Aspirin and lung cancer in women

The association between aspirin use and lung cancer risk in women was examined in a case-control study nested in the New York University Women's Health Study, a large cohort in New York. Case subjects were all the 81 incident lung cancer cases who had provided information about aspirin use at enrollment and during the 1994-1996 follow up. Ten controls per case were randomly selected from among study participants who matched a case by age, menopausal status, and dates of enrollment and follow-up. Relative to no aspirin use, the odds ratio for lung cancer (all histological sub-types combined) among subjects who reported aspirin use three or more times per week for at least 6 months was 0.66 (95% confidence interval 0.34-1.28), after adjustment for smoking and education. A stronger inverse association was observed in analyses restricted to non-small cell lung cancer (adjusted odds ratio 0.39, 95% confidence interval 0.16-0.96). These results suggest that regular aspirin use might be inversely associated with risk of lung cancer in women, particularly the non-small cell sub-type.     

Aspirin and lung cancer risk in a cohort study of women: dosage, duration and latency

Aspirin may reduce the risk of cancer at some sites but its effect at the lung is unclear. We prospectively examined associations between aspirin use and risk of lung cancer in 109,348 women in the Nurses' Health study from 1980 to 2004. During this time, 1,360 lung cancers were documented in participants 36-82 years of age. Aspirin use and smoking were assessed every 2 years. Risk of lung cancer was a non-significant 16% lower for regular aspirin users of one or two tablets per week and a significant 55% higher for users of 15 or more tablets per week compared with women who never regularly used aspirin. Results were similar when limited to never smokers. For both the low and high quantity aspirin users, risk of lung cancer did not decline or increase with longer durations of use, and associations attenuated as the latency period between aspirin assessment and lung cancer diagnosis was lengthened. Our findings, together with those from previous clinical trials and prospective studies, do not provide consistent evidence that aspirin influences the development of lung cancer and further investigation is required with adjustment for smoking.     

Long-term aspirin use and colorectal cancer risk: a cohort study in Sweden

In a prospective cohort study of 74 250 Swedish women and men, with 7.2 years of follow-up and 705 incident colorectal cancer cases, long duration of aspirin use (>20 years) was associated with a reduced risk of colorectal cancer (multivariate rate ratio: 0.65; 95% confidence interval: 0.45-0.94). Aspirin use for a shorter period was not associated with risk.     

Anthropometry and prostate cancer risk: a prospective study of 22,248 Norwegian men

Objectives: Few risk factors for prostate cancer are known, but both endocrine changes and dietary factors have been implicated in the etiology of the disease. Anthropometry may therefore provide a tool in the search for carcinogenic mechanisms connected to these suggested causal components.Methods: We have studied the association between body size and prostate cancer risk in a prospective study of 22,248 Norwegian men. During 12 years of follow-up, 642 men developed cancer of the prostate. A possible association between anthropometry (height, weight, body mass index (BMI), and lean body mass (LBM)) and prostate cancer risk was assessed using Cox regression analysis.Results: Overall, we observed no significant trend for any of the variables studied, although an excess risk of prostate cancer with increasing height was suggested by an age-adjusted relative risk of 1.2 (95% CI=0.9–1.6) for the tallest compared to the shortest quintile of men. None of the other three variables (weight, BMI, and LBM) displayed any consistent relation with the risk of prostate cancer.Conclusions: We conclude that these results do not indicate a strong association between anthropometric factors and risk of prostate cancer.Also affiliated with the Norwegian Cancer Society, Oslo, Norway     

肺癌的化学预防研究进展

肺癌是目前全球癌症死亡的首要原因,已经成为全球共同面对和急需解决的公共卫生问题之一。虽然在多学科治疗以及精准医学理念的指导下,肺癌疗效在不断提高,但远期生存率仍较低,因此,预防其发生意义重大。预防包括生物预防和化学预防,本文就化学预防研究进展进行综述。     

Green tea consumption and lung cancer risk: the Ohsaki study

We examined the risk of lung cancer in relation to green tea consumption in a population-based cohort study in Japan among 41,440 men and women, aged 40-79 years, who completed a questionnaire in 1994 regarding green tea consumption and other health-related lifestyle factors. During the follow-up period of 7 years (from 1995 to 2001), 302 cases of lung cancer were identified, and the Cox proportional hazards regression model was used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs). The multivariable-adjusted HRs of lung cancer incidence for green tea consumption of 1 or 2, 3 or 4, and 5 or more cups/day as compared to less than 1 cup/day were 1.14 (95% CI: 0.80-1.62), 1.18 (95% CI: 0.83-1.66), and 1.17 (95% CI: 0.85-1.61), respectively (P for trend=0.48). This cohort study has found no evidence that green tea consumption is associated with lung cancer.     

