Search

Bcl-2 and TGF-β receptors type II (RII) in colon carcinomas were studied in a series of 113 patients, to determine their prognostic significance and to correlate their expression with other prognostic indicators. Bcl-2 expression in the tumor cells showed a reverse relation with tumor size (P = 0.018), histological grade (P = 0.04), and stage (P = 0.013). Univariate survival analysis using the log rank test showed that the survival of patients with bcl-2-positive tumors was significantly better than the survival of patients with bcl-2-negative tumors (P = 0.02). However, when entered into a multivariate analysis model, it was not found to be of independent prognostic significance. TGF-β RII expression was correlated with stage (P = 0.03), while no statistically significant correlation was found between TGF-β RII expression and histological grade or survival. In conclusion, these results provide additional evidence for the role of bcl-2 and TGF-β RII in carcinogenesis of the colon, while they do not support the use of these factors as prognostic markers in patients with colon cancer. [ABSTRACT FROM AUTHOR]

Background: Adverse pregnancy outcomes have reached epidemic proportions in recent years with serious health ramifications, especially for diverse cancers risk. Therefore, we carried out an umbrella review to systematically evaluate the validity and strength of the data and the extent of potential biases of the established association between adverse pregnancy outcomes and cancers risk in both mother and offspring. Methods: PubMed, Embase, and Web of Science databases were searched from inception until 18 January 2024. Meta-analyses of observational studies investigating the relationship between adverse pregnancy outcomes and multiple cancers risk in both mother and offspring were included. Evidence certainty was assessed using Grading of Recommendations, Assessment, Development, and Evaluation. The protocol for this umbrella review was prospectively registered in PROSPERO (CRD42023470544). Results: The search identified 129 meta-analyses of observational studies and 42 types of cancer. Moderate certainty of evidence, exhibiting statistical significance, has been observed linking per kilogram increase in birth weight to a heightened risk of breast cancer (OR = 1.07, 95% CI = 1.02–1.12), prostate cancer (OR = 1.02, 95% CI = 1.00–1.05), leukemia (OR = 1.18, 95% CI = 1.13–1.23), and acute lymphoblastic leukemia in offspring (OR = 1.18, 95% CI = 1.12–1.23); rubella infection during pregnancy to an increased risk of leukemia in offspring (OR = 2.79, 95% CI = 1.16–6.71); and a linear dose–response association between an increase in the proportion of optimal birth weight and an elevated risk of acute lymphoblastic leukemia in offspring (OR = 1.16, 95% CI = 1.09–1.24), respectively. Conclusions: Although some adverse pregnancy outcomes have clinically promising associations with risk of several cancers in both mother and offspring, it is essential to conduct additional research to solidify the evidence, evaluate causality, and ascertain clinical utility. [ABSTRACT FROM AUTHOR]

Cancer continues to pose a significant global health challenge, as evidenced by the increasing incidence rates and high mortality rates, despite the advancements made in chemotherapy. The emergence of chemoresistance further complicates the effectiveness of treatment. However, there is growing interest in the potential of metformin, a commonly prescribed drug for type 2 diabetes mellitus (T2DM), as an adjuvant chemotherapy agent in cancer treatment. Although the precise mechanism of action of metformin in cancer therapy is not fully understood, it has been found to have pleiotropic effects, including the modulation of metabolic pathways, reduction in inflammation, and the regulation of cellular proliferation. This comprehensive review examines the anticancer properties of metformin, drawing insights from various studies conducted in vitro and in vivo, as well as from clinical trials and observational research. This review discusses the mechanisms of action involving both insulin-dependent and independent pathways, shedding light on the potential of metformin as a therapeutic agent for different types of cancer. Despite promising findings, there are challenges that need to be addressed, such as conflicting outcomes in clinical trials, considerations regarding dosing, and the development of resistance. These challenges highlight the importance of further research to fully harness the therapeutic potential of metformin in cancer treatment. The aims of this review are to provide a contemporary understanding of the role of metformin in cancer therapy and identify areas for future exploration in the pursuit of effective anticancer strategies. [ABSTRACT FROM AUTHOR]

Diabetes and cancer are two complicated and common diseases that have received a lot of attention in the fields of medical and public health. The goal of this in-depth review article is to offer a full analysis of the complex connection between cancer and diabetes. The review starts out by exploring the epidemiological data connecting these two illnesses, underlining the elevated risk of cancer among those with diabetes. The various underlying mechanisms are then explored, including hyperglycemia, insulin resistance, persistent inflammation, and common risk factors including obesity. This article additionally explores how managing diabetes affects cancer outcomes and vice versa. It highlights the value of interdisciplinary care approaches and clarifies the difficulties faced by those who deal with both disorders. The review also emphasizes recent advances in the field, such as the use of antidiabetic drugs in the treatment and prevention of cancer, as well as the possibility of precision medicine to personalize care for those who have both cancer and diabetes. This comprehensive review highlights the complex interactions between cancer and diabetes and stresses the necessity for a multidisciplinary approach to care, early detection, and management techniques that address both disorders simultaneously. For those who are impacted by these difficult co-morbidities, the changing landscape of research in this area offers promise for improved outcomes and a higher quality of life. [ABSTRACT FROM AUTHOR]

Gastrointestinal (GI) cancers, which are a diverse group of malignant diseases, represent a major healthcare problem around the world. Due to the lack of specific symptoms in the early stages as well as insufficient diagnostic possibilities, these malignancies occupy the leading position in the causes of death worldwide. The currently available tests have too many limitations to be part of routine diagnostics. Therefore, new potential biomarkers that could be used as diagnostic and prognostic factors for these cancers are still being sought. Among the proteins that might fit this role are serpins, which are serine protease inhibitors. Although the serpins themselves have been known for many years, they have recently become the centre of attention for many authors, especially due to the fact that a number of proteins in this family are involved in many stages of neoplasia formation, from angiogenesis through tumour growth to progression. Therefore, the aim of this review is to present the current knowledge about the significance of serpins in GI malignancies, especially their involvement in the development and progression of oesophageal, gastric, pancreatic and colorectal cancers. This review summarises and confirms the important roles of selected serpins in the pathogenesis of various GI cancers and also points to their promising roles as therapeutic targets. However, due to the relatively nonspecific nature of serpins, future research should be carried out to elucidate the mechanisms involved in tumour pathogenesis in more detail. [ABSTRACT FROM AUTHOR]

