Publications

Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: a consortia-based evaluation and replication study

Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII®) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.

Bladder cancer mortality of workers exposed to aromatic amines: an updated analysis

Trends in mortality from coronary heart and cerebrovascular disease in Switzerland, 1969?87

Overweight and colorectal cancer risk.

Epidemiological studies on risk factors for colorectal cancer have focused mainly on diet. Weight and height have also been studied, partly because they reflect the balance between energy intake and expenditure in different age periods. Energy intake, body size, physical activity and colorectal cancer risk will be reviewed in this paper focusing mostly on recent data coming from Italian, English and Scandinavian studies. Overweight has long been recognised as a risk factor for hormone related and other cancers, including colorectal cancer. In addition, the epidemiological evidence consistently shows that physical activity reduces the risk of colon cancer. On the contrary, evidence on rectal cancer is less impressive. In conclusion, body size control along all life and physical activity represent important factors to prevent colon cancer and a wide range of chronic conditions. Therefore, strategies to favour these goals through counselling from health-care providers, regulatory changes, and programs aimed at individuals and communities should be implemented.

Supplementary Figures S1-S7 from Leveraging Tissue-Specific Enhancer–Target Gene Regulatory Networks Identifies Enhancer Somatic Mutations That Functionally Impact Lung Cancer

&lt;p&gt;Supplementary Figures S1-S7&lt;/p&gt;

Adrenergic signaling induces a pro-tumorigenic B cell state in colorectal cancer

Abstract The importance of neuron-tumor crosstalk has gained increasing attention, yet its influence on the cellular and molecular landscape of colorectal cancer (CRC) remains largely unexplored. Here, we show that colonic innervation shapes the tumor immune microenvironment in a murine model of colitis-associated CRC. Although neuronal density does not affect tumor number, size, or overall burden, transcriptomic profiling of cells isolated from the tumor of hypo-innervated mice revealed extensive differential gene expression, including genes involved in immunoglobulin (Ig) signaling and the cancer-relevant hallmark ‘avoiding immune destruction’. Flow cytometry analysis of leukocyte populations demonstrated a significant reduction of B cells in the cancerous colon of hypo-innervated mice, notably a decrease in germinal center B cells and an altered class-switching profile, characterized by reduced IgA and increased IgD expression. Fluorescence and transmission electron microscopy showed that colonic B cells are primarily localized in the submucosa near neuronal processes containing varicose release sites, suggesting direct neuron-B cell interactions. Functional assays revealed that adrenergic stimulation of B cells promotes their proliferation and maturation, enhances IL-10 secretion, and alters immunoglobulin profiles. Strikingly, the transcriptome of epinephrine-treated B cells closely mirrors that of plasma cells from human CRC tissues, and the transcriptomic signature of these epinephrine-stimulated B cells associates with poorer patient survival. Together, these findings uncover an adrenergic neuron - B cell axis in CRC, providing evidence for direct neuroimmune interactions that affect B cell maturation and may influence tumor progression and therapeutic responses.

Lung cancer mortality in European women: recent trends and perspectives

Dietary glycemic load and gastric cancer risk in Italy

We investigated gastric cancer risk in relation to dietary glycemic index (GI) and glycemic load (GL), which represent indirect measures of carbohydrate absorption and consequently of dietary insulin demand, in a case-control study conducted in northern Italy between 1997 and 2007, including 230 patients with the incident, histologically confirmed gastric cancer and 547 frequency matched controls, admitted to the same hospitals as cases with acute non-neoplastic conditions. We used conditional logistic regression models, including terms for major recognised gastric cancer risk factors and non-carbohydrate energy intake. The odds ratios (ORs) in the highest vs lowest quintile were 1.9 (95% CI: 1.0-3.3) for GI and 2.5 (95% CI: 1.3-4.9) for GL. Compared with participants reporting low GL and high fruits/vegetables intake, the OR rose across strata of high GL and low fruits/vegetables, to reach 5.0 (95% CI: 2.2-11.5) for those reporting low fruits/vegetables intake and high GL. Our study may help to explain the direct relation observed in several studies between starchy foods and gastric cancer risk.

Long-term oral contraceptive use increased the risk of cervical cancer in HPV-positive women

Second neoplasms after oesophageal cancer

The authors considered the incidence of second neoplasms among 1,672 oesophageal cancers diagnosed between 1974 and 2004 in the Cancer Registries of the Swiss Cantons of Vaud and Neuchâtel, and followed-up to 2004. A total of 141 second neoplasms were observed versus 38.5 expected, corresponding to a standardized incidence ratio (SIR) of 3.7 (95% confidence interval: 3.1-4.3). The SIRs were statistically significant for cancers of the oral cavity and pharynx (57.3), larynx (24.3), lung (6.6) and intestines (2.6). The SIRs were higher in subjects diagnosed below age 50 and in the first year after diagnosis. The SIR of upper digestive and respiratory tract neoplasms was higher for oesophageal cancers diagnosed in the upper (87.5) and middle (68.1), as compared with the lower third (19.4). There was no rise of second oral, pharyngeal and laryngeal cancer with advancing age, and their incidence tended indeed to decline from 100/1,000 at age 40-49 to 25/1,000 at age 70-79. There was no tendency to rise with age in the incidence of first oesophageal cancer in subjects who subsequently developed another upper digestive or respiratory tract neoplasm. The excess risks of upper digestive and respiratory tract neoplasms are attributable to increased diagnosis and registration of second neoplasms following a diagnosis of oesophageal cancer, as well as to heavy tobacco and alcohol consumption in oesophageal cancer cases. The absence of rise in incidence with age is also compatible with the existence of a subset of the population of susceptible individuals.