吸入性糖皮质激素对肺癌的化学预防作用及其机制简

研究证实COPD是肺癌的独立危险因素,吸烟为COPD和肺癌的共同危险因素,而炎症反应、氧化应激、表观遗传等在肺癌发生中也起着重要作用。动物模型及临床研究均证实吸入性糖皮质激素（ICS）具有肺癌化学预防作用,但其机制并不完全清楚。深入研究糖皮质激素参与调节肺癌发生的机制,可能有助于制定新的肺癌预防和治疗策略。本文就糖皮质激素在抗炎效应、调控遗传信息及细胞周期、诱导细胞凋亡等途径的作用机制作一综述,以期为深入探究糖皮质激素参与调节肺癌发生提供依据。     

Individual and joint use of statins and low-dose aspirin and risk of colorectal cancer: a population-based case-control study

Recent research has drawn attention to protective effects of statins on colorectal cancer (CRC) and possible joint effects with other drugs. Because statins are often administered in combination with low-dose aspirin for the prevention of cardiovascular disease, the aim of our study was to investigate individual and combined effects of statins and low-dose aspirin on CRC risk. We assessed use of statins and low-dose aspirin in 540 cases with histologically confirmed incident CRC and 614 control subjects in a population-based case-control study in Germany. Multiple logistic regression was used to estimate the impact of regular use of either low-dose aspirin or statins, and of both drugs combined on CRC risk. We found modest risk reduction of CRC for regular use of low-dose aspirin (adjusted odds ratio 0.77, 95% confidence interval 0.55-1.07) and a stronger association with regular use of statins (OR 0.65, 95% CI 0.43-0.99) or use of both drugs (OR 0.63, 95% CI 0.36-1.10). Combined use of low-dose aspirin and statins was associated with risk reduction by 62% after 5 or more years (OR 0.38, 95% CI 0.15-0.97). Combinational chemoprevention with low-dose aspirin and statins might provide stronger risk reduction than either of the single drugs after at least 5 years use, but confirmation is needed, preferably in prospective cohort studies and eventually by randomized controlled trials.     

Aspirin and other non-steroidal anti-inflammatory drug use and colorectal cancer survival: a cohort study

Background:

Aspirin has been widely reported to reduce the incidence of colorectal cancer. Recently, a survival benefit after diagnosis has also been suggested. Data regarding such a benefit are to date contradictory. This study examines the effect of non-steroidal anti-inflammatory drug (NSAID) use on mortality in colorectal cancer in a larger patient cohort than previously to further clarify this effect, especially in terms of exposure timing and dosing.

Methods:

A study using the General Practice Research Database assessed whether aspirin or NSAID exposure in the year immediately following diagnosis affected all-cause mortality in a cohort of 13 994 colorectal cancer patients. Cox proportional hazards modelling adjusted for age, gender, smoking, body mass index and comorbidity.

Results:

Overall mortality was slightly lower in patients treated with aspirin, (hazard ratio (HR)=0.91; 95% confidence interval (CI)=0.82–1.00). This effect was observed only in patients treated with prophylaxis-dose aspirin (HR=0.89, CI=0.80–0.98) and only in patients taking aspirin before diagnosis (HR=0.86, CI=0.76–0.98). Differential effects were observed depending on the time after diagnosis. Up to 5 years, a reduction in mortality was observed for aspirin users (HR=0.83, CI=0.75–0.92), whereas after 10 years there was an increase in mortality (HR=1.94, CI=1.26–2.99). For NSAID use, no significant effect was observed on overall mortality (HR=1.07, CI=0.98–1.15). High-dose NSAID use was associated with a slight increase in mortality (HR=1.41, CI=1.26–1.56).

Interpretation:

These findings provide further indication that aspirin may be beneficial in reducing mortality in colorectal cancer during the first 5 years. The same cannot be said for other NSAIDs, where a small increase in mortality was observed.     