Background Hepatocellular carcinoma (HCC) is the sixth most common cancer globally, and is attributable mainly to viral hepatitis, alcohol and nonalcoholic fatty liver disease. Methods Three hundred Greek patients diagnosed with HCC between 2000 and 2019 were retrospectively evaluated for patient and HCC characteristics. Patients were classified as before 2011 (A) or after 2011 (B) and HCC risk factors were compared with historic Greek cohorts. Results The median age was 64 years and 86% were male; 45% had chronic hepatitis B virus (HBV) infection, 26% chronic hepatitis C virus (HCV) infection, and 30% non-viral liver diseases (nvLD). No change was observed among liver diseases between periods A and B. However, there was a trend towards a decrease in virally and an increase in non-virally induced HCC (P=0.075). Patients in period B (vs. A) were more likely to be diagnosed with fewer (<3, P=0.006) and smaller (<3 cm, P=0.005) nodules. Compared with 1558 Greek HCC patients from 1974-2000, there was a decrease in HBV and an increase in HCV and nvLD-related HCCs (P<0.001). Conclusions In Greece, after 2000, there was a decrease in the proportion of HBV and an increase in the proportion of HCV and nvLD-related HCC, while over the last 2 decades there has been a trend towards a decrease in virally and an increase in non-virally induced HCC. Since 2011, HCC is being diagnosed at an earlier stage, possibly reflecting improved surveillance strategies. [ABSTRACT FROM AUTHOR]

Open in new tab Download slide Open in new tab Download slide OBJECTIVES Our goal was to analyse a consecutive series of patients with solid organ tumours undergoing coronary artery bypass grafting (CABG) by defining the risk factors for early and long-term outcomes. METHODS Between 2005 and 2016, a consecutive series of 4079 patients underwent isolated CABG at our institution. Of 103 patients (2.5%) with active malignancy, we enrolled 82 patients (mean age 71 ± 7 years) with solid organ tumours, divided into 4 subgroups: lung (9 patients—11%), gastroenteric (16 patients—20%), urinary (48 patients—58%) and other solid tumours (9 patients—11%). A deterministic record linkage between the clinical database and the National Hospital Information System allowed identification of long-term survival rates and freedom from major adverse cardiovascular events (acute myocardial infarction, repeated admissions for percutaneous coronary intervention and heart failure). RESULTS The most common forms of cancer were prostate, colon and carcinoma of the lung. Compared to patients without cancer, patients with neoplasms were significantly older and had a higher rate of comorbidities, without significant differences among the cancer subgroups. The 30-day mortality rate was significantly higher in patients with cancer compared to those without cancer (4.9% vs 1.8%). However, on logistic regression analysis, cancer was an independent risk factor for postoperative pulmonary dysfunction but not for in-hospital death. The median follow-up time was 58 ± 12 months. The overall 5-year survival rate was 60% [95% confidence interval (CI) 47–71%], with a dismal 32% (95% CI 5–65%) survival rate among patients who had lung tumours only. The 5-year freedom from major adverse cardiovascular events was 64% (95% CI 52–74%), without significant differences among subgroups, and was comparable to that of the non-cancer population. Resolution of coronary heart disease allowed safe cancer surgical resection in 80% of the population. CONCLUSIONS Based on the results from the present study, CABG should not be denied to patients with solid organ tumours by claiming a worse prognosis or less graft durability. Further studies with larger numbers are warranted. [ABSTRACT FROM AUTHOR]

Although increasing dairy product intake has been associated with risk of several cancers, epidemiological studies on hepatocellular carcinoma are sparse and have yielded inconsistent results. We prospectively assessed the associations of dairy products (total, milk, butter, cheese and yogurt) and their major components (calcium, vitamin D, fats and protein) with the risk of hepatocellular carcinoma development among 51,418 men and 93,427 women in the Health Professionals Follow‐Up Study and the Nurses' Health Study. Diets were collected at baseline and updated every 4 years using validated food frequency questionnaires. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards regression model. During up to 32 years of follow‐up, a total of 164 hepatocellular carcinoma cases were documented. After adjustment for most known hepatocellular carcinoma risk factors, higher total dairy product intake was associated with an increased risk of hepatocellular carcinoma (highest vs. lowest tertile, HR = 1.85, 95% CI: 1.19–2.88; ptrend = 0.009). For the same comparison, we observed significant positive associations of high‐fat dairy (HR = 1.81, 95% CI: 1.19–2.76; ptrend = 0.008) and butter (HR = 1.58, 95% CI: 1.06–2.36; ptrend = 0.04) with hepatocellular carcinoma risk. There was a nonsignificant inverse association between yogurt intake and hepatocellular carcinoma risk (HR = 0.72, 95% CI: 0.49–1.05; ptrend = 0.26). Our data suggest that higher intake of high‐fat dairy foods was associated with higher, whereas higher yogurt consumption might be associated with lower risk of developing hepatocellular carcinoma among U.S. men and women. What's new? In the US, liver cancer incidence has increased considerably in the last 30 years. Meanwhile, Americans are also eating more dairy products. These authors investigated the association between dairy consumption and risk of hepatocellular carcinoma (HCC). From participants in the Nurses' Health Study and the Health Professionals Follow‐Up Study, they collected diet information at baseline and again every 4 years. Although they considered individual components of dairy food, including calcium, fat, protein, and vitamin D, they found no association between HCC risk and any individual nutrient. They did find higher total dairy intake associated with higher risk of HCC, particularly for high‐fat products. Higher yogurt intake appears to be associated with a suggestive lower risk, which deserves further investigations. [ABSTRACT FROM AUTHOR]

The goal of this study was to review the scientific basis for the recognition of occupational cancer, in relation to hepatitis viral infections in Korea. Most Hepatitis B virus (HBV) infections in Korea occur as vertical infections, but these are decreasing rapidly due to vaccination. Hepatitis C virus (HCV) is known to be transmitted through parenteral routes, but the transmission route is often unclear. Most occupational infections of hepatitis virus involve accidental injuries of medical institution workers while using virus-contaminated medical devices. Many cohort studies and case-control studies have consistently reported that HBV and HCV infection increases the risk of hepatocellular carcinoma (HCC) and the strength of this association is high. Non-Hodgkin's lymphoma appears to be associated with HCV. Cholangiocarcinoma, pancreatic cancer, leukemia, and thyroid cancer are considered to be less related or unrelated to epidemiological causation. There are no uniform international specific criteria for occupational cancer caused through occupational exposure to a hepatitis virus. In establishing appropriate standards applicable to Korea, there should be sufficient consideration of latency, virus exposure levels and frequency, and other cancers, apart from HCC. In conclusion, we recommend keeping the current specific criteria. However, if a worker is injured at work when using a sharp medical device, and HBV and HCV viral infections are confirmed through serologic tests; if the worker is diagnosed as having a chronic HBV or HCV infection, a subsequent HCC (or Non-Hodgkin's lymphoma following chronic HCV infection) can then be considered highly related to the worker's occupation. [ABSTRACT FROM AUTHOR]

