Progression of anal high‐grade squamous intraepithelial lesions to invasive anal cancer among HIV‐infected men who have sex with men

The incidence of anal cancer is elevated in human immunodeficiency virus (HIV)‐infected men‐who‐have‐sex‐with‐men (MSM) compared to the general population. Anal high‐grade squamous intraepithelial lesions (HSIL) are common in HIV‐infected MSM and the presumed precursors to anal squamous cell cancer; however, direct progression of HSIL to anal cancer has not been previously demonstrated. The medical records were reviewed of 138 HIV‐infected MSM followed up at the University of California, San Francisco, who developed anal canal or perianal squamous cancer between 1997 and 2011. Men were followed up regularly with digital anorectal examination (DARE), high‐resolution anoscopy (HRA) and HRA‐guided biopsy. Although treatment for HSIL and follow‐up were recommended, not all were treated and some were lost to follow‐up. Prevalent cancer was found in 66 men. Seventy‐two HIV‐infected MSM developed anal cancer while under observation. In 27 men, anal cancer developed at a previously biopsied site of HSIL. An additional 45 men were not analyzed in this analysis due to inadequate documentation of HSIL in relation to cancer location. Of the 27 men with documented progression to cancer at the site of biopsy‐proven HSIL, 20 men progressed from prevalent HSIL identified when first examined and seven men from incident HSIL. Prevalent HSIL progressed to cancer over an average of 57 months compared to 64 months for incident HSIL. Most men were asymptomatic, and cancers were detected by DARE. Anal HSIL has clear potential to progress to anal cancer in HIV‐infected MSM. Early diagnosis is facilitated by careful follow‐up. Carefully controlled studies evaluating efficacy of screening for and treatment of HSIL to prevent anal cancer are needed.     

Smoking cessation among men following cancer diagnosis: a matched cohort study

Purpose

Cigarette smoking among cancer survivors increases the risk of recurrence and secondary cancers. We sought to investigate smoking cessation following diagnosis of cancer compared to those not diagnosed with cancer. We also investigated cessation following diagnosis of a smoking-related and non-smoking-related cancer separately.

Methods

We conducted a matched cohort study within the Health Professionals Follow-Up Study (HPFS). We identified 566 men diagnosed with cancer who were current cigarette smokers at the time of diagnosis between 1986 and 2010 (exposed). Men diagnosed with cancer were age-matched 1:4 to men without a diagnosis of cancer who were also current cigarette smokers (unexposed). Multivariable conditional logistic regression models were used to calculate odds ratios (OR) and 95% confidence intervals (CI) to evaluate the association between a cancer diagnosis and smoking cessation within 2 and 4 years post diagnosis adjusted for potential confounders, overall and for smoking-related and non-smoking-related cancers.

Results

Of the men with cancer, 38% quit within 2 years and 42% within 4 years of diagnosis. Men diagnosed with cancer were more likely to quit smoking within 2 (OR?=?2.5, 95% CI: 2.0–3.0) and 4 years (OR?=?1.6, 95% CI: 1.3–2.0) post diagnosis, compared to matched men without cancer. The association was similar for smoking-related (OR?=?3.4, 95%: 1.6–7.2) and non-smoking-related cancers (OR?=?3.8, 95%: 2.8–5.2).

Conclusions

Men diagnosed with cancer were more likely to quit smoking compared to men not diagnosed with cancer. A cancer diagnosis may be a “teachable moment” in which strategies to promote smoking cessation for individuals diagnosed with smoking-related and non-smoking-related cancers should be investigated.

Implications for Cancer Survivors

There is a continued need for the widespread implementation of cessation interventions for cancer survivors.