Glycemic load in relation to hepatocellular carcinoma among patients with chronic hepatitis infection

Cervical cancer mortality among young women in Latin America and the Caribbean: trend analysis from 1997 to 2030

Mortality trends of cervical cancer among young women have large variability in LAC countries. Cervical cancer screening programs have a high priority for the region. Primary and secondary prevention in the community are necessary to accelerate a reduction of cervical cancer mortality by 2030.

Tea consumption and cancer risk

The relationship between tea consumption and cancer risk has been analyzed using data from an integrated series of case-control studies conducted in northern Italy between 1983 and 1990. The dataset included 119 histologically confirmed cancers of the oral cavity and pharynx, 294 of the esophagus, 564 of the stomach, 673 of the colon, 406 of the rectum, 258 of the liver, 41 of the gallbladder, 303 of the pancreas, 149 of the larynx, 2,860 of the breast, 567 of the endometrium, 742 of the ovary, 107 of the prostate, 365 of the bladder, 147 of the kidney, 120 of the thyroid, and a total of 6,147 controls admitted to hospital for acute nonneoplastic conditions unrelated to long-term dietary modifications. Multivariate relative risks (RR) for tea consumption were derived after allowance for age, sex, area of residence, education, smoking, and coffee consumption. All the estimates for tea consumption were close to unity, the highest values being 1.4 for rectum, gallbladder, and endometrium. There was no association with cancers of the oral cavity (RR = 0.6), esophagus (RR = 1.0), stomach (RR = 1.0), bladder (RR = 0.8), kidney (RR = 1.1), prostate (RR = 0.9), or any other site considered. Although in northern Italy tea was consumed daily by only a limited proportion of the population, this integrated series of studies offers further reassuring evidence on the relationship between tea and cancer risk.

Nitrosamine intake and gastric cancer risk

The association between intake of N-nitrosodimethylamine (NDMA), the most commonly occurring of the volatile nitrosamines derived from foods, and gastric cancer risk has been investigated using data from a case-control study conducted in Northern Italy between 1985 and 1993, including 746 incident cases of gastric cancer and 2,053 controls admitted to hospital for acute, non-neoplastic and non-digestive tract diseases, not related to long-term modifications of diet. Information was collected on frequency of consumption of 29 food items, including selected sources of NDMA. Compared with subjects in the lowest tertile of NDMA intake, the odds ratios (ORs) were 1.1 in the intermediate and 1.6 in the highest tertile of intake. These estimates were not appreciably modified after allowance for total energy intake, other major dietary and non-dietary correlates of gastric cancer, and estimated intake of nitrite and nitrate: the multivariate OR for the highest NDMA intake tertile was 1.4 (95% CI 1.1-1.7). The association was consistent across strata of sex and age, but somewhat stronger in males and in subjects below age 60 (OR in the highest tertile, 1.8). Limitations of exposure assessment and absence of information on other N-nitrosamines preclude, however, any definite assessment of the possible role of exogenous N-nitrosamines in gastric carcinogenesis.

Persistence with oral and transdermal hormone replacement therapy and hospitalisation for cardiovascular outcomes

SFigure2 from Cyclic Fasting–Mimicking Diet Plus Bortezomib and Rituximab Is an Effective Treatment for Chronic Lymphocytic Leukemia

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Cancer Mortality in a Cohort of Continuous Glass Filament Workers

Although limited in size, this study provides no evidence that continuous glass filament workers experience a significant increased risk of cancer, including respiratory cancer.

Number of siblings and subsequent gastric cancer risk

The number of siblings is an indirect indicator of living and, possibly, dietary conditions in childhood and adolescence. The relationship between the number of siblings and subsequent gastric cancer risk was analysed using data from a case--control study conducted in Italy between 1985 and 1992 on 723 cases of incident, histologically confirmed gastric cancer and 2,024 controls in hospital for acute, non-neoplastic, non-digestive tract disorders. After allowance for age and sex, there was a significant trend of increasing gastric cancer risk with increasing number of siblings (P < 0.01). Compared with subjects with no siblings, the relative risk (RR) was 1.1 for those with one, 1.3 for 2, 1.4 for 3-6 and 1.7 for 7 or more siblings. The association was stronger in subjects above the age of 60: the RR for > or = 5 siblings was 1.8, as compared with 1.2 for younger subjects. These patterns of trends are consistent with the hypothesis that domestic crowding and deprivation in childhood and adolescence is a correlate of subsequent gastric cancer risk, and offer therefore interesting clues to our understanding of the process of gastric carcinogenesis.