Prostate cancer (PCa) has become the most frequent type of cancer in men. Recent data suggest that diabetic patients taking metformin have a lower incidence of certain cancer, including PCa. Metformin is the most common drug used in type II diabetes mellitus; its use has been shown to lower the incidence of several cancers, although there are ambiguous data about the anticancer activity of metformin. A large number of studies examined the potential antineoplastic mechanism of metformin although it is not still completely understood. This review summarizes the literature concerning the effects of metformin on PCa cells, highlighting its numerous mechanisms of action through which it can act. We analyze the possible causes of the discordances regarding the impact of metformin on risk of PCa; we discuss the latest findings in this field, suggesting that metformin may have a future role in the management of PCa both as monotherapy and in combination with other drugs. [ABSTRACT FROM AUTHOR]

Obesity has been an epidemic worldwide over the past decades and significantly increases the risk of developing a variety of deadly diseases including type 2 diabetes, cardiovascular diseases and many cancers. The relationship between obesity and type 2 diabetes and cardiovascular disease has been well documented. The drastically increased frequency of a number of cancers in obesity has attracted growing interest. On one hand, how increased adiposity promotes cancer development remains poorly understood, despite the fact that considerable epidemiological evidence has suggested links between them. On the other hand, however, numerous studies have shown that tumorigenesis leads to substantial weight loss in a large portion of cancer patients. Here, we summarize the recent advances on our understanding of the link between obesity and cancer development with a focus on the molecular mechanisms accounting for the rising cancer incidence in the context of obesity. In addition, we also discuss how cancer-associated anorexia and cachexia causes weight loss. © 2017 IUBMB Life, 69(10):776-784, 2017 [ABSTRACT FROM AUTHOR]

Cancers have been the leading cause of death worldwide and the prevalence of obesity is also increasing in these few decades. Interestingly, there is a direct association between cancer and obesity. Each year, more than 90,000 cancer deaths are caused by obesity or overweight. The dietary pattern in Crete, referred as the traditional Mediterranean diet, is believed to confer Crete people the low mortality rates from cancers. Nevertheless, the antiobesity effect of the Mediterranean diet is less studied. Given the causal relationship between obesity and cancer, the antiobesity effect of traditional Mediterranean diet might contribute to its anticancer effects. In this regard, we will critically review the anticancer and antiobesity effects of this diet and its dietary factors. The possible mechanisms underlying these effects will also be discussed. [ABSTRACT FROM PUBLISHER]

Background: The aetiology of nasopharyngeal carcinoma (NPC) remains enigmatic in endemic and non-endemic areas. Early-life infection with Epstein-Barr virus (EBV) may predispose to NPC development, whereas delayed primary infection with EBV may cause infectious mononucleosis (IM).Methods: We used Swedish population and health registers to investigate whether potential indicators of early EBV infection, such as birth order, sibship size, maternal age and paternal age, are related to the subsequent risks for NPC and IM. We conducted two nested case-control studies, one for each health outcome, based on 251 NPC case patients, 11 314 IM case patients and five population control subjects per case matched by birth year and sex. We used conditional logistic regression modelling to estimate odds ratios (ORs) and their 95% confidence intervals (CIs) for NPC and IM.Results: The multivariate-adjusted ORs of developing NPC increased with number of siblings; the ORs associated with having one, two and three or more siblings, compared with none, were 1.59 (95% CI = 0.97, 2.62), 1.94 (95% CI = 1.17, 3.22), and 2.03 (95% CI = 1.23, 3.35), respectively (Ptrend = 0.006). This increased risk of NPC was explained mainly by having older rather than younger siblings. In contrast, lower risks of IM were observed among individuals with an increasing number of older siblings, younger siblings and total siblings.Conclusions: Early-life social environment, possibly related to EBV infection, contributes to NPC pathogenesis in non-endemic areas. This hypothesis is further supported by the clearly contrasting findings between NPC and IM. [ABSTRACT FROM AUTHOR]

There is a growing understanding that several infectious agents are acquired in early life and this is the reason why available vaccines target the new born, infants, and adolescents. Infectious agents are associated with cancer development and it is estimated that about 20% of the world’s cancer burden is attributed to infectious agents. There is a growing evidence that certain infectious agents acquired in early life can give rise to cancer development, but estimates of the cancer burden from this early-life acquisition is unknown. In this article, we have selected five cancers (cervical, liver, Burkitt’s lymphoma-leukemia, nasopharyngeal carcinoma, and adult T-cell leukemia-lymphoma) and examine their links to infectious agents (HPV, HBV, HCV, EBV, and HTLV-1) acquired in early life. For these agents, the acquisition in early life is from mother-to- child transmission, perinatal contact (with genital tract secretions, amniotic fluids, blood, and breast milk), saliva, sexual intercourse, and blood transfusion. We also discuss prevention strategies, address future directions, and propose mechanisms of action after a long latency period from the time of acquisition of the infectious agent in early life to cancer development. [ABSTRACT FROM AUTHOR]

Cosmic radiation can cause genetic and cytogenetic damage. Certain occupations including airline pilots and cabin crew are acknowledged to have a greater exposure to cosmic radiation. In a systematic search of MEDLINE, performed from 1990 to 2014, we analyzed clinical studies using the keywords: cosmic radiation, cancer, chromosome aberration, pilots and astronauts. Increased incidence of skin cancers among airline cabin crew has been reported in a number of studies and appears to be the most consistent finding. However, as with other cancers, it is unclear whether increased exposure to cosmic radiation is a factor in the increased incidence or whether this can be explained by lifestyle factors. Further research is needed to clarify the risk of cancer in relation to cosmic radiation. [ABSTRACT FROM AUTHOR]

Epidemiological studies have shown that overweight and cancer are closely related, even though obesity alone does not apparently heighten cancer risk by the same amount. Given the low overall risk of all cancers with obesity, it is unlikely that obesity alone causes cancer, but should instead be considered as a tumor promoter. There are three main hypotheses that could explain how obesity might contribute to cancer development and growth: the inflammatory cytokines from adipose tissue hypothesis, the insulin resistance and hyperinsulinemia hypothesis, and the unopposed estrogen cancer hypothesis. The link between obesity and cancer is that adipocytes constitute a major component of the tumor microenvironment for breast and abdominally metastasizing cancers, promoting tumor growth. This review will mainly focus attention on the relationship between adipose tissue, estrogens, and cancer risk. [ABSTRACT FROM AUTHOR]