     

Antibody responses following incident anal and penile infection with human papillomavirus in teenage men who have sex with men

Men who have sex with men (MSM) are at risk for human papillomavirus (HPV)‐related anal cancer. Few data exist on antibody responses following incident anogenital infection with HPV in teenage MSM. A cohort of 200 MSM aged 16–20 years from Melbourne, Australia were assessed at baseline, 3, 6 and 12 months. At each visit anal and penile swabs were collected for HPV DNA and serum for HPV antibodies for genotypes 6, 11, 16 and 18 (Merck's Multiplex Assays using Luminex). The main outcome, seroconversion, was defined as the detection of HPV antibodies following a negative antibody result for the same HPV type at baseline. The seroincidence rates for HPV types 6, 11, 16 and 18 were: 19 (95% CI 12–26), 7 (3–12), 4 (1–8) and 6 (3–11) per 100 person‐years, respectively. Men who experienced incident anal HPV infections from types 6/11 were significantly more likely to develop serum antibodies to the same HPV type(s) than those who experienced incident anal infections from types 16/18 [73 vs. 18%, odds ratio (OR) = 15, 95% CI: 2–118]. The median time between incident anal HPV infection and seroconversion for HPV 6, 11, 16 and 18 was: 91, 38, 161 and 182 days, respectively. Antibody responses against HPV types 6/11 were significantly more likely to occur following incident anal compared with incident penile infection with HPV types 6/11 (OR = 6, 95% CI: 2–21). The likelihood of antibody responses following anogenital HPV infections depends on the HPV type and site of infection.     

Cigarette smoking and lung cancer risk according to histologic type in Japanese men and women

Although cigarette smoking is a well‐known risk factor for lung cancer, histology‐specific risk has not been fully clarified in Japan. This case‐control study evaluated the associations between smoking and lung cancer risk according to sex and histologic type. From among patients aged 30 years and over admitted to a single hospital in Japan between 1997 and 2009, 1670 lung cancer cases and 5855 controls were selected. History of smoking, quantity and duration of smoking, and passive smoking from spouses were assessed using a self‐administered questionnaire. Odds ratios (ORs) and 95% confidence intervals (CIs) for each exposure were estimated by unconditional logistic regression. Ever‐smoking was significantly associated with a higher risk of squamous cell and small cell carcinoma. The OR for these two histologic types combined was larger in women (OR = 24.98, 95% CI: 13.50–46.23) than in men (OR = 9.43, 95% CI: 5.73–15.51). Analysis of the quantity and duration of smoking showed that the OR for each exposure level tended to be larger in women than in men. For adenocarcinoma, clear positive associations with quantity and duration‐related factors were observed among men, and a significant positive association with passive smoking from spouses was found among non‐smoking women (OR = 1.44, 95% CI: 1.06–1.95). These results suggest sex‐ and histologic type‐ differences in the association of smoking with lung cancer risk. Although smoking control should be continued to prevent lung cancers, further studies are required to better clarify differences in smoking‐related lung cancer risk between the sexes and histologic types.     

Immunodeficiency and the risk of cervical intraepithelial neoplasia 2/3 and cervical cancer: A nested case‐control study in the Swiss HIV cohort study

HIV‐infected women are at increased risk of cervical intraepithelial neoplasia (CIN) and invasive cervical cancer (ICC), but it has been difficult to disentangle the influences of heavy exposure to HPV infection, inadequate screening and immunodeficiency. A case‐control study including 364 CIN2/3 and 20 ICC cases matched to 1,147 controls was nested in the Swiss HIV Cohort Study (1985–2013). CIN2/3 risk was significantly associated with low CD4+ cell counts, whether measured as nadir [odds ratio (OR) per 100‐cell/μL decrease = 1.15, 95% CI: 1.08, 1.22], or at CIN2/3 diagnosis (1.10, 95% CI: 1.04, 1.16). An association was evident even for nadir CD4+ 200–349 versus ≥350 cells/μL (OR = 1.57, 95% CI: 1.09, 2.25). After adjustment for nadir CD4+, a protective effect of >2‐year cART use was seen against CIN2/3 (OR versus never cART use = 0.64, 95% CI: 0.42, 0.98). Despite low study power, similar associations were seen for ICC, notably with nadir CD4+ (OR for 50 vs. >350 cells/μL= 11.10, 95% CI: 1.24, 100). HPV16‐L1 antibodies were significantly associated with CIN2/3, but HPV16‐E6 antibodies were nearly exclusively detected in ICC. In conclusion, worsening immunodeficiency, even at only moderately decreased CD4+ cell counts, is a significant risk factor for CIN2/3 and cervical cancer.     

