p53 gene mutations in early colorectal carcinoma. de novo vs. adenoma-carcinoma sequence

p53 gene mutations in early and advanced colorectal cancer were detected by PCR-SSCP analysis. Early colorectal cancer was classified intode novo cancer and polyp-forming cancer, respectively, according to morphology and presence of adenomatous components. A total of 94 paraffin-embedded tissue specimens from patients with colorectal cancer were analysed.p53 gene mutations were detected in 40.0% (12/30) of de novo cancer, 36.7% (11/30) of polyp-forming cancer, and 44% (15/34) of advanced cancer. p53 mutations were detected at a high frequency in both types of early colorectal cancer as well as in advanced cancer. No correlations were found between p53 mutations and clinicopathological data. Our data suggest that the p53 gene mutations occurred in the early colorectal cancer stage of carcinogenesis regardless of the pathway. © 1995 Wiley-Liss, Inc.     

B.W.S. Robinson, A.P. Chahinian (eds). Mesothelioma

B.W.S. Robinson, A.P. Chahinian (eds). Martin Dunitz Ltd, London,2002, 380 pp, £95.00, US$145.00 The incidence of mesothelioma is approaching its peak, and theprognosis for this cancer remains extremely poor. The impossibilityof predicting cancer appearance after asbestos exposure, thedifficulty of     

Dietary patterns and risk of prostate cancer in U.S. men.

We prospectively investigated the associations between dietary patterns and risk of prostate cancer in the Health Professionals Follow-up Study. Between 1986 and 2000, 3,002 incident prostate cancer cases were identified in our cohort. Using factor analysis, two major dietary patterns were identified, a prudent and a western dietary pattern. Dietary patterns were not appreciably associated with risk of total prostate cancer. For the highest versus the lowest quintiles, the multivariable relative risk (RR) for the prudent pattern was 0.94 [95% confidence interval (CI), 0.83-1.06], and for the western pattern, the multivariable RR was 1.03 (95% CI, 0.92-1.17). Neither were these associated with risk of advanced prostate cancer [highest versus lowest quintile, prudent pattern (RR, 1.01; 95% CI, 0.68-1.49); western pattern (RR, 1.13; 95% CI, 0.77-1.67)]. Higher western pattern scores were suggestively associated with a greater risk of advanced prostate cancer among older men [highest versus lowest quintile (RR, 1.35; 95% CI, 0.97-1.90)], but not after adding processed meat to the model [highest versus lowest quintile (RR, 1.11; 95% CI, 0.75-1.65)]. We did not find any evidence for a protective association between prudent pattern and risk of prostate cancer. The lack of association between a western dietary pattern as identified by factor analysis in our cohort and prostate cancer risk suggests that dietary risk factors for prostate cancer are likely to differ from those for other conditions, such as cardiovascular disease and type 2 diabetes, that have been associated with a western dietary pattern in this cohort.     

P.W. Kantoff, P.R. Carroll, A.V. D'Amico (eds). Prostate Cancer: Principles and Practice

P.W. Kantoff, P.R. Carroll, A.V. D’Amico (eds). LippincottWilliams & Wilkins, 2001, 704 pp, €199.00, £109.00,US$169.00 Reviewing the sum of knowledge concerning prostate cancer isa real necessity. Prostate Cancer: Principles and Practice providesa review of all aspects of prostate cancer from     

Cholesterol-lowering drugs and advanced prostate cancer incidence in a large U.S. cohort.

BACKGROUND: 3-Hydroxy-3-methylglutaryl CoA reductase inhibitors, commonly known as statins, account for the great majority of cholesterol-lowering drug use in the United States. Long-duration statin use was associated with substantially reduced risk of advanced prostate cancer in a recent large prospective study. METHODS: We examined the association between use of cholesterol-lowering drugs and prostate cancer incidence by disease stage and grade among 55,454 men in the Cancer Prevention Study II Nutrition Cohort. Proportional hazards modeling was used to calculate RRs. RESULTS: During follow-up from 1997 to 2003, we identified 3,413 cases of incident prostate cancer, including 317 cases of advanced prostate cancer. After adjustment for age, history of prostate-specific antigen testing, and other potential prostate cancer risk factors, current use of cholesterol-lowering drugs for 5 or more years was not associated with overall prostate cancer incidence (multivariate adjusted rate ratio, 1.06; 95% confidence interval, 0.93-1.20), but was associated with a marginally statistically significant reduction in risk of advanced prostate cancer (rate ratio, 0.60; 95% confidence interval, 0.36-1.00). CONCLUSION: These results provide some support for the hypothesis that long-term statin use is associated with reduced risk of advanced prostate cancer.     