Phosphoinositide 3-kinases (PI3Ks) regulate several cellular functions that are critical for cancer progression and development, including cell survival, proliferation and migration. Three classes of PI3Ks exist with the class I PI3K encompassing four isoforms of the catalytic subunit known as p110α, p110β, p110γ, and p110δ. Although for many years attention has been mainly focused on p110α recent evidence supports the conclusion that p110β, p110γ, and p110δ can also have a role in cancer. Amongst these, accumulating evidence now indicates that p110γ is involved in several cellular processes associated with cancer and indeed this specific isoform has emerged as a novel important player in cancer progression. Studies from our laboratory have identified a specific overexpression of p110γ in human pancreatic ductal adenocarcinoma (PDAC) and in hepatocellular carcinoma (HCC) tissues compared to their normal counterparts. Our data have further established that selective inhibition of p110γ is able to block PDAC and HCC cell proliferation, strongly suggesting that pharmacological inhibition of this enzyme can directly affect growth of these tumors. Furthermore, increasing evidence suggests that p110γ plays also a key role in the interactions between cancer cells and tumor microenvironment and in particular in tumor-associated immune response. It has also been reported that p110γ can regulate invasion of myeloid cells into tumors and tumor angiogenesis. Finally p110γ has also been directly involved in regulation of cancer cell migration. Taken together these data indicate that p110γ plays multiple roles in regulation of several processes that are critical for tumor progression and metastasis. This review will discuss the role of p110γ in gastrointestinal tumor development and progression and how targeting this enzyme might represent a way to target very aggressive tumors such as pancreatic and liver cancer on multiple fronts. [ABSTRACT FROM AUTHOR]

Background We evaluated mortality among 5,964 former U.S. commercial cockpit crew (pilots and flight engineers). The outcomes of a priori interest were non-chronic lymphocytic leukemia, central nervous system (CNS) cancer (including brain), and malignant melanoma. Methods Vital status was ascertained through 2008. Life table and Cox regression analyses were conducted. Cumulative exposure to cosmic radiation was estimated from work history data. Results Compared to the U.S. general population, mortality from all causes, all cancer, and cardiovascular diseases was decreased, but mortality from aircraft accidents was highly elevated. Mortality was elevated for malignant melanoma but not for non-chronic lymphocytic leukemia. CNS cancer mortality increased with an increase in cumulative radiation dose. Conclusions Cockpit crew had a low all-cause, all-cancer, and cardiovascular disease mortality but elevated aircraft accident mortality. Further studies are needed to clarify the risk of CNS and other radiation-associated cancers in relation to cosmic radiation and other workplace exposures. [ABSTRACT FROM AUTHOR]

Gallstones and cholecystectomy may be related to digestive system cancer through inflammation, altered bile flux, and changes in metabolic hormone levels. Although gallstones are recognized causes of gallbladder cancer, associations with other cancers of the digestive system are poorly established. We used the Surveillance, Epidemiology, and End Results (SEER)-Medicare linked database (1992–2005), which includes 17 cancer registries that cover approximately 26% of the US population, to identify first primary cancers (n = 236,850) occurring in persons aged ≥66 years and 100,000 cancer-free population-based controls frequency-matched by calendar year, age, and gender. Odds ratios and 95% confidence intervals were calculated using logistic regression analysis, adjusting for the matching factors. Gallstones and cholecystectomy were associated with increased risk of noncardia gastric cancer (odds ratio (OR) = 1.21 (95% confidence interval (CI): 1.11, 1.32) and OR = 1.26 (95% CI: 1.13, 1.40), respectively), small-intestine carcinoid (OR = 1.27 (95% CI: 1.01, 1.60) and OR = 1.78 (95% CI: 1.41, 2.25)), liver cancer (OR = 2.35 (95% CI: 2.18, 2.54) and OR = 1.26 (95% CI: 1.12, 1.41)), and pancreatic cancer (OR = 1.24 (95% CI: 1.16, 1.31) and OR = 1.23 (95% CI: 1.15, 1.33)). Colorectal cancer risk associated with gallstones and cholecystectomy decreased with increasing distance from the common bile duct (P-trend < 0.001). Hence, gallstones and cholecystectomy are associated with the risk of cancers occurring throughout the digestive tract. [ABSTRACT FROM PUBLISHER]

Background: Few studies have examined the broad health effects of occupational exposures in flight attendants apart from disease-specific morbidity and mortality studies. We describe the health status of flight attendants and compare it to the U.S. population. In addition, we explore whether the prevalence of major health conditions in flight attendants is associated with length of exposure to the aircraft environment using job tenure as a proxy. Methods: We surveyed flight attendants from two domestic U.S. airlines in 2007 and compared the prevalence of their health conditions to contemporaneous cohorts in the National Health and Nutrition Survey (NHANES), 2005-2006 and 2007-2008. We weighted the prevalence of flight attendant conditions to match the age distribution in the NHANES and compared the two populations stratified by gender using the Standardized Prevalence Ratio (SPR). For leading health conditions in flight attendants, we analyzed the association between job tenure and health outcomes in logistic regression models. Results: Compared to the NHANES population (n =5,713), flight attendants (n = 4,011) had about a 3-fold increase in the age-adjusted prevalence of chronic bronchitis despite considerably lower levels of smoking. In addition, the prevalence of cardiac disease in female flight attendants was 3.5 times greater than the general population while their prevalence of hypertension and being overweight was significantly lower. Flight attendants reported 2 to 5.7 times more sleep disorders, depression, and fatigue, than the general population. Female flight attendants reported 34% more reproductive cancers. Health conditions that increased with longer job tenure as a flight attendant were chronic bronchitis, heart disease in females, skin cancer, hearing loss, depression and anxiety, even after adjusting for age, gender, body mass index (BMI), education, and smoking. Conclusions: This study found higher rates of specific diseases in flight attendants than the general population. Longer tenure appears to explain some of the higher disease prevalence. Conclusions are limited by the cross-sectional design and recall bias. Further study is needed to determine the source of risk and to elucidate specific exposure-disease relationships over time. [ABSTRACT FROM AUTHOR]