Serum cholesterol levels in relation to the incidence of cancer: The JPHC study cohorts

An inverse association between serum total cholesterol and cancer mortality cast a controversy for cause or result of low cholesterol on cancer risk. Therefore, we examined a total of 33,368 Japanese men and women aged 40–69 years, who were free of prior diagnosis of cancer and cardiovascular disease, undertook serum total cholesterol measurement and completed a food frequency questionnaire between 1990 and 1994. They were followed to ascertain incident total and major sites of cancer until the end of 2004 to examine sex‐specific associations between cholesterol and cancer risk by incident time, stage and virus infection. After 412,714 person‐years of follow‐up, 2,728 incident cancers were documented. Serum total cholesterol levels were inversely associated with risk of total cancer in men, with strong inverse associations with stomach cancer in men and liver cancer in both sexes. After exclusion for first 3‐year incident cases and advanced cases with metastasis, the inverse association diminished for total and stomach cancers but remained for liver cancer. The multivariable hazard ratios (95% CI) for serum total cholesterol <4.14 mmol/l versus 4.65–5.16 mmol/l were 1.15(0.92–1.43); p‐trend across the overall cholesterol categories = 0.25 for total cancer and 1.18(0.79–1.75), p‐trend = 0.04 for stomach cancer and 5.12(1.65–15.9), p‐trend = 0.0011 for liver cancer in men, and 5.73(1.57–20.9), p‐trend = 0.0007 for liver cancer in women. The sustained excess risk of liver cancer associated with low cholesterol was observed regardless of hepatitis‐C‐virus infection and drinking habits. Although the inverse association for liver cancer remained to be examined further, our findings do not support that low serum total cholesterol levels increase risks of total cancer and other major sites. © 2009 UICC     

Higher Dihydrotestosterone Is Associated with the Incidence of Lung Cancer in Older Men

Advancing age is associated with increased cancer incidence, but the role of sex hormones as risk predictors for common cancers in older men remains uncertain. This study was performed to assess associations of testosterone (T), dihydrotestosterone (DHT) and estradiol (E2), with incident prostate, lung and colorectal cancer in community-dwelling older men. Plasma T, DHT and E2 were assayed using liquid chromatography-mass spectrometry between 2001 and 2004 in 3690 men. Cancer outcomes until 20 June 2013 were ascertained using data linkage. Analyses were performed using proportional hazards competing-risks models, and adjustments were made for potential confounding factors including smoking status. Results are expressed as subhazard ratios (SHR). There were 348, 107 and 137 cases of prostate, lung and colorectal cancers respectively during a median of 9.1-year follow-up. Mean T was comparable in current and non-smokers, whilst mean DHT was lower in ex- and current smokers compared to non-smokers. After adjusting for confounders including smoking, higher T or DHT was associated with an increased incidence of lung cancer (SHR = 1.30, 95% CI 1.06–1.60; p = 0.012 per 1 SD increase in T and SHR = 1.29, 95% CI 1.08–1.54; p = 0.004 for DHT). Sex hormones were not associated with prostate or colorectal cancer. In older men, higher T or DHT predict increased incidence of lung cancer over the next decade. Sex hormones are not associated with incident prostate or colorectal cancer. Further studies are warranted to determine if similar associations of sex hormones with lung cancer are present in other populations and to investigate potential underlying mechanisms.     

Prospective investigation of the cigarette smoking-head and neck cancer association by sex