Establishing cancer units.

The creation of effective cancer units is central to the implementation of the report A Policy Framework for Commissioning Cancer Services, produced by the Chief Medical Officers of England and Wales, recently issued by the Department of Health in April 1995. While cancer units are described in this report a range of important questions remain about their nature and how they should be developed. This paper addresses these issues in three ways. A definition of the cancer unit is suggested and its main implications spelt out. The problems of establishing cancer units are covered under three headings. Where should cancer units be? Which cancer sites should the unit cover? What is needed to establish the cancer unit? Finally two checklists are presented, describing the task from the perspectives of the district health authority and hospital(s) concerned. The underlying theme is that real changes in clinical practice and organisation are the goal, and these can only be achieved where there is extensive local dialogue in which the relevant issues are addressed in a structured and rigorous manner. Cosmetic changes in hospital designation will not achieve the consistent quality of cancer service that is the cornerstone of the ''Calman'' policy.     

Recent trends in breast cancer incidence rates by age and tumor characteristics among U.S. women

Introduction  

A recent abstract presented in a breast cancer symposium attributed the sharp decrease in female breast cancer incidence rates from 2002 to 2003 in the Surveillance, Epidemiology, and End Results (SEER) cancer registries of the United States to the reduced use of hormone replacement therapy since July 2002. However, this hypothesis does not explain the decrease that began in 1999 in the age-standardized incidence rate of invasive breast cancer in the nine oldest SEER cancer registry areas, although the trend through 2003 was not statistically significant. In this paper, we examine temporal trends in invasive and in situ female breast cancer by age, stage, tumor size, and estrogen receptor/progestin receptor (ER/PR) status in the nine oldest SEER cancer registry areas and consider the implication of these trends in relation to risk factors and screening.     

Aspirin and other nonsteroidal anti-inflammatory drugs and breast cancer incidence in a large U.S. cohort.

Use of nonsteroidal anti-inflammatory drugs (NSAIDs), particularly aspirin, has consistently been associated with reduced risk of breast cancer in case-control studies. However, results from prospective studies have been less consistent. We examined the association between NSAID use and breast cancer incidence, adjusting for multiple breast cancer risk factors among 77,413 women in the Cancer Prevention Study II Nutrition Cohort. During follow-up from 1992 to 2001, we observed 3,008 cases of incident breast cancer. Information on NSAID use was obtained from a questionnaire completed at enrollment in 1992 or 1993 and was updated using follow-up questionnaires in 1997 and 1999. NSAID use was modeled using time-dependent variables to update exposure status. Neither current total NSAID use (aspirin and other NSAIDs combined) nor current aspirin use were associated with breast cancer incidence even at relatively high levels of use [rate ratio (RR), 1.07; 95% confidence interval (95% CI), 0.96-1.21 for > or =60 NSAID pills per month compared with no reported use of NSAIDs; RR, 1.01; 95% CI, 0.84-1.20 for > or =60 aspirin per month compared with no reported use of aspirin]. Even long-duration regular use (> or =30 pills per month for > or =5 years) was not associated with breast cancer incidence (RR, 1.05; 95% CI, 0.88-1.26 for total NSAIDs; RR, 0.88; 95% CI, 0.69-1.12 for aspirin). Although we cannot exclude a small reduction in breast cancer risk associated with NSAID use, the results of this study provide evidence against a large reduction in risk.     

J. Cassidy, D. Bisset, R.A.J. Spence (eds). Oxford Handbook of Oncology

J. Cassidy, D. Bisset, R.A.J. Spence (eds). Oxford UniversityPress, Oxford, 2002, 698 pp, €29.95, £21.95, $24.95 As is presented in the preface, this handbook is designed asa primer for those who are involved with cancer patients orthe study of cancer, and should be an easy guide for studentsand trainees as well as for professionals. The great majority     

Cancer morbidity in alcohol abusers.

