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Sökning: L773:0143 3334

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211.
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212.
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213.
  • Sinnott, Jennifer A., et al. (författare)
  • Molecular differences in transition zone and peripheral zone prostate tumors
  • 2015
  • Ingår i: Carcinogenesis. - Oxford, United Kingdom : Oxford University Press. - 0143-3334 .- 1460-2180. ; 36:6, s. 632-638
  • Tidskriftsartikel (refereegranskat)abstract
    • Prostate tumors arise primarily in the peripheral zone (PZ) of the prostate, but 20-30% arise in the transition zone (TZ). Zone of origin may have prognostic value or reflect distinct molecular subtypes; however, it can be difficult to determine in practice. Using whole-genome gene expression, we built a signature of zone using normal tissue from five individuals and found that it successfully classified nine tumors of known zone. Hypothesizing that this signature captures tumor zone of origin, we assessed its relationship with clinical factors among 369 tumors of unknown zone from radical prostatectomies (RPs) and found that tumors that molecularly resembled TZ tumors showed lower mortality (P = 0.09) that was explained by lower Gleason scores (P = 0.009). We further applied the signature to an earlier study of 88 RP and 333 transurethral resection of the prostate (TURP) tumor samples, also of unknown zone, with gene expression on ~6000 genes. We had observed previously substantial expression differences between RP and TURP specimens, and hypothesized that this might be because RPs capture primarily PZ tumors, whereas TURPs capture more TZ tumors. Our signature distinguished these two groups, with an area under the receiver operating characteristic curve of 87% (P < 0.0001). Our findings that zonal differences in normal tissue persist in tumor tissue and that these differences are associated with Gleason score and sample type suggest that subtypes potentially resulting from different etiologic pathways might arise in these zones. Zone of origin may be important to consider in prostate tumor biomarker research.
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214.
  • SKOG, K, et al. (författare)
  • EFFECT OF COOKING TEMPERATURE ON THE FORMATION OF HETEROCYCLIC AMINES IN FRIED MEAT-PRODUCTS AND PAN RESIDUES
  • 1995
  • Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 16:4, s. 861-867
  • Tidskriftsartikel (refereegranskat)abstract
    • Frequent consumers of meat have an increased risk of colorectal cancer and possibly also of breast, stomach, pancreas and urinary bladder cancer. Bacon, 'Falusausage', ground beef, meatballs, pork belly, pork chops and sliced beef account for more than one-third of the intake of fried meat of the population of Stockholm of age 50-75. These dishes were fried at four temperatures (150, 175, 200 and 225 degrees C) representing normal household cooking practices in Stockholm. Heterocyclic amines in these dishes were analysed using solid-phase extraction and HPLC. The heterocyclic amines 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,8-dimethylimidazo [4,5-f]quinoxaline (MeIQx), 2-amino-3,4,8-trimethylimidazo [4,5-f]quinoxaline (DiMeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were recovered. The formation of IQ was favoured by moderate cooking temperatures; IQ was detected in one meat sample cooked at 150 degrees C and in some pan residues. The yield of MeIQx, DiMeIQx and PhIP increased with the temperature. For several of the meat dishes, the content of heterocyclic amines in the pan residue was as large or larger than for corresponding piece of meat. The highest levels of MeIQx were 23.7 ng/g in the meat and 23.3 ng/g in the pan residue, Corresponding data for DiMeIQx were 2.7 and 4.1 ng/g and for PhIP 12.7 and 82.4 ng/g. The study leaves little doubt that mutagenic heterocyclic amines are ingested by the population of Stockholm, and added to previous epidemiological studies from the same area, the combined data are consistent with human carcinogenicity of heterocyclic amines, However, analytical epidemiological studies are needed before any statement on causality can be made.
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215.
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216.
  • Sonestedt, Emily, et al. (författare)
  • Plant foods and estrogen receptor {alpha} and {beta} defined breast cancer: observations from the Malmo Diet and Cancer cohort.