BACKGROUND: Men are approximately 3 times more likely to develop squamous cancers of the head and neck (oral cavity, pharynx, and larynx) than women. Very few prospective studies have examined the association between cigarette smoking and cancers of the head and neck in women, even though the rates of smoking in women are increasing rapidly worldwide. METHODS: The association between cigarette smoking and head and neck cancer was investigated in 476,211 participants, aged 50-71 years, of the National Institutes of Health/American Association of Retired Persons (NIH-AARP) diet and health study by using age-standardized incidence rates and hazard ratios from Cox models adjusted for other risk factors for these cancers. RESULTS: Over the course of follow-up (1995 through 2000), 584 men and 175 women were diagnosed with head and neck cancer. Nonsmoking (24.4), former smoking (36.9), and current smoking (147.3) men had higher rates of incident head and neck cancer per 100,000 person-years of follow-up than women did in each equivalent category of cigarette use (non: 4.8; former: 17.2; current: 75.7). The hazard ratios associated with smoking were significantly larger in women (12.96; 95% confidence interval [CI], 7.81-21.52) than in men (5.45, 95% CI, 4.22-7.05; P for interaction: <.001) for head and neck cancer overall and also for the 3 subsites (oral cavity, oro-hypopharynx, and larynx) examined in stratified analyses. Ever-smoking accounted for 45% of head and neck cancers in men and 75% in women, assuming causality. CONCLUSIONS: Cigarette smoking is a strong risk factor for head and neck cancer in both men and women. Incidence rates of head and neck cancer were higher in male smokers than female smokers, but smoking may explain a higher proportion of head and neck cancer in women than in men.     

CTX、G-CSF 动员造血干细胞过程中NK 细胞检测

 目的　探讨环磷酰胺 ( CTX)、粒细胞集落刺激因子 ( G- CSF)动员癌症患者造血干细胞过程中 NK细胞数量和活性的变化。方法　 2 1例诊断明确的癌症患者 ,经 CTX4.0 g/m2和 G- CSF(惠尔血 ) 1 5 0 μg/d动员。动员前 (前期 )、WBC降至最低点时 (极期 )、WBC开始恢复后 3天 (恢复早期 )、WBC开始恢复后 6天 (恢复期 )用流式细胞仪计数 CD34 +细胞和 NK细胞 ,用乳酸脱氢酶释放法测量 NK细胞活性。结果　动员过程中 ,NK细胞极期显著低于前期 ,恢复期则显著高于前期 ,P<0 .0 1 ;其变化与 WBC、MNC、血小板 ( BPC)、CD34 + 细胞呈显著正相关 ,P<0 .0 5。 NK细胞活性无显著差别 ,P>0 .0 5。结论　动员过程中 NK细胞数量增加 ,活性无改变。     

Racial differences in prostate cancer risk in young HIV-positive and HIV-negative men: a prospective cohort study

Purpose

African American men have the highest incidence of prostate cancer among ethnic groups, and racial disparity is highest in younger men. Prostate cancer prevalence is rising in HIV-infected men due to improved survival on antiretroviral therapies, yet little is known about racial differences in prostate cancer risk by HIV-infection status and age.

Methods

This is a prospective cohort study of prostate cancer risk in 2,800 HIV-infected and -uninfected men who have sex with men (MSM) aged 40–70 years (22% African American) who were enrolled in the multicenter AIDS cohort study from 1996 to 2010. Poisson regression models were used to examine associations between race and HIV-infection status and prostate cancer risk among men aged 40–70, 40–55, and 56–70 years.

Results

Among men aged 40–70 years, incidence rates (IR) per 100,000 person-years were 169 among all men and 276 among African American HIV-infected men. Prostate cancer risk was similar by HIV-infection status (IRR 1.0, 95% CI 0.55–1.82), but nearly threefold higher in African Americans compared to non-African Americans in adjusted models (IRRs 2.66 and 3.22, 95% CIs 1.36–5.18 and 1.27–8.16 for all or HIV-infected men, respectively). Racial disparity in prostate cancer risk was greatest in African American men aged 40–55 years (adjusted IRR 3.31, 95% CI 1.19–9.22). Prostate cancer risk showed associations with family history of prostate cancer (p = 0.001), but not heavy smoking, androgen supplement use, or HIV-related factors.

Conclusions

Among MSM, African American HIV-positive and HIV-negative men aged 40–55 years have threefold increased risk of young-onset prostate cancer compared to non-African American men, highlighting the need to make informed decisions about screening in this population.

