease of 2.77 (95% CI, 1.95 to 3.95). In contrast, subjects in the highest versus lowest BMI category had a relative risk of death from lung cancer of 0.94 (95% CI, 0.75 to 1.17) and of death from chronic respiratory disease of 1.18 (95% CI, 0.89 to 1.56).

Conclusions

Increased abdominal fat measured by WC was related to a higher risk of deaths from major specific causes, including deaths from lung cancer and chronic respiratory disease, independent of BMI.     

Breast cancer risk and 6q22.33: combined results from Breast Cancer Association Consortium and Consortium of Investigators on Modifiers of BRCA1/2

Recently, a locus on chromosome 6q22.33 (rs2180341) was reported to be associated with increased breast cancer risk in the Ashkenazi Jewish (AJ) population, and this association was also observed in populations of non-AJ European ancestry. In the present study, we performed a large replication analysis of rs2180341 using data from 31,428 invasive breast cancer cases and 34,700 controls collected from 25 studies in the Breast Cancer Association Consortium (BCAC). In addition, we evaluated whether rs2180341 modifies breast cancer risk in 3,361 BRCA1 and 2,020 BRCA2 carriers from 11 centers in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). Based on the BCAC data from women of European ancestry, we found evidence for a weak association with breast cancer risk for rs2180341 (per-allele odds ratio (OR)?=?1.03, 95% CI 1.00-1.06, p?=?0.023). There was evidence for heterogeneity in the ORs among studies (I(2)?=?49.3%; p?=?<0.004). In CIMBA, we observed an inverse association with the minor allele of rs2180341 and breast cancer risk in BRCA1 mutation carriers (per-allele OR?=?0.89, 95%CI 0.80-1.00, p?=?0.048), indicating a potential protective effect of this allele. These data suggest that that 6q22.33 confers a weak effect on breast cancer risk.     

Deaths in Canada from lung cancer due to involuntary smoking.

Recently published evidence indicates that involuntary smoking causes an increased risk of lung cancer among nonsmokers. Information was compiled on the proportion of people who had never smoked among victims of lung cancer, the risk of lung cancer for nonsmokers married to smokers and the prevalence of such exposure. On the basis of these data we estimate that 50 to 60 of the deaths from lung cancer in Canada in 1985 among people who had never smoked were caused by spousal smoking; about 90% occurred in women. The total number of deaths from lung cancer attributable to exposure to tobacco smoke from spouses and other sources (mainly the workplace) was derived by applying estimated age- and sex-specific rates of death from lung cancer attributable to such exposure to the population of Canadians who have never smoked; about 330 deaths from lung cancer annually are attributable to such exposure.     

Update analysis of studies on the MMP-9 ?1562 C>T polymorphism and cancer risk

Polymorphisms in the matrix metalloproteinase (MMP) gene have been hypothesized to be functional and may contribute to genetic susceptibility to cancers. The common sequence variation in MMP-9 ?1562 C>T (rs3918242), has been involved in cancer risk. However, results of the related published studies were somewhat controversial and underpowered in general. To clarify the role of MMP-9 ?1562 C>T genotype in global cancer, we performed a meta-analysis of all the available published studies involving 4,124 cancer patients and 4,728 control subjects. The overall results indicated that there was no major association of the variant on cancer risk. However, stratified analysis by cancer type showed that the MMP-9 ?1562 C>T polymorphism has a lower risk in colorectal cancer (OR?=?0.80, 95%CI?=?0.66?C0.96, P _{heterogeneity}?=?0.391) and lung cancer (OR?=?0.70, 95%CI?=?0.51?C0.96, P _{heterogeneity}?=?0.959) by allelic contrast. Furthermore, association of the MMP-9 ?1562 C>T polymorphism and cancer risk was also observed in hospital-based studies under the dominant genetic model (OR?=?0.87, 95%CI?=?0.78?C0.97, P _{heterogeneity}?=?0.355), allelic contrast (OR?=?0.85, 95%CI?=?0.75?C0.96, P _{heterogeneity}?=?0.271) and heterozygote comparison (OR?=?0.89, 95%CI?=?0.79?C0.99, P _{heterogeneity}?=?0.402). This pooled analysis showed evidence that the MMP-9 ?1562 C>T polymorphism may decrease both the colorectal and lung cancer risk. Further prospective studies with larger numbers of participants worldwide are required to evaluate the association in more detail.     

Risk of cancer in relation to serum concentrations of selenium and vitamins A and E: matched case-control analysis of prospective data.

The independent and joint associations of serum selenium and vitamin A (retinol) and E (alpha tocopherol) concentrations with the risk of death from cancer were studied in 51 case-control pairs--that is, 51 patients with cancer, each paired with a control matched for age, sex, and smoking. Case-control pairs came from a random sample of some 12000 people aged 30-64 years resident in two provinces of eastern Finland who were followed up for four years. Patients who died of cancer during the follow up period had a 12% lower mean serum selenium concentration (p = 0.015) than the controls. The difference persisted when deaths from cancer in the first follow up year were excluded. The adjusted risk of fatal cancer was 5.8-fold (95% confidence interval 1.2-29.0) among subjects in the lowest tertile of selenium concentrations compared with those with higher values. Subjects with both low selenium and low alpha tocopherol concentrations in serum had an 11.4-fold adjusted risk. Among smoking men with cancer serum retinol concentrations were 26% lower than in smoking controls (p = 0.002). These data suggest that dietary selenium deficiency is associated with an increased risk of fatal cancer, that low vitamin E intake may enhance this effect, and that decreased vitamin or provitamin A intake contributes to the risk of lung cancer among smoking men with a low selenium intake.