Epidemiological studies investigating the association between dietary intake and oesophageal cancer have mostly focused on nutrients and food groups instead of dietary patterns. We conducted a population-based case–control study, which included 365 oesophageal adenocarcinoma (OAC), 426 oesophagogastric junction adenocarcinoma (OGJAC) and 303 oesophageal squamous cell carcinoma (OSCC) cases, with frequency matched on age, sex and geographical location to 1580 controls. Data on demographic, lifestyle and dietary factors were collected using self-administered questionnaires. We used principal component analysis to derive three dietary patterns: ‘meat and fat’, ‘pasta and pizza’ and ‘fruit and vegetable’, and unconditional logistic regression models to estimate risks of OAC, OGJAC and OSCC associated with quartiles (Q) of dietary pattern scores. A high score on the meat-and-fat pattern was associated with increased risk of all three cancers: multivariable-adjusted OR 2·12 (95 % CI 1·30, 3·46) for OAC; 1·88 (95 % CI 1·21, 2·94) for OGJAC; 2·84 (95 % CI 1·67, 4·83) for OSCC (P-trend < 0·01 for all three cancers). A high score on the pasta-and-pizza pattern was inversely associated with OSCC risk (OR 0·58, 95 % CI 0·36, 0·96, P for trend = 0·009); and a high score on the fruit-and-vegetable pattern was associated with a borderline significant decreased risk of OGJAC (OR for Q4 v. Q1 0·66, 95 % CI 0·42, 1·04, P = 0·07) and significantly decreased risk of OSCC (OR 0·41, 95 % CI 0·24, 0·70, P for trend = 0·002). High-fat dairy foods appeared to play a dominant role in the association between the meat-and-fat pattern and risk of OAC and OGJAC. Further investigation in prospective studies is needed to confirm these findings. [ABSTRACT FROM PUBLISHER]

Increased cancer risk is associated with select dietary factors. Dietary lifestyles can alter systemic acid-base balance over time. Acidogenic diets, which are typically high in animal protein and salt and low in fruits and vegetables, can lead to a sub-clinical or low-grade state of metabolic acidosis. The relationship between diet and cancer risk prompts questions about the role of acidosis in the initiation and progression of cancer. Cancer is triggered by genetic and epigenetic perturbations in the normal cell, but it has become clear that microenvironmental and systemic factors exert modifying effects on cancer cell development. While there are no studies showing a direct link between diet-induced acidosis and cancer, acid-base disequilibrium has been shown to modulate molecular activity including adrenal glucocorticoid, insulin growth factor (IGF-1), and adipocyte cytokine signaling, dysregulated cellular metabolism, and osteoclast activation, which may serve as intermediary or downstream effectors of carcinogenesis or tumor promotion. In short, diet-induced acidosis may influence molecular activities at the cellular level that promote carcinogenesis or tumor progression. This review defines the relationship between dietary lifestyle and acid-base balance and discusses the potential consequences of diet-induced acidosis and cancer occurrence or progression. [ABSTRACT FROM AUTHOR]

ObjectiveIntake of nutrients may influence the risk of endometrial cancer (EC). We aimed to estimate the association of intake of individual nutrients from food and from food plus supplements with EC occurrence.DesignA population-based case–control study conducted in Canada (2002–2006).SettingNutrient intakes from food and supplements were assessed using an FFQ. Logistic regression was used to estimate EC risk within quartile levels of nutrient intakes.SubjectsIncident EC cases (n 506) were identified from the Alberta Cancer Registry, and population controls were frequency- and age-matched to cases (n 981).ResultsThere existed little evidence of an association with EC for the majority of macronutrients and micronutrients examined. We observed a statistically significant increased risk associated with the highest, compared with the lowest, quartile of intake of dietary cholesterol (multivariable-adjusted OR = 1·51, 95 % CI 1·08, 2·11; P for trend = 0·02). Age-adjusted risk at the highest level of intake was significantly reduced for Ca from food sources (OR = 0·73, 95 % CI 0·54, 0·99) but was attenuated in the multivariable model (OR = 0·82, 95 % CI 0·59, 1·13). When intake from supplements was included in Ca intake, risk was significantly reduced by 28 % with higher Ca (multivariable-adjusted OR = 0·72, 95 % CI 0·51, 0·99, P for trend = 0·04). We also observed unexpected increased risks at limited levels of intakes of dietary soluble fibre, vitamin C, thiamin, vitamin B6 and lutein/zeaxanthin, with no evidence for linear trend.ConclusionsThe results of our study suggest a positive association between dietary cholesterol and EC risk and an inverse association with Ca intake from food sources and from food plus supplements. [ABSTRACT FROM PUBLISHER]

Objective: Improving the prognostic stratification of unresectable hepatocellular carcinoma (HCC) patients is critically needed. Since patients' survival is closely linked to the severity of the underlying liver disease, and insulin-like growth factor-1 (IGF-1) is produced predominantly in the liver, we hypothesized that IGF-1 may correlate with patients' survival and hence improve the prognostic ability of the Cancer of the Liver Italian Program (CLIP) score. Methods: Baseline plasma IGF-1 and clinicopathologic parameters were available from 288 patients. Multivariate Cox regression models, Kaplan-Meier curves, and the log-rank test were applied. Recursive partitioning was used to determine the optimal cut point for IGF-1 using training/validation samples. Prognostic ability of the I-CLIP (I = IGF) was compared to CLIP using C-index. Results: IGF-1 significantly correlated with the clinicopathologic features. With an optimal IGF-1 cut point of 26 ng/ml, the overall survival of patients with IGF-1 >26 was 17.7 months (95% CI 13.6-22.8), and with IGF-1 ≤26 was 5.8 months (95% CI 4.0-12.5), p < 0.0001. The concordance probabilities for CLIP and I-CLIP were 0.7037 and 0.7096, respectively (p < 0.0001). Conclusions: Our preliminary results indicate that I-CLIP significantly improved prognostic stratification of patients with advanced HCC. However, independent validation of our study is warranted. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article discusses the link between fruit and vegetable consumption and risk of bladder cancer based on the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The variety of fruits and vegetable consumed by study participants was quantified through diet diversity scores (DDSs). The effect of the DDSs on risk of bladder cancer was evaluated using multivariable Cox proportional hazard models. The study found no significant link between DDSs and bladder cancer risk.

Objective The objective is to systematically estimate the current cancer incidence and mortality from the six leading cancer types globally and by sub-regions resulting from exposure to known risk factors such as tobacco use, elevated body weight, alcohol consumption, inadequate physical activity, unhealthy diet and infections. Methods Cancer incidence, mortality and burden of disease caused by the main cancer risk factors were calculated using comparative risk assessment methods and updated data on mortality and risks. Results Lung cancer was the most common cancer in men and breast cancer the most common cancer in women, both in terms of incidence and mortality. The five leading behavioral and dietary risks—high body mass index, low fruit and vegetable intake, physical inactivity, tobacco use and alcohol use—were responsible for 24% of new cancer cases and 30% of cancer deaths. Cancers with the largest proportions attributable to preventable risk factors were cervical cancer (100%) and lung cancer (71%). Seventy percent of liver cancers and 60% of stomach cancers were due to infectious agents. A higher proportion of cancer deaths was attributed to infections in low- and middle-income than in high-income countries. Conclusions The cancer burden is driven by changes in exposure to influential risk factors and can be influenced by preventive interventions aimed at reducing these exposures. [ABSTRACT FROM PUBLISHER]