     

Anal squamous intraepithelial lesions are frequent among young HIV‐infected men who have sex with men followed up at the Spanish AIDS Research Network Cohort (CoRIS‐HPV)

The aim of our study was to determine the baseline prevalence of anal squamous intraepithelial lesions (SIL) and associated risk factors in HIV‐infected men who have sex with men (MSM) in a Spanish ongoing multicenter cohort. CoRIS‐HPV started in 2007, nested in the Spanish AIDS Research Network Cohort (CoRIS). Anal liquid cytology testing was performed. High‐risk human papillomavirus (HR‐HPV) infection was determined, and positive samples were genotyped. We analyzed all subjects up to April 2011. Multivariate logistic regression analyses were performed. A total of 551 subjects with baseline anal liquid cytologies were analyzed; 37.0% negative for intraepithelial lesion, 9.0% atypical squamous cells of uncertain significance (ASCUS), 41.0% low‐grade SIL, 4.0% high‐grade SIL and 9.0% inadequate. Prevalence of anal SIL (excluding ASCUS) in valid samples (n = 450) was 54.7% (95% confidence interval [CI] = 49.9–59.3). Globally HR‐HPV prevalence was 81.7% (95% CI = 78.0–85.2). Multiple infections (≥2 HR‐HPV genotypes) were documented in 77.7% (95% CI = 73.1–82.0). The only risk factor associated with anal SIL was the number of HR‐HPV types; MSM with five or more HR‐HPV genotypes had an odds ratio (OR) of anal SIL seven times greater (OR = 7.4; 95% CI = 2.8–19.6) than those with one HR‐HPV genotype. No associations were found for age, educational level, smoking, geographical origin, CD4 T‐cell count, antiretroviral treatment or number of sexual partners. The prevalence of anal SIL in young HIV‐positive MSM is high, and the main risk factor is multiple infections with HR‐HPV types.     

Weight change and cancer risk in a cohort of more than 65,000 adults in Austria.

BACKGROUND: To investigate relations between weight loss or weight gain and the incidence of cancer. PATIENTS AND METHODS: Weight change was assessed in a population-based cohort of >65 000 Austrian adults (28 711 men and 36 938 women) for a period of 7 years, after which participants were followed for incident cancers over 8 years on average. Incident cancers (other than nonmelanoma skin cancers) were ascertained by a population-based cancer registry (n = 3128). Cox proportional hazards models were used to estimate hazard rate ratios (HRs) stratified by age and adjusted for smoking, occupational group, blood glucose and body mass index at baseline. RESULTS: In both men and women, neither weight loss nor weight gain was clearly associated with the incidence of all cancers combined. Weight loss (>0.10 kg/m(2)/year) was inversely associated with colon cancer in men [HR 0.50; 95% confidence interval (CI) 0.29-0.87], while high weight gain (> or =0.50 kg/m(2)/year) was inversely associated with prostate cancer (HR 0.43; 95% CI 0.24-0.76). Among women, high weight gain was positively associated with ovarian cancer (HR 2.48; 95% CI 1.05-5.85). CONCLUSION: These findings indicate that recent weight change may influence the incidence of several types of cancer.     

Hormonal and reproductive factors and risk of upper gastrointestinal cancers in men: A prospective cohort study within the UK Biobank

Incidence of upper gastrointestinal cancers of the oesophagus and stomach show a strong unexplained male predominance. Hormonal and reproductive factors have been associated with upper gastrointestinal cancers in women but there is little available data on men. To investigate this, we included 219,425 men enrolled in the UK Biobank in 2006–2010. Baseline assessments provided information on hormonal and reproductive factors (specifically hair baldness, number of children fathered, relative age at first facial hair and relative age voice broke) and incident oesophageal or gastric cancers were identified through linkage to U.K. cancer registries. Unadjusted and adjusted hazard ratios (HR) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. During 8 years of follow‐up, 309 oesophageal 210 gastric cancers occurred. There was some evidence that male pattern baldness, was associated with gastric cancer risk (adjusted HR 1.35, 95% CI 0.97, 1.88), particularly for frontal male pattern baldness (adjusted HR 1.52, 95% CI 1.02, 2.28). There was little evidence of association between other hormonal and reproductive factors and risk of oesophageal or gastric cancer, overall or by histological subtype. In the first study of a range of male hormonal and reproductive factors and gastric cancer, there was a suggestion that male pattern baldness, often used as a proxy of sex hormone levels, may be associated with gastric cancer. Future prospective studies that directly test circulating sex steroid hormone levels in relation to upper gastrointestinal cancer risk are warranted.     