Nutrition and lung cancer

Epidemiologic evidence on the relationship between nutrition and lung cancer is reviewed. Observational studies of diet and lung cancer, both prospective and retrospective, continue to suggest strongly that increased vegetable and fruit intake is associated with reduced risk in men and women; in various countries; in smokers, ex-smokers, and never-smokers; and for all histologic types of lung cancer. Prospective studies of blood -carotene levels, arguably the best available biomarker of vegetable and fruit intake, indicate that low levels are predictive of increased lung cancer incidence. However, in a randomized, placebo-controlled clinical trial in male smokers, lung cancer incidence and total mortality were increased significantly among the men receiving -carotene supplements. If -carotene can prevent lung carcinogenesis, which the trial cannot rule out, then the dosage, duration of use, method of administration, and/or subpopulation are critical. Ongoing clinical trials, some of which include women, will provide much-needed information. Other carotenoids, other phytochemicals, and associated dietary patterns may explain the beneficial effects of vegetables and fruits and have not been explored adequately in epidemiologic work. Several observational epidemiologic studies, both prospective and retrospective, have indicated that diets high in fat, saturated fat, and cholesterol may increase the risk of lung cancer and that the effect is not mediated through vegetable and fruit intake. The relationship, although not yet established, merits further investigation. Since -carotene can function as an antioxidant, other micronutrients with this potential, specifically vitamins E and C and selenium, also have been proposed to reduce lung cancer risk. However, the totality of the epidemiologic evidence is not, at present, persuasive for any one of these micronutrients.     

Prospective investigation of emotional control and cancer risk in men (the Zutphen Elderly Study) (The Netherlands)

Objectives: Emotional control is hypothesized to increase cancer incidence and cancer mortality risk. We tested the hypothesis prospectively on all cancers in elderly men. Methods: The Zutphen Elderly Study on lifestyle and chronic diseases started in 1985. The total sample consisted of 939 men born between 1900 and 1920 and living in Zutphen (response 74%). In 1985, emotional control was measured by questionnaire with the Courtald Emotional Control Scale (CECS). The CECS consists of three dimensions (anger, anxiety and depression). Emotional control scores were grouped in tertiles. Information on cancer incidence and mortality was collected until December 1994 through general practitioners and hospital administration (119 incidence cases, and 71 deaths from cancer). Cox proportional hazards analyses were performed, adjusted for sociodemographic, psychosocial, and lifestyle-related factors. Results: Overall emotional control and emotional control of anger and of anxiety were not convincingly related to cancer risk. Intermediate control of depression was related to cancer incidence (fully adjusted RR = 1.7, 95% CI = 1.0–2.8). Both intermediate and high control of depression were related to cancer mortality (RR = 2.2, 95% CI = 1.1–4.6 and RR = 2.1, 95% CI = 1.0–4.3, respectively). Conclusion: Our findings provide evidence that control of depression is related to cancer risk.     

Prognosis in HIV-infected patients with non-small cell lung cancer

Background:

We conducted a population-based study to evaluate whether non-small cell lung cancer (NSCLC) prognosis was worse in HIV-infected compared with HIV-uninfected patients.

Methods:

Using the Surveillance, Epidemiology and End Results (SEER) registry linked to Medicare claims, we identified 267 HIV-infected patients and 1428 similar controls with no evidence of HIV diagnosed with NSCLC between 1996 and 2007. We used conditional probability function (CPF) analyses to compare survival by HIV status accounting for an increased risk of non-lung cancer death (competing risks) in HIV-infected patients. We used multivariable CPF regression to evaluate lung cancer prognosis by HIV status adjusted for confounders.

Results:

Stage at presentation and use of stage-appropriate lung cancer treatment did not differ by HIV status. Median survival was 6 months (95% confidence interval (CI): 5–8 months) among HIV-infected NSCLC patients compared with 20 months (95% CI: 17–23 months) in patients without evidence of HIV. Multivariable CPF regression showed that HIV was associated with a greater risk of lung cancer-specific death after controlling for confounders and competing risks.

Conclusion:

NSCLC patients with HIV have a poorer prognosis than patients without evidence of HIV. NSCLC may exhibit more aggressive behaviour in the setting of HIV.     