Food fat plays an important role in the human diet. On the one hand, fats provide the body with energy, contribute to the absorption of fat-soluble vitamins, and act as structural elements of cell walls. On the other hand, a high fat intake is associated with obesity, type 2 diabetes, cancer, and coronary heart disease. Animal fats, which contain a high proportion of saturated fatty acids, are often the focus of attention when it comes to reducing the share of fat in the diet. The present overview of the literature describes the amount of total fat and the percentage of individual fatty acid groups in meat and meat products, documents the contribution of meat and meat products to fat intake, and investigates the connection between meat fat and various diseases. The information given is based mainly on data material from Switzerland; data from other countries have been included for comparison. [ABSTRACT FROM AUTHOR]

Evidence derived from a vast array of laboratory studies and epidemiological investigations have implicated diets rich in fruits and vegetables with a reduced risk of certain cancers. However, these approaches cannot demonstrate causal relationships and there is a paucity of randomized, controlled trials due to the difficulties involved with executing studies of food and behavioral change. Rather than pursuing the definitive intervention trials that are necessary, the thrust of research in recent decades has been driven by a reductionist approach focusing upon the identification of bioactive components in fruits and vegetables with the subsequent development of single agents using a pharmacologic approach. At this point in time, there are no chemopreventive strategies that are standard of care in medical practice that have resulted from this approach. This review describes an alternative approach focusing upon development of tomato-based food products for human clinical trials targeting cancer prevention and as an adjunct to therapy. Tomatoes are a source of bioactive phytochemicals and are widely consumed. The phytochemical pattern of tomato products can be manipulated to optimize anticancer activity through genetics, horticultural techniques, and food processing. The opportunity to develop a highly consistent tomato-based food product rich in anticancer phytochemicals for clinical trials targeting specific cancers, particularly the prostate, necessitates the interactive transdisciplinary research efforts of horticulturalists, food technologists, cancer biologists, and clinical translational investigators. [ABSTRACT FROM AUTHOR]

The International Agency for Research on Cancer (IARC) classified occupational painting as a human carcinogen based on lung and bladder cancers; however, no specific exposures were implicated. The authors conducted comprehensive meta-analyses of the epidemiological literature on occupational painting and these cancers. The authors abstracted study results and confounder information, and used quantile plots and regression models to evaluate heterogeneity and publication bias. Summary risk estimates were derived and sensitivity analyses performed to evaluate smoking, socioeconomic status (SES), and exposure variables. Where applicable, a Bayesian approach was used to externally adjust for smoking, a major risk factor for both cancers. For lung cancer cohort mortality studies, publication bias and heterogeneity were seen, and earlier studies reported higher risk estimates than later studies. Overall lung cancer summary risk estimates were 1.29 for case-control and 1.22 and 1.36 for cohort morbidity and mortality studies, respectively, and risk estimates for bladder cancer were 1.28 for case-control and 1.14 and 1.27 for cohort morbidity and mortality studies, respectively (all statistically significant). Risks did not differ between painters and mixed occupations. Nonsignificant summary estimates resulted for lung and bladder cancers when controlling for SES, or externally adjusting for smoking in lung cancer studies. Summary risks varied by control source for case-control studies. Residual confounding by smoking and SES, lack of exposure group effect, and publication bias limit the ability of the meta-analyses to explain associations observed between occupational painting and lung and bladder cancers. Given the long latencies for lung and bladder cancers, these weak associations, if real, may not be elucidated through studies of occupational painting today. [ABSTRACT FROM AUTHOR]

Radiation causes DNA damage, increases risk of cancer, and is associated with psychological stress responses. This article proposes an evidence-based integrative model in which psychological factors could interact with radiation by either augmenting or moderating the adverse effects of radiation on DNA integrity and eventual tumorigenesis. Based on a review of the literature, we demonstrate the following: (1) the effects of low-dose radiation exposures on DNA integrity and on tumorigenesis; (2) the effects of low-dose radiation exposure on psychological distress; (3) the relationship between psychological factors and DNA damage; and (4) the possibility that psychological stress augments and that psychological resource variables moderate radiation-induced DNA damage and risk of cancer. The additional contribution of psychological processes to radiation-DNA damage-cancer relationships needs further study, and if verified, has clinical implications. [ABSTRACT FROM AUTHOR]

Use of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs) may reduce the risk of gastric or oesophageal adenocarcinomas. We examined the association between self-reported use of aspirin or non-aspirin NSAIDs in the earlier 12 months and gastric non-cardia (N=182), gastric cardia (N=178), and oesophageal adenocarcinomas (N=228) in a prospective cohort (N=311 115) followed for 7 years. Hazard ratios (HRs) and 95% confidence intervals (CIs) come from Cox models adjusted for potential confounders. Use of any aspirin (HR, 95% CI: 0.64, 0.47-0.86) or other NSAIDs (0.68, 0.51-0.92) was associated with a significantly lower risk of gastric non-cardia adenocarcinoma. Neither aspirin (0.86, 0.61-1.20) nor other NSAIDs (0.91, 0.67-1.22) had a significant association with gastric cardia cancer. We found no significant association between using aspirin (1.00, 0.73-1.37) or other NSAIDs (0.90, 69-1.17) and oesophageal adenocarcinoma. We also performed a meta-analysis of the association between the use of NSAIDs and risk of gastric and oesophageal adenocarcinoma. In this analysis, aspirin use was inversely associated with both gastric and oesophageal adenocarcinomas, with summary odds ratios (95% CI) for non-cardia, cardia, and oesophageal adenocarcinomas of 0.64 (0.52-0.80), 0.82 (0.65-1.04), and 0.64 (0.52-0.79), respectively. The corresponding numbers for other NSAIDs were 0.68 (0.57-0.81), 0.80 (0.67-0.95), and 0.65 (0.50-0.85), respectively. [ABSTRACT FROM AUTHOR]

To investigate the relationship between air pollution and risk of death from bladder cancer, the authors conducted a matched case-control study using deaths that occurred in Taiwan from 1995 through 2005. Data on all eligible bladder cancer deaths were obtained from the Bureau of Vital Statistics of the Taiwan Provincial Department of Health. The control group consisted of people who died from causes other than cancer or diseases associated with genitourinary problems. The controls were pair matched to the cases by sex, year of birth, and year of death. Each matched control was selected randomly from the set of possible controls for each case. Classification of exposure to municipality air pollution was based on the measured levels of nitrogen dioxide and sulfur dioxide. The results of the present study show that there is a significant positive association between the levels of air pollution and bladder cancer mortality. The adjusted odds ratios (95% confidence interval) were 1.37 (1.03-1.82) for the group with medium air pollution level and 1.98 (1.36-2.88) for the group with high air pollution level when compared to the group with the low air pollution level. Trend analyses showed statistically significant trend in risk of death from bladder cancer with increasing air pollution level. The findings of this study warrant further investigation of the role of air pollutants in the etiology of bladder cancer. [ABSTRACT FROM AUTHOR]