Data on the association between alcohol abuse and cancer morbidity are scarce in large cohorts of non-hospitalised alcoholic men and women. Of 18,368 alcohol abusers who entered an outpatient clinic in Copenhagen during 1954-87, 18,307 were followed and their cancer incidence was compared with that of the total Danish population. On average the 15,214 men were observed for 12.9 years and the 3,093 women for 9.4 years. The overall morbidity of cancer was increased significantly. Of the men, 1,441 developed cancer [relative risk (RR) = 1.6; 95% confidence interval (CI) = 1.5-1.7], while 182 women did (RR = 1.5; 95% CI 1.3-1.8). Significantly increased incidences were found of cancer in the tongue, mouth, pharynx, oesophagus, liver, larynx, lung and pleura and secondary cancer. The women had significantly increased risk of cervical cancer (RR = 2.0; 95% CI 1.2-3.0). The men developed prostatic cancer significantly more frequently than expected (RR = 1.4; 95% CI 1.2-1.8). The risk of melanomas (RR = 0.5; 95% CI 0.2-0.8) was significantly lower than expected. The relative risks of cancer of the stomach, pancreas, kidney and endocrine system were only slightly increased. The study group did not develop more colonic (RR = 1.0; 95% CI 0.8-1.3) or rectal cancer (RR = 1.0; CI 0.7-1.3) than expected. The risk of breast cancer in women was slightly increased (RR = 1.3; 95% CI 0.9-1.7), but not statistically significant. Thus, the associations between alcohol and cancer of the upper digestive and respiratory tract and the liver are confirmed. In addition, this study indicates an increased occurrence of cancer of the prostate gland, pleura and uterine cervix in alcohol abusers.     

Reproductive factors and incidence of endometrial cancer in U.S. black women

Purpose

Previous studies have shown that reproductive history is a strong determinant of endometrial cancer risk among white women. Less is known about how reproductive history affects endometrial cancer risk among black women, whose incidence and mortality differ from white women. We investigated the associations of age at menarche, parity, timing of births, and menopausal age with endometrial cancer in the Black Women’s Health Study, a prospective cohort study.

Methods

Every 2 years from 1995 to 2013, 47,555 participants with intact uteri at baseline in 1995 completed questionnaires on reproductive and medical history, and lifestyle factors. Self-reported cases of endometrial cancer were confirmed by medical record, cancer registry, or death certificate when available. Cox proportional hazards regression was used to estimate multivariable incidence rate ratios (IRR) and 95% confidence intervals (CI).

Results

During 689,501 person-years of follow-up, we identified 300 incident cases of endometrial cancer. The strongest associations with endometrial cancer were found for early age at menarche (<11 vs. 12–13 years: IRR 1.82, 95% CI 1.31, 2.52), and later age at first birth (≥30 vs. <20 years: IRR 0.26, 95% CI 0.13, 0.50). Parous women were less likely than nulliparous women to develop endometrial cancer (IRR 0.77, 95% CI 0.57, 1.05), but there was little evidence of a dose–response relationship for number of births.

Conclusion

Associations between reproductive factors and endometrial cancer among black women were generally consistent with those in studies of white women.

     

Smoking and cancer mortality among U.S. veterans: A 26-year follow-up

On the 30th anniversary of the U.S. Surgeon General's report Smoking and Health, we present updated results from one of the original cohort studies that comprised the groundbreaking document. A 26-year follow-up of 248,046 U.S. veterans evaluating the risks of cigarette smoking revealed strong dose-response effects between smoking and total cancer and a large number of cancer sites. Over 50% of cancer deaths among current smokers and 23% of cancer deaths among former smokers were attributable to cigarette smoking. These findings further demonstrate the large and unique role cigarette smoking plays in cancer etiology and the importance of smoking cessation to reduce this enormous public health burden. © 1995 Wiley-Liss, Inc.     

Recreational physical activity and risk of prostate cancer in a large cohort of U.S. men.

Physical activity has been proposed as a modifiable risk factor for prostate cancer because of its potential effects on circulating hormones such as testosterone and insulin. We examined the association of various measures of physical activity with prostate cancer risk among men in the American Cancer Society Cancer Prevention Study II Nutrition Cohort, a large prospective study of U.S. adults. Information on recreational physical activity was obtained from a self-administered questionnaire completed at cohort enrollment in 1992/1993, as well as from a questionnaire completed as part of an earlier study in 1982. During the 9-year prospective follow-up, 5,503 incident prostate cancer cases were identified among 72,174 men who were cancer-free at enrollment. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) for measures of recreational physical activity and to adjust for potential confounding factors. We observed no difference in risk of prostate cancer between men who engaged in the highest level of recreational physical activity (>35 metabolic equivalent-hours/wk) and those who reported no recreational physical activity at baseline (RR, 0.90; 95% confidence interval, 0.78-1.04; P for trend = 0.31). We also did not observe an association between prostate cancer and recalled physical activity at age 40 or exercise reported in 1982. However, the incidence of aggressive prostate cancer was inversely associated with >35 metabolic equivalent-hours/wk of recreational physical activity compared with that in men who reported no recreational physical activity (RR, 0.69; 95% confidence interval, 0.52-0.92; P for trend = 0.06). Our findings are consistent with most previous studies that found no association between recreational physical activity and overall prostate cancer risk but suggest physical activity may be associated with reduced risk of aggressive prostate cancer.     

