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  • Resultat 961-970 av 1473
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961.
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962.
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963.
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964.
  • Murovska, Modra, et al. (författare)
  • Human retrovirus 5 sequences in peripheral blood cells of patients with B-cell non-Hodgkin's lymphoma
  • 2000
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 85:6, s. 762-70
  • Tidskriftsartikel (refereegranskat)abstract
    • A recently described sequence from a probable 5th human exogenous retrovirus, HRV-5, is related to type A, B and D retroviruses. It was initially detected in a salivary gland biopsy from a patient with Sjögren's syndrome, but it is not consistently associated with this disease. We searched for the HRV-5 sequence in DNA extracted from whole blood of 300 blood donors, 81 patients with hematological malignancy and 21 patients with neurological disease using PCR. While samples from none of the blood donors and the neurological patients became positive, 3 of the 81 patients with hematological malignancy were HRV-5 DNA positive. All 3 had B-cell non-Hodgkin's lymphoma of low grade. The difference in frequency between NHL and controls is statistically significant. HRV-5 DNA was found in DNA from whole blood and in plastic-adherent cells but not in tumor cell DNA. Thus, monocytes/macrophages may be preferred targets for HRV-5. Our result, together with a previous finding of HRV-5 DNA in 2 NHL cases, is compatible with an association between HRV-5 and NHL, whether causal or not.
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965.
  • Murphy, Neil, et al. (författare)
  • A prospective evaluation of plasma polyphenol levels and colon cancer risk
  • 2018
  • Ingår i: International Journal of Cancer. - : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 143:7, s. 1620-1631
  • Tidskriftsartikel (refereegranskat)abstract
    • Polyphenols have been shown to exert biological activity in experimental models of colon cancer; however, human data linking specific polyphenols to colon cancer is limited. We assessed the relationship between pre-diagnostic plasma polyphenols and colon cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition study. Using high pressure liquid chromatography coupled to tandem mass spectrometry, we measured concentrations of 35 polyphenols in plasma from 809 incident colon cancer cases and 809 matched controls. We used multivariable adjusted conditional logistic regression models that included established colon cancer risk factors. The false discovery rate (qvalues ) was computed to control for multiple comparisons. All statistical tests were two-sided. After false discovery rate correction and in continuous log2 -transformed multivariable models, equol (odds ratio [OR] per log2 -value, 0.86, 95% confidence interval [95% CI] = 0.79-0.93; qvalue  = 0.01) and homovanillic acid (OR per log2 -value, 1.46, 95% CI = 1.16-1.84; qvalue  = 0.02) were associated with colon cancer risk. Comparing extreme fifths, equol concentrations were inversely associated with colon cancer risk (OR = 0.61, 95% CI = 0.41-0.91, ptrend  = 0.003), while homovanillic acid concentrations were positively associated with colon cancer development (OR = 1.72, 95% CI = 1.17-2.53, ptrend  < 0.0001). No heterogeneity for these associations was observed by sex and across other colon cancer risk factors. The remaining polyphenols were not associated with colon cancer risk. Higher equol concentrations were associated with lower risk, and higher homovanillic acid concentrations were associated with greater risk of colon cancer. These findings support a potential role for specific polyphenols in colon tumorigenesis.
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966.
  • Myte, Robin, et al. (författare)
  • Metabolic factors and the risk of colorectal cancer by KRAS and BRAF mutation status
  • 2019
  • Ingår i: International Journal of Cancer. - : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 145:2, s. 327-337
  • Tidskriftsartikel (refereegranskat)abstract
    • Factors related to energy metabolism and the metabolic syndrome, such as higher body mass index (BMI), blood glucose, or blood lipids, and blood pressure, are associated with an increased risk of colorectal cancer (CRC). However, CRC is a heterogeneous disease, developing through distinct pathways with differences in molecular characteristics and prognosis, and possibly also in risk factors. For subtypes defined by KRAS and BRAF mutation status, BMI is the only metabolic factor previously studied, with inconsistent findings. We investigated whether associations between BMI, blood glucose, blood lipids, and blood pressure and CRC risk differed by tumor KRAS and BRAF mutation status in 117,687 participants from two population-based cohorts within the Northern Sweden Health and Disease Study (NSHDS). Hazard ratios (HRs) for overall CRC and CRC subtypes by metabolic factors were estimated with Cox proportional hazards regression, using multiple imputation to handle missing exposure and tumor data. During a median follow-up of 15.6 years, we acquired 1,250 prospective CRC cases, of which 766 cases had complete baseline and molecular tumor data. Consistent with previous evidence, higher BMI, total cholesterol, triglyceride levels, and blood pressure were associated with an increased risk of overall CRC (HRs per 1 standard deviation increase: 1.07 to 1.12). These associations were similar regardless of CRC subtype by KRAS and BRAF mutation status (all pheterogeneity > 0.05). The same was true for subtypes based on microsatellite instability status. Poor metabolic health may therefore be a universal mechanism for colorectal cancer, acting across multiple developmental pathways.
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967.