Objective: Pregnancies reduce the risk of ovarian cancer, and among multiparous women, levels of circulating progesterone might be higher during pregnancies with wider birth spacing. We hypothesized that childbirth with wider birth spacing might reduce maternal risk of invasive epithelial ovarian cancer more than births with narrower spacing.Methods: We conducted a case-control study nested in a nationwide cohort of Swedish women from 1961 to 2001. We selected five individually age-matched controls for each case of invasive epithelial ovarian cancer, and analysis for the effect of birth spacing was performed for 5,341 cases and 29,047 controls. We applied unconditional logistic regression analyses adjusting for age, ages at childbirth, educational level, area of residence, and gender of offspring.Results: Relative risk of invasive epithelial ovarian cancer associated with each one-year increase in average birth spacing is 1.00 (95% CI = 0.98-1.01) among all women and 0.99 (0.98-1.01) among those born before 1935 and less likely to have used oral contraceptives. Further analyses on the biparous and triparous women did not find a consistent association between birth spacing and the risk of ovarian cancer.Conclusions: Birth spacing is unlikely to be a major determinant underlying the protective effects of childbirth on ovarian cancer risk. [ABSTRACT FROM AUTHOR]

The role of low penetrance genes and environmental factors in the etiology of bladder cancer (CaB) is unclear, but may involve genetic and environmental factors. Most environmental pro-carcinogens require metabolic activation by phase I enzymes (CYP450s), However, phase II enzyme (i.e., microsomal epoxide hydrolase: mEH) is mainly involved in the detoxification of wide variety of endogenous or exogenous carcinogens. Genetic differences in CYP1A1 gene and the mEH gene polymorphisms have been reported to be associated with susceptibility to various cancers. In our case–control study, we assess whether Msp1 polymorphism of CYP1A1 (CYP1A1*2A), and His113 in exon 3 and Arg139 in exon 4 of the mEH susceptibility genotypes, tobacco-use and age factors contribute to bladder cancer risk among Indians. A case–control study was conducted in 106 bladder cancer (CaB) patients and 160 age matched controls from similar ethnic background. The CYP1A1*2A and mEH genotypes were determined by polymerase chain reaction/restriction fragment length polymorphism method from DNA extracted from peripheral blood samples. Binary logistic regression model was used for assessing differences in genotype prevalence between patients and the controls. The Arlequin software package was used to compute haplotype frequencies. We observed non-significant association in T/C polymorphism of the CYP1A1 gene (CYP1A1*2A); however, the exon 3 His genotype of the mEH gene polymorphism alone (odds ratio = 2.67, P = 0.001) or in combination with tobacco-users were significantly associated with the risk of bladder cancer. No associations were observed with stage or grade of bladder tumor with these genotypes. In conclusion, our study demonstrated that exon 3 His genotype of the mEH are more prone to the risk of sporadic bladder cancer in North India. [ABSTRACT FROM AUTHOR]

Ovarian cancer is the fifth most frequently occurring cancer among women and leading cause of gynecological cancer deaths in North America. Although the etiology of ovarian cancer is not clear, certain factors are implicated in the etiology of this disease, such as ovulation, gonadotropic and steroid hormones, germ cell depletion, oncogenes and tumor suppressor genes, growth factors, cytokines, and environmental agents. Family history of breast or ovarian cancer is a prominent risk factor for ovarian cancer, with 5-10% of ovarian cancers due to heritable risk. Reproductive factors such as age at menopause and infertility contribute to greater risk of ovarian cancer, whereas pregnancy, tubal ligation, and hysterectomy reduce risk. Oral contraceptive (OC) use has clearly been shown to be protective against ovarian cancer. In contrast, large epidemiologic studies found hormone replacement therapy (HRT) to be a greater risk factor for ovarian cancer. The marked influence of hormones and reproductive factors on ovarian cancer suggests that endocrine disrupters may impact risk; however, there is a notable lack of research in this area. Lifestyle factors such as cigarette smoking, obesity, and diet may affect ovarian cancer risk. Exposure to certain environmental agents such as talc, pesticides, and herbicides may increase risk of ovarian cancer; however, these studies are limited. Further research is needed to strengthen the database of information from which an assessment of environmental and toxicological risk factors for ovarian cancer can be made. [ABSTRACT FROM AUTHOR]

Young pre-menopausal women with breast carcinomas have an overall worse prognosis than older, post-menopausal women. Because histologic grade is a major predictor of tumor behavior and correlates with biomarker expression, we assessed the immunohistochemical expression of epidermal growth factor receptor (EGFR), p185erbB-2 and Bcl-2, and nuclear accumulation of p53 in breast carcinomas in pre- and post-menopausal women with equivalent histologic grades. This allowed identification of differences in biomarker expression and prognostic significance in pre- and post-menopausal women independent of histologic grade. We investigated 100 infiltrating ductal carcinomas (IDC) in pre-menopausal women, ages 45 years and younger, and 100 IDC in post-menopausal women, ages 65 years and older. The IDC were selected so that the proportions of high and low/moderate grade carcinomas were equal in the pre- and post-menopausal groups. Prognostic utility of biomarker expression in pre- and post-menopausal groups was determined by product limit and multivariate analysis of survival. There were statistically significant differences in cytoplasmic expression of EGFR and Bcl-2 and nuclear accumulation of p53, but not in the expression of p185erbB-2, in carcinomas of high vs. low histologic grade. There was no difference in the expression of EGFR, p185erbB-2 or Bcl-2, or in nuclear accumulation of p53 in these IDC from pre- vs. post-menopausal women. Bcl-2 and the nuclear accumulation of p53 were of prognostic significance in our overall study population; however, when assessing pre- and post-menopausal women separately, Bcl-2 and p53 were of prognostic significance only in pre-menopausal, but not post-menopausal women. In summary expression of EGFR and Bcl-2 and nuclear accumulation of p53 were significantly associated with histologic grade, but not with menopausal status. In addition, there were differences in the prognostic effectiveness of these biomarkers in pre- vs. post-menopausal women. [ABSTRACT FROM AUTHOR]