Metabolic syndrome is associated with colorectal cancer in men

Aim of the studyWe assessed the relation between metabolic syndrome (MetS) and its components and colorectal cancer.MethodsWe analysed data from a multicentre case–control study conducted in Italy and Switzerland, including 1378 cases of colon cancer, 878 cases of rectal cancer and 4661 controls. All cases were incident and histologically confirmed. Controls were subjects admitted to the same hospitals as cases with acute non-malignant conditions. MetS was defined according to the International Diabetes Federation criteria. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were estimated by multiple logistic regression models, including terms for major identified confounding factors for colorectal cancer.ResultsWith reference to each component of the MetS, the ORs of colorectal cancer in men were 1.27 (95% CI, 0.95–1.69) for diabetes, 1.24 (95% CI, 1.03–1.48) for hypertension, 1.14 (95% CI, 0.93–1.40) for hypercholesterolaemia and 1.26 (95% CI, 1.08–1.48) for overweight at age 30. The corresponding ORs in women were 1.20 (95% CI, 0.82–1.75), 0.87 (95% CI, 0.71–1.06), 0.83 (95% CI, 0.66–1.03) and 1.06 (95% CI, 0.86–1.30). Colorectal cancer risk was increased in men (OR = 1.86; 95% CI, 1.21–2.86), but not in women (OR = 1.13; 95% CI, 0.66–1.93), with MetS. The ORs were 2.09 (95% CI, 1.38–3.18) in men and 1.15 (95% CI, 0.68–1.94) in women with ?3 components of the MetS, as compared to no component. Results were similar for colon and rectal cancers.ConclusionThis study supports a direct association between MetS and both colon and rectal cancers in men, but not in women.     

Small cell lung cancer in women: risk associated with smoking, prior respiratory disease, and occupation

Small cell carcinoma of the lung (SCLC) occurs most frequently in heavy smokers, yet exhibits a lesser predominance among men than other smoking-associated lung cancers. Incidence rates have increased more rapidly in women than men and at a faster rate among women than other cell types. To investigate the importance of smoking and other risk factors, a case-control study of SCLC in women was conducted. A total of 98 women with primary SCLC and 204 healthy controls, identified by random-digit dialing and frequency matched for age, completed telephone interviews. Data collected include demographics, medical history, family cancer history, residence history, and lifetime smoking habits. Odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated using logistic regression analysis. Risk for small cell carcinoma in women is strongly associated with current use of cigarettes. Ninety-seven of 98 cases had smoked cigarettes; 79% of cases were current smokers and 20% were former smokers at the time of diagnosis compared to 13% current and 34% former smokers among controls. The ORs associated with smoking are 108.7 (95% CI 14.8-801) for ever-use of cigarettes, 278.9 (95% CI 37.0-2102) for current smoking, and 31.5 (95% CI 4. 1-241) for former smoking. Risk increases steeply with pack-years of smoking and decreases with duration of smoking cessation. After adjusting for age, education, and lifetime smoking history, medical history of physician-diagnosed respiratory disease including chronic bronchitis, emphysema, pneumonia, tuberculosis, asthma, and hay fever is not associated with a significant increase in lung cancer risk. Employment in blue collar, service, or other high risk occupations is associated with a two to three-fold non-significant increase in risk for small cell carcinoma after adjusting for smoking.     

Lycopene,tomato products and prostate cancer‐specific mortality among men diagnosed with nonmetastatic prostate cancer in the Cancer Prevention Study II Nutrition Cohort

