European Journal of Cancer Prevention 

About: European Journal of Cancer Prevention is an academic journal published by Lippincott Williams & Wilkins. The journal publishes majorly in the area(s): Cancer & Population. It has an ISSN identifier of 0959-8278. Over the lifetime, 2734 publications have been published receiving 70522 citations. The journal is also known as: Eur J Cancer Prev.

The Malmö Diet and Cancer Study: representativity, cancer incidence and mortality in participants and non-participants.

Abstract: In order to investigate potential selection bias in population-based cohort studies, participants (n = 28098) and non-participants (n = 40807) in the Malmo Diet and Cancer Study (MDCS) were compared with regard to cancer incidence and mortality. MDCS participants were also compared with participants in a mailed health survey with regard to subjective health, socio-demographic characteristics and lifestyle. Cancer incidence prior to recruitment was lower in non-participants, Cox proportional hazards analysis yielded a relative risk (RR) with a 95% confidence interval of 0.95 (0.90-1.00), compared with participants. During recruitment, cancer incidence was higher in non-participants, RR: 1.08 (1.01-1.17). Mortality was higher in non-participants both during, 3.55 (3.13-4.03), and following the recruitment period, 2.21 (2.03-2.41). The proportion reporting good health was higher in the MDCS than in the mailed health survey (where 74.6% participated), but the socio-demographic structure was similar. We conclude that mortality is higher in non-participants than in participants during recruitment and follow-up. It is also suggested that non-participants may have a lower cancer incidence prior to recruitment but a higher incidence during the recruitment period.

Intestinal flora and endogenous vitamin synthesis

Abstract: It is well established that the rumen microbial flora are a rich source of vitamins to the ruminant, and that the faecal bacterial flora are a major vitamin source for coprophagic rodents. There is also good evidence that the gut bacterial flora are a significant source of a range of vitamins to the human. In this paper evidence is presented that gut bacteria are a significant source of a range of vitamins, particularly those of the B group and vitamin K.

Annual or biennial CT screening versus observation in heavy smokers: 5-year results of the MILD trial.

Abstract: The efficacy and cost-effectiveness of low-dose spiral computed tomography (LDCT) screening in heavy smokers is currently under evaluation worldwide Our screening program started with a pilot study on 1035 volunteers in Milan in 2000 and was followed up in 2005 by a randomized trial comparing annual or biennial LDCT with observation, named Multicentric Italian Lung Detection This included 4099 participants, 1723 randomized to the control group, 1186 to biennial LDCT screening, and 1190 to annual LDCT screening Follow-up was stopped in November 2011, with 9901 person-years for the pilot study and 17 621 person-years for Multicentric Italian Lung Detection Forty-nine lung cancers were detected by LDCT (20 in biennial and 29 in the annual arm), of which 17 were identified at baseline examination; 63% were of stage I and 84% were surgically resectable Stage distribution and resection rates were similar in the two LDCT arms The cumulative 5-year lung cancer incidence rate was 311/100 000 in the control group, 457 in the biennial, and 620 in the annual LDCT group (P=0036); lung cancer mortality rates were 109, 109, and 216/100 000 (P=021), and total mortality rates were 310, 363, and 558/100 000, respectively (P=013) Total mortality in the pilot study was similar to that observed in the annual LDCT arm at 5 years There was no evidence of a protective effect of annual or biennial LDCT screening Furthermore, a meta-analysis of the four published randomized trials showed similar overall mortality in the LDCT arms compared with the control arm

Role of oxidative DNA damage in cancer initiation and promotion.

Abstract: Normal aerobic metabolism produces huge amounts of potentially dangerous oxidants, controlled by a variety of antioxidant systems An imbalance between the generated and exogenously inflicted oxidants and the oxidant system is termed oxidative stress Even without oxidative stress, ie under normal physiological conditions, the damage to vital cellular micromolecules, such as DNA, is extensive, amounting to hundreds of hits per cell per day More than one hundred different oxidative modifications in DNA have been described The hydroxylation of guanine in the 8-position is the most frequent and most mutagenic lesion described The 8-hydroxylation of guanine leads to lack of base pairing specifically and misreading of the modified base and adjacent residues The modifications to DNA are so frequent that extensive and specific repair is needed for survival Indeed, multiple repair enzyme systems to mediate and remove/repair oxidative DNA modification are described Within DNA, hot-spots of oxidative modification and subsequent mutation have been described, and some specificity appears as compared to other agents that can lead to modification of DNA, ie aflatoxin and benzo[a]pyrene Numerous publications from epidemiology and intervention studies with antioxidants point at oxidative modification as an important factor in cancer development at certain sites Yet, direct evidence linking oxidative DNA modification to cancer has not been published With regard to antoxidant prevention of cancer no effective single substance has so far been identified

Review of anthropometric factors and breast cancer risk

Abstract: Epidemiological evidence implicating anthropometric risk factors in breast cancer aetiology is accumulating. For premenopausal women, breast cancer risk increases with increasing height, but decreases with higher weight or body mass index, and no association with increased central adiposity exists. For postmenopausal women, an increased risk of breast cancer is found with increasing levels of all the anthropometric variables including height, weight, body mass index, waist-hip ratio, waist circumference and weight gain. Weight loss appears to decrease risk, particularly if it occurs later in life. Breast size may be a risk factor for breast cancer, however, the current evidence is inconclusive. Several hypothesized biologic mechanisms exist to explain how anthropometric factors influence breast cancer risk. Obesity may increase levels of circulating endogenous sex hormones, insulin and insulin-like growth factors that all, in turn, increase breast cancer risk. Genetic predisposition to obesity and to specific body fat distributions are also implicated. With obesity, there are increased levels of fat tissue that can store toxins and can serve as a continuous source of carcinogens. Recommendations for future research on anthropometric factors and breast cancer are provided. Sufficient evidence exists to support strategies to avoid weight gain throughout life as a means of reducing postmenopausal breast cancer risk.