  • Möller, Henrik, et al. (författare)
  • Breast cancer survival in England, Norway and Sweden : a population-based comparison
  • 2010
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 127:11, s. 2630-2638
  • Tidskriftsartikel (refereegranskat)abstract
    • Several international studies have found that survival from breast cancer is lower in the United Kingdom than in some other European countries. We have compared breast cancer survival between the national populations of England, Norway and Sweden, with a view to identifying subsets of patients with particularly good or adverse survival outcomes. We extracted cases of breast cancer in women diagnosed 1996-2004 from the national cancer registries of the 3 countries. The study comprised 303,657 English cases, 24,919 Norwegian cases and 57,512 cases from Sweden. Follow-up was in 2001-2004. The main outcome measures were 5-year cumulative relative survival and excess death rates, stratified by age and period of follow-up. In comparison with Norway and Sweden, the excess mortality in England was particularly pronounced in the first month and in the first year after diagnosis, and generally more marked in the oldest age groups. Compared with Norwegian patients, 81% of the excess deaths in the English patients occurred in the first 2 years after diagnosis. Our findings emphasise the importance of awareness of symptoms and early detection as the main strategy to improve breast cancer survival in the United Kingdom.
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968.
  • Møller, Henrik, et al. (författare)
  • Prostate cancer incidence, clinical stage and survival in relation to obesity : A prospective cohort study in Denmark.
  • 2015
  • Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 136:8, s. 1940-1947
  • Tidskriftsartikel (refereegranskat)abstract
    • There is no clear link between obesity and prostate cancer incidence but an association has been reported between obesity and fatal prostate cancer. We report on two prospective cohort analyses on (i) the incidence of prostate cancer in relation to obesity in a cohort of men with no previous cancer, and on (ii) the stage distribution and prostate cancer specific mortality in relation to obesity among men with prostate cancer. The "Diet, Cancer and Health" prospective cohort study was established in Denmark in 1993-1997 and accrued 26,944 men aged 50-64 years. Data were extracted on height, weight, body mass index (BMI), waist circumference and body fat percentage. Information on cancer incidence and deaths were obtained by record linkage with the Danish Cancer Register and the Danish Death Register. The incidence rate of prostate cancer was similar or slightly lower in obese men compared with nonobese men, but obese men tended to be diagnosed with more advanced prostate cancer. The proportion of Stage 3-4 cancers was 37% in the lowest BMI quartile and 48% in the highest (p = 0.006). Obese men with prostate cancer had higher prostate cancer specific mortality. The hazard ratio comparing the highest and the lowest quartiles of BMI was 1.48 (95% confidence interval: 1.06-2.05; p-value for trend: 0.002). The association was attenuated but not eliminated by statistical adjustment for stage, and the data are suggestive of a stage-independent causal pathway where prostate cancer in obese men has higher fatality, even in early-stage disease.
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969.
  • Nadeem, Aftab, et al. (författare)
  • Suppression of β-catenin signaling in colon carcinoma cells by a bacterial protein
  • 2021
  • Ingår i: International Journal of Cancer. - : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 149:2, s. 442-459
  • Tidskriftsartikel (refereegranskat)abstract
    • Colorectal cancer is one of the leading causes of cancer-related death worldwide. The adenomatous polyposis coli (APC) gene is mutated in hereditary colorectal tumors and in more than 80% of sporadic colorectal tumors. APC mutations impair β-catenin degradation, leading to its permanent stabilization and increased transcription of cancer-driving target genes. In colon cancer, impairment of β-catenin degradation leads to its cytoplasmic accumulation, nuclear translocation, and subsequent activation of tumor cell proliferation. Suppressing β-catenin signaling in cancer cells therefore appears to be a promising strategy for new anticancer strategies. Recently, we discovered a novel Vibrio cholerae cytotoxin, motility-associated killing factor A (MakA), that affects both invertebrate and vertebrate hosts. It promotes bacterial survival and proliferation in invertebrate predators but has unknown biological role(s) in mammalian hosts. Here, we report that MakA can cause lethality of tumor cells via induction of apoptosis. Interestingly, MakA exhibited potent cytotoxic activity, in particular against several tested cancer cell lines, while appearing less toxic toward nontransformed cells. MakA bound to the tumor cell surface became internalized into the endolysosomal compartment and induced leakage of endolysosomal membranes, causing cytosolic release of cathepsins and activation of proapoptotic proteins. In addition, MakA altered β-catenin integrity in colon cancer cells, partly through a caspase- and proteasome-dependent mechanism. Importantly, MakA inhibited β-catenin-mediated tumor cell proliferation. Remarkably, intratumor injection of MakA significantly reduced tumor development in a colon cancer murine solid tumor model. These data identify MakA as a novel candidate to be considered in new strategies for development of therapeutic agents against colon cancer.
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970.
  • Nagel, Gabriele, et al. (författare)
  • Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE)
  • 2018
  • Ingår i: International Journal of Cancer. - : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 143:7, s. 1632-1643
  • Tidskriftsartikel (refereegranskat)abstract
    • Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancersof the stomach and upper aerodigestive tract (UADT). We investigated the association of long-term exposure to ambient airpollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land-useregression models for particulate matter (PM) below 10mm (PM10), below 2.5mm (PM2.5), between 2.5 and 10mm (PMcoarse),PM2.5absorbance and nitrogen oxides (NO2and NOX) as well as approximated by traffic indicators. Cox regression modelswith adjustment for potential confounders were used for cohort-specific analyses. Combined estimates were determined withrandom effects meta-analyses. During average follow-up of 14.1 years of 305,551 individuals, 744 incident cases of gastriccancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5mg/m3of PM2.5was 1.38 (95% CI 0.99; 1.92)for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures consid-ered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influencemarkedly the effect estimate for PM2.5and gastric cancer. Higher estimated risks of gastric cancer associated with PM2.5wasfound in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study showsan association between long-term exposure to PM2.5and gastric cancer, but not UADT cancers, suggesting that air pollutionmay contribute to gastric cancer risk.
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