Obesity, recreational physical activity, and risk of pancreatic cancer in a large U.S. Cohort.

BACKGROUND: Obesity and physical activity, in part through their effects on insulin sensitivity, may be modifiable risk factors for pancreatic cancer. METHODS: The authors analyzed data from the American Cancer Society Cancer Prevention Study II Nutrition Cohort to examine the association between measures of adiposity, recreational physical activity, and pancreatic cancer risk. Information on current weight and weight at age 18, location of weight gain, and recreational physical activity were obtained at baseline in 1992 via a self-administered questionnaire for 145,627 men and women who were cancer-free at enrollment. During the 7 years of follow-up, 242 incident pancreatic cancer cases were identified among these participants. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) and to adjust for potential confounding factors including personal history of diabetes and smoking. RESULTS: We observed an increased risk of pancreatic cancer among obese [body mass index (BMI) >/= 30] men and women compared with men and women of normal BMI [<25; RR, 2.08; 95% confidence interval (95% CI), 1.48-2.93, P(trend) = 0.0001]. After adjustment for between BMI, risk of pancreatic cancer was independently increased among men and women who reported a tendency for central weight gain compared with men and women reporting a tendency for peripheral weight gain (RR, 1.45; 95% CI, 1.02-2.07). We observed no difference in pancreatic cancer incidence rates between men and women who were most active (>31.5 metabolic equivalent hours per week) at baseline compared with men and women who reported no recreational physical activity (RR, 1.20; 95% CI, 0.63-2.27). CONCLUSION: This study, along with several recent studies, supports the hypothesis that obesity and central adiposity are associated with pancreatic cancer risk.     

Preventing the lung cancer epidemic.

There are approximately 11 million new cases of cancer diagnosedworldwide each year [1] of which one in eight is a lung cancer.Over one million people die from lung cancer each year. In Europe,in 2004, there were approximately 3 million new cases of cancerand 1.7 million deaths from cancer [2]. Lung cancer was thecommonest incident form of cancer (375 000 new cases) and thecommonest cause of death from cancer (340 000 deaths).     

Advances in prostate cancer.

The causes of prostate cancer reflect a complex interaction between environmental and genetic factors. Improvement in screening has reduced the incidence of prostate cancer, and risk assessment schemata have enhanced therapy, both for localized disease and for locally recurrent prostate cancer. The use of hormone therapy has been further evaluated, as primary therapy for locally advanced cancers, for lymph node-positive cancers, and for de novo metastatic cancer. Modest inroads have been made in the treatment and understanding of androgen-independent prostate cancer. Advances have been made in the understanding of the risk factors, genetic and environmental, associated with the development and progression of prostate cancer; in screening; and in optimizing therapy for localized, locally recurrent, and advanced disease. This article reviews the most salient observations reported between November 1, 1997 and October 31, 1998.     

Comprehensive cancer control in the U.S.: summarizing twenty years of progress and looking ahead

In order to celebrate the accomplishments of the Centers for Disease Control and Prevention’s (CDC) National Comprehensive Cancer Control Program (NCCCP), the Comprehensive Cancer Control National Partners (CCCNP) developed this Special Issue on Cancer Causes and Control. This, the third Special Issue on Comprehensive Cancer Control (CCC), is a reflection of 20 years of building successful partnerships to prevent and control cancer; planning and implementing strategic cancer control; collaborating to address national cancer prevention and control priorities; evaluating efforts; sharing successes; and, in later years, serving as a model for global cancer control planning and implementation. The CDC currently supports cancer control planning and implementation in all 50 states, the District of Columbia, eight tribes or tribal organizations, and seven Pacific Island Jurisdictions and U.S. territories through the NCCCP. CCC is an approach that brings together multi-sector partners to address the cancer burden in a community collectively by leveraging existing resources and identifying and addressing cancer related issues and needs. The Comprehensive Cancer Control National Partnership (CCCNP), a partnership of national organizations, has been committed to supporting comprehensive cancer control efforts since 1999. We summarize the efforts described in this Special Issue. We also describe opportunities and critical elements to continue the momentum for comprehensive cancer control well into the future.     