While dietary lycopene and tomato products have been inversely associated with prostate cancer incidence, there is limited evidence for an association between consumption of lycopene and tomato products and prostate‐cancer specific mortality (PCSM). We examined the associations of prediagnosis and postdiagnosis dietary lycopene and tomato product intake with PCSM in a large prospective cohort. This analysis included men diagnosed with nonmetastatic prostate cancer between enrollment in the Cancer Prevention Study II Nutrition Cohort in 1992 or 1993 and June 2011. Prediagnosis dietary data, collected at baseline, were available for 8,898 men, of whom 526 died of prostate cancer through 2012. Postdiagnosis dietary data, collected on follow‐up surveys in 1999 and/or 2003, were available for 5,643 men, of whom 363 died of prostate cancer through 2012. Cox proportional hazards regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for PCSM. Neither prediagnosis nor postdiagnosis dietary lycopene intake was associated with PCSM (fourth vs. first quartile HR = 1.00, 95% CI 0.78–1.28; HR = 1.22, 95% CI 0.91–1.64, respectively). Similarly, neither prediagnosis nor postdiagnosis consumption of tomato products was associated with PCSM. Among men with high‐risk cancers (T3–T4 or Gleason score 8–10, or nodal involvement), consistently reporting lycopene intake ≥ median on both postdiagnosis surveys was associated with lower PCSM (HR = 0.41, 95% CI 0.17–0.99, based on ten PCSM cases consistently ≥ median intake) compared to consistently reporting intake < median. Future studies are needed to confirm the potential inverse association of consistently high lycopene intake with PCSM among men with high‐risk prostate cancers.     

Cigarette smoking and subsequent risk of lung cancer by histologic type in middle-aged Japanese men and women: the JPHC study

In order to update the findings of relative risk associated with cigarette smoking for lung cancer by histologic type in Japan, the data from a population-based cohort study of 91,738 men and women were analyzed. During 1990-1999, 422 lung cancer incident cases were identified. The relative risk for all incident cases associated with current smokers versus non-smokers was 4.5 [95% confidence interval (CI): 3.0-6.8] and 4.2 (95% CI: 2.4-7.2), for men and women, respectively. When divided by histologic type, relative risk for squamous cell carcinoma and small cell carcinoma was 12.7 (95% CI: 4.7-34.7) and 17.5 (95% CI: 4.9-62.1), while for adenocarcinoma it was 2.8 (95% CI: 1.6-4.9) and 2.0 (95% CI: 0.8-5.0) for men and women, respectively. We confirmed that the lung cancer risk in men rose with increasing cigarette smoking, especially the duration of smoking among current smokers and decreased after the cessation of smoking among former smokers. Unlike the US or European countries, the relative risk did not increase in this updated study, compared with previous studies in 1960s to 1990s in Japan either for all incident cases or for specific histologic types and the magnitude of relative risks was substantially lower than that observed in the US or European countries, especially for adenocarcinoma.     

Sex differences in lung-cancer risk associated with cigarette smoking

The importance of cigarette smoking as a risk factor for specific histologic types of lung cancer in men and women has been examined in a case-control analysis of data from the Cancer Surveillance Program of Orange County, a population-based registry. Smoking habits were abstracted from medical records for 1153 men and 833 women diagnosed with primary lung cancer in 1984–1986 and 1851 men and 1656 women aged 30 or older diagnosed with cancers not associated with smoking. Ninety-six percent of men and 89% of women with lung cancer were current or former cigarette smokers, as compared with 55% of men and 34% of women with other cancers. The age and ethnicity-adjusted odds ratios (OR) for ever-smoking were 19.7 for men and 15.0 for women. Men and women who smoked 2 or more packs per day experienced nearly equal risks. Comparison of the most common cell types showed that women smokers had equal or lower ORs for squamous-cell carcinoma and adenocarcinoma, but higher OR for small-cell carcinoma, as compared with men smokers. While the smoking-associated OR were equal for small-cell and squamous-cell carcinomas in men, the OR for women were significantly higher for small-cell carcinoma than for squamous-cell carcinoma.     

Alcohol drinking and renal cell carcinoma in women and men.

The role of alcohol consumption on the risk of renal cell cancer was investigated separately for women and men, in a case-control study of 348 people with incident histologically confirmed cancer and 1048 hospital controls from northern Italy. No significant relationship emerged, nor any differences between the sexes. The odds ratios were 1.2 (95% confidence interval, 0.6-2.4) for the highest tertile of intake in women (>or=3 drinks per day) and 0.8 (0.4-1.3) for the highest quartile of intake in men (>or=6 drinks per day).