Using the Swedish Family-Cancer Database, among a total of 1 030 806 women followed from 1993 through 2004, invasive and borderline epithelial ovarian cancer was identified in 3306 and 822 women respectively, with data on family history, reproductive variables, residential region and socioeconomic status. Relative risks and population-attributable fractions (PAFs) were estimated by Poisson regression. The overall PAFs of invasive epithelial ovarian cancer for family history and for reproductive factors were 2.6 and 22.3%, respectively, for serous/seropapillary cystadenocarcinoma (3.0 and 19.1%), endometrioid carcinoma (2.6 and 26.6%), mucinous cystadenocarcinoma (0.5 and 23.9%) and clear-cell carcinoma (2.6 and 73.9%). The corresponding PAFs of borderline tumours due to family history were lower, but higher due to reproductive factors. Family history, low parity and young age at first birth were associated with elevated risks. The risks for women with a family history were among the highest, but these women accounted for the smallest proportion of the cases, giving the lowest PAFs.British Journal of Cancer (2008) 98, 199–205. doi:10.1038/sj.bjc.6604135 www.bjcancer.com Published online 11 December 2007 [ABSTRACT FROM AUTHOR]

This review focuses on the possible role in human health of the consumption of lignan-rich foods. Most of the plant lignans in human foods are converted by the intestinal microflora in the upper part of the large bowel to enterolactone and enterodiol, called mammalian or enterolignans. The protective role of these compounds, particularly in chronic Western diseases, is discussed. Evidence suggests that fiber- and lignan-rich whole-grain cereals, beans, berries, nuts, and various seeds are the main protective foods. Many factors, in addition to diet, such as intestinal microflora, smoking, antibiotics, and obesity affect circulating lignan levels in the body. Lignan-rich diets may be beneficial, particularly if consumed for life. Experimental evidence in animals has shown clear anticarcinogenic effects of flaxseed or pure lignans in many types of cancer. Many epidemiological results are controversial, partly because the determinants of plasma enterolactone are very different in different countries. The source of the lignans seems to play a role because other factors in the food obviously participate in the protective effects. The results are promising, but much work is still needed in this area of medicine. [ABSTRACT FROM AUTHOR]

Abstract Background  Because dietary fat has been postulated to affect obesity and estrogen levels, two important risk factors for endometrial cancer, its association with this disease has received some attention. We summarize here the current evidence for several dietary lipids. Methods  Searches were conducted to identify peer-reviewed manuscripts up to December 2006. Two cohort studies and nine case–control studies were included in meta-analyses. Results  Random-effects summary estimates for case–control studies were 1.24 (95% CI: 1.10, 1.41) per 10% kcal from total fat and 1.28 (95% CI: 1.12, 1.47) per 10 g/1,000 kcal of saturated fat. The only cohort study evaluating total fat and saturated fat did not find an association. We estimated a 35% increased risk (95% CI: 0.96, 1.90) per 150 mg/1,000 kcal of cholesterol intake, based on six case–control studies. For animal fat (per 10 g/1,000 kcal) the summary estimates were 0.78 (95% CI: 0.63, 0.96) and 1.34 (95% CI: 1.06, 1.69) for two cohort and four case–control studies, respectively. Conclusions  Case–control data suggest an increased risk for total, saturated, and animal fat. However, the limited available cohort data do not support these associations. Additional data, particularly from prospective studies, are needed before conclusions can be drawn. [ABSTRACT FROM AUTHOR]

Abstract Objective  We examined subsite- and histology-specific esophageal and gastric cancer incidence patterns among Hispanics/Latinos and compared them with non-Hispanic whites and non-Hispanic blacks. Methods  Data on newly diagnosed esophageal and gastric cancers for 1998–2002 were obtained from 37 population-based central cancer registries, representing 66% of the Hispanic population in the United States. Age-adjusted incidence rates (2000 US) were computed by race/ethnicity, sex, anatomic subsite, and histology. The differences in incidence rates between Hispanics and non-Hispanics were examined using the two-tailed z-statistic. Results  Squamous cell carcinoma accounted for 50% and 57% of esophageal cancers among Hispanic men and women, respectively, while adenocarcinoma accounted for 43% among Hispanic men and 35% among Hispanic women. The incidence rate of squamous cell carcinoma was 48% higher among Hispanic men (2.94 per 100,000) than non-Hispanic white men (1.99 per 100,000) but about 70% lower among Hispanics than non-Hispanic blacks, for both men and women. In contrast, the incidence rates of esophageal adenocarcinoma were lower among Hispanics than non-Hispanic whites (58% lower for men and 33% for women) but higher than non-Hispanic blacks (70% higher for men and 64% for women). Cardia adenocarcinoma accounted for 10–15% of gastric cancers among Hispanics, and the incidence rate among Hispanic men (2.42 per 100,000) was 33% lower than the rate of non-Hispanic white men (3.62 per 100,000) but 37% higher than that of non-Hispanic black men. The rate among Hispanic women (0.86 per 100,000), however, was 20% higher than that of non-Hispanic white women (0.72 per 100,000) and 51% higher than for non-Hispanic black women. Gastric non-cardia cancer accounted for approximately 50% of gastric cancers among Hispanics (8.32 per 100,000 for men and 4.90 per 100,000 for women), and the rates were almost two times higher than for non-Hispanic whites (2.95 per 100,000 for men and 1.72 per 100,000 for women) but about the same as the non-Hispanic blacks. Conclusion  Subsite- and histology-specific incidence rates of esophageal and gastric cancers among Hispanics/Latinos differ from non-Hispanics. The incidence rates of gastric non-cardia cancer are almost two times higher among Hispanics than non-Hispanic whites, both men and women. The rates of gastric cardia cancer are lower among Hispanics than non-Hispanic whites for men but higher for women. The rates of esophageal and gastric cardia adenocarcinomas are higher among Hispanics than non-Hispanic blacks. [ABSTRACT FROM AUTHOR]

Background: For more than 50 years, the traditional Mediterranean diet has been considered health-promoting, but it was not until the mid-1990s that the topic began to receive increased scrutiny and prominence.Objective: To highlight the health benefits of the Mediterranean diet as documented by studies undertaken mostly within a large countrywide general population cohort in Greece.Methods: The Greek EPIC (European Prospective Investigation into Cancer) cohort, a prospective study based on volunteers from the general population of Greece, and other investigations with converging objectives. In the Greek EPIC cohort of more than 28,000 volunteers being followed for more than 10 years, several findings on the association of diet with chronic diseases have been published in the international scientific literature.Results: The traditional Mediterranean diet of Greece is associated with reduced total mortality as well as reduced mortality from coronary heart disease and cancer. It is applicable in other Western populations, where it has also been shown to be inversely related to total mortality. Moreover, the traditional Mediterranean diet may be optimal for patients who have suffered a coronary infarct, and it does not promote obesity. Traditional foods are integral components of the Mediterranean diet and may contribute to its health-promoting attributes.Conclusions: The traditional Mediterranean diet may be an optimal diet both for healthy people and for patients with coronary heart disease and other chronic conditions. [ABSTRACT FROM AUTHOR]