Chemoprevention of lung cancer: current status and future prospects

Lung cancer is the leading cause of cancer death in the United States. The current mainstays of lung cancer therapy are surgery, radiation and chemotherapy. These interventions have produced slight declines in mortality rates in the last 5 years however, it appears unlikely that marked improvements will occur in the near future. This grim overview argues strongly for new, emerging approaches for controlling this disease. Chemoprevention is the use of specific natural or synthetic substances with the objective of reversing, suppressing or preventing carcinogenic progression to invasive cancer. Whether primary, secondary or tertiary settings, prevention has the highest potential to improve the dismal statistics associated with this cancer. Several randomized clinical or translational chemoprevention trials have been conducted. All have so far produced either neutral or harmful primary endpoint results showing that lung cancer was not prevented by alpha-tocopheral, beta-carotene, retinal, retinyl palmitate, N-acetylcysteine or isotretinoin in smokers. Secondary results supporting treatment with isotretinoin in 'never' and former smokers and data from prevention trials involving selenium and vitamin E however, are encouraging and offer a promising direction for future clinical study. Other areas of promise for future lung cancer chemoprevention study include the study of molecular markers of risk and drug activity, molecular targeting study, improved imaging techniques and new drug delivery systems.     

1988～1997年广西扶绥县居民肺癌死亡分析

目的　探讨广西扶绥县居民 1988年～ 1997年肺癌死亡的流行病特征及变动趋势。方法　根据扶绥县 1988～ 1997年人口死亡及恶性肿瘤 (含肺癌 )监测资料 ,建立肺癌死亡资料数据库 ,用DIS和STAT2软件进行统计分析。结果　扶绥县人口肺癌粗死亡率为 4 74/ 10万 (其中男性为 7 0 6 / 10万 ,女性为 2 2 1/ 10万 ) ,男女性别比为 3 19∶1,年龄别死亡率呈负偏态分布 ,死者中位年龄为 5 9 4 6岁。结论　扶绥县人口肺癌死亡情况处于我国较低水平 ,男性死亡率明显高于女性 ,逐年老龄化的趋势也很明显 ,罕见于少年儿童。     

Racial differences in lung cancer

Although race, in and of itself, is not a relevant biologic variable, racial differences in disease characteristics and outcomes have been reported in many malignancies, including lung cancer. The lung cancer incidence rate in blacks has been consistently higher than that in whites for many years. This racial disparity is seen primarily in men and is significantly greater in younger age groups. The reason for higher lung cancer incidence rates in blacks remains unclear, but racial differences in smoking habits, socioeconomic variables, and the metabolism of tobacco carcinogens may all play an important role. Blacks are also more likely than whites to present with squamous cell carcinoma and with advanced-stage disease. A significant racial difference in survival rates has developed over the past 30 years, with a poorer prognosis noted in black patients, particularly those with local- and regional-stage disease. This disparity appears to be due to a lack of improvement in the survival of black patients with lung cancer, but the biological and/or societal basis for racial variations in survival have not been determined. In summary, significant racial differences exist in lung cancer incidence and survival rates. Further research is required to determine the factors responsible for these differences and to develop effective preventative and therapeutic interventions that will impact favorably on the incidence and prognosis of this disease.     

Association of microsomal epoxide hydrolase polymorphisms and lung cancer risk

Microsomal epoxide hydrolase (mEH) plays a dual role in the detoxification and activation of tobacco procarcinogens. Two polymorphisms affecting enzyme activity have been described in the exons 3 and 4 of the mEH gene, which result in the substitution of amino acids histidine to tyrosine at residue 113, and arginine to histidine at residue 139, respectively. We performed a hospital-based case-control study consisting of 277 newly diagnosed lung cancer patients and 496 control subjects to investigate a possible association between these two polymorphisms and lung cancer risk. The polymorphisms were determined by polymerase chain reaction/restriction fragment length polymorphism and TaqMan assay using DNA from peripheral white blood cells. Logistic regression was performed to calculate odds ratios (ORs), confidence limits (CL) and to control for possible confounders. The exon 3 polymorphism of the mEH gene was associated with a significantly decreased risk of lung cancer. The adjusted OR, calculated relative to subjects with the Tyr113/Tyr113 wild type, for the His113/His113 genotype was 0.38 (95% CL 0.20-0.75). An analysis according to histological subtypes revealed a statistically significant association for adenocarcinomas; the adjusted OR for the His113/His113 genotype was 0.40 (95% CL 0.17-0.94). In contrast, no relationship between the exon 4 polymorphism and lung cancer risk was found. The adjusted OR, calculated relative to the His139/His139 wild type, was for the Arg139/Arg139 genotype 1.83 (0.76-4.44). Our results support the hypothesis that genetically reduced mEH activity may be protective against lung cancer.