Heterocyclic aromatic amine pesticide use and human cancer risk: Results from the U.S. Agricultural Health Study

Imazethapyr, a heterocyclic aromatic amine, is a widely used crop herbicide first registered for use in the United States in 1989. We evaluated cancer incidence among imazethapyr‐exposed pesticide applicators enrolled in the Agricultural Health Study (AHS). The AHS is a prospective cohort of 57,311 licensed pesticide applicators in the U.S., enrolled from 1993–1997. Among the 49,398 licensed pesticide applicators eligible for analysis, 20,646 applicators reported use of imazethapyr and 2,907 incident cancers developed through 2004. Imazethapyr exposure was classified by intensity‐weighted lifetime exposure days calculated as [years of use × days per year × intensity level]. Poisson regression analysis was used to evaluate the relationship between imazethapyr exposure and cancer incidence. We found significant trends in risk with increasing lifetime exposure for bladder cancer (p for trend 0.01) and colon cancer (p for trend 0.02). Rate ratios (RRs) were increased by 137% for bladder cancer and 78% for colon cancer when the highest exposed were compared to the nonexposed. The excess risk for colon cancer was limited to proximal cancers, (RR = 2.73, 95% confidence intervals 1.42, 5.25, p for trend 0.001). No association was observed for prostate, lung, rectum, kidney, oral, pancreas, lymphohematopoietic cancers or melanoma. These findings provide new evidence that exposure to aromatic amine pesticides may be an overlooked exposure in the etiology of bladder and colon cancer. The use of imazethapyr and other imidazolinone compounds should continue to be evaluated for potential risk to humans. Published 2008 Wiley‐Liss, Inc.     

Body mass index and risk of prostate cancer in U.S. health professionals

The relationship between body mass index (BMI) and prostate cancer risk may be complex because obesity is associated with various hormonal factors and because the influence of BMI may differ according to whether the cancers are hereditary or sporadic. We used data from the Health Professionals Follow-Up Study, in which 2896 incident cases of prostate cancer were reported from February 1, 1986, through January 31, 2000, to determine prospectively whether BMI was associated with the risk of hereditary (men <60 years of age or with a positive family history of prostate cancer) and sporadic (men > or =60 years of age and without such a family history) prostate cancer. The risk of prostate cancer in men with a higher BMI (> or =30 kg/m2) was lower than that in men with a lower BMI (23-24.9 kg/m2) but only if they were younger (<60 years old) (relative risk = 0.52, 95% confidence interval = 0.33 to 0.83; P(trend)<.001) or had a family history of prostate cancer (relative risk = 0.74, 95% confidence interval = 0.45 to 1.19; P(trend) =.01). However, for groups with more sporadic cancers, BMI had a weak, non-statistically significant positive association with prostate cancer. We observed statistically significant interactions between BMI and age (P(interaction)<.001, two-sided Wald test) and between BMI and family history of prostate cancer (P(interaction) =.006, two-sided Wald test). Patterns for BMI and waist circumference were similar. Because obesity is associated with lower circulating concentrations of testosterone, our results suggest the hypothesis that androgens may play a more direct role for early-onset or hereditary prostate cancers than for sporadic prostate cancers.     

Endometriosis and risk of ovarian and endometrial cancers in a large prospective cohort of U.S. nurses

Purpose

Endometriosis is associated with ovarian cancer, but the relation with endometrial cancer is unclear. Prior studies generally were retrospective and had potential limitations, including use of self-reported endometriosis, failure to account for delays between symptom onset and endometriosis diagnosis, and changes in risk factors post-endometriosis diagnosis. We evaluated whether these limitations obscured a weak association with endometrial cancer and the extent to which these limitations impacted associations with ovarian cancer.

Methods

Cox proportional hazards regression models were used to assess associations between endometriosis and cancer risk, evaluating the impacts of self-reported vs. laparoscopically confirmed endometriosis, delayed diagnosis, and post-endometriosis diagnosis changes in risk factor exposures on relative risk estimates.

Results

Over 18 years of follow-up, we identified 228 ovarian and 166 endometrial cancers among 102,025 and 97,109 eligible women, respectively. Self-reported endometriosis was associated with ovarian cancer [relative risk (RR): 1.81; 95% confidence interval (CI): 1.26–2.58]; this association was stronger for laparoscopically confirmed endometriosis (HR: 2.14; 95% CI 1.45–3.15). No association was observed with endometrial cancer (self-report RR: 0.78; 95% CI 0.42–1.44; laparoscopic-confirmation RR: 0.76; 95% CI 0.35–1.64). Accounting for diagnosis delays or post-endometriosis diagnosis changes in risk factors had a little impact.

Conclusions

This study adds to the evidence that endometriosis is not strongly linked to endometrial cancer risk and that the association with ovarian cancer is robust to misclassification, diagnostic delay, and changes in exposures post-endometriosis diagnosis. Our analysis suggests that confounding and misclassification do not obscure a weak association for endometrial cancer risk, although our results should be replicated.