  • 2008
  • Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 29:11, s. 2203-2209
  • Tidskriftsartikel (refereegranskat)abstract
    • The associations between plant foods and breast cancer incidence are inconsistent. The objective of this study was to examine prospectively the association between dietary fibre, plant foods and breast cancer, especially the association between plant food intake and estrogen receptor (ER) alpha and beta defined breast cancer. Among women without prevalent cancer from the population-based prospective Malmö Diet and Cancer cohort (n = 15,773, 46-75 years at baseline), 544 women were diagnosed with incident invasive breast cancer during a mean follow-up of 10.3 years. Information on dietary habits was collected by a modified diet history method. ER status of the tumours was determined by immunohistochemistry using tissue microarray. Cox proportional hazards regression estimated hazard ratios (HR) and 95% confidence intervals (CI) of breast cancer associated with fibre and 11 plant food groups. High-fibre bread was significantly associated with a decreased breast cancer incidence (HR, 0.75, 95 % CI, 0.57-0.98, for highest compared to lowest quintile). The other plant food groups were not significantly associated with breast cancer incidence. There was a tendency for a negative association for high-fibre bread among ERalpha (+) breast cancer (p for trend = 0.06) and ERbeta (+) breast cancer (p for trend = 0.06). Fried potatoes were statistically significantly associated with increased risk of ERbeta (-) breast cancer (p = 0.01). This study suggests that different plant foods may be differently associated with breast cancer, with fibre-rich bread showing an inverse association. We did not observe strong evidence for differences in incidence according to the ER alpha and beta status of breast cancer.
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217.
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218.
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219.
  • Stenstrom, Bjorn, et al. (författare)
  • Swedish moist snuff accelerates gastric cancer development in Helicobacter pylori-infected wild-type and gastrin transgenic mice
  • 2007
  • Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 28:9, s. 2041-2046
  • Tidskriftsartikel (refereegranskat)abstract
    • The Swedish variant of moist oral smokeless tobacco (snus) is popular in Sweden and Norway, banned from sale within the European Union and is currently being introduced in USA. The aim of the present study was to determine if snus is carcinogenic to the stomach, particularly in Helicobacter pylori (H.P.)-infected hosts at increased risk for gastric cancer development. Snus (General (TM); Swedish Match, Sweden) was mixed with powdered standard mouse chow at a concentration of 5-9% (wt/wt) and given to wild-type (WT, FVB) and gastrin transgenic (INS-GAS, FVB) mice for 6 months with or without H.P. (strain 67:21, CagA(+), VacA(+)) infection. At necropsy, pathological evaluation of stomachs from uninfected snus-treated WT mice showed mild morphological changes, whereas 50% snus-treated INS-GAS mice developed carcinoma in situ (CIS), compared with 25% not exposed to snus. When snus was given to H.P.-infected mice, 9 of 17 WT mice developed CIS with intramucosal invasion, and the remaining 8 of 17 WT mice developed high-grade dysplasia (score > 1.5) that was associated with increased gastritis, epithelial defects, oxyntic atrophy, hyperplasia and intestinal metaplasia. Twelve of 12 H.P.-infected INS-GAS mice developed CIS with intramucosal invasion and submucosal herniation. We suggest that snus is a potential gastric carcinogen in mice. The development of CIS was associated with increased rates of the epithelial cell proliferation and apoptosis, common features of gastric carcinogenesis.
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220.
  • Stepien, Magdalena, et al. (författare)
  • Pre-diagnostic copper and zinc biomarkers and colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition cohort
  • 2017
  • Ingår i: Carcinogenesis. - : OXFORD UNIV PRESS. - 0143-3334 .- 1460-2180. ; 38:7, s. 699-707
  • Tidskriftsartikel (refereegranskat)abstract
    • Adequate intake of copper and zinc, two essential micronutrients, are important for antioxidant functions. Their imbalance may have implications for development of diseases like colorectal cancer (CRC), where oxidative stress is thought to be etiologically involved. As evidence from prospective epidemiologic studies is lacking, we conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort to investigate the association between circulating levels of copper and zinc, and their calculated ratio, with risk of CRC development. Copper and zinc levels were measured by reflection X-ray fluorescence spectrometer in 966 cases and 966 matched controls. Multivariable adjusted odds ratios (OR) and 95% confidence intervals (CI) were calculated using conditional logistic regression and are presented for the fifth versus first quintile. Higher circulating concentration of copper was associated with a raised CRC risk (OR = 1.50; 95% CI: 1.06, 2.13; P-trend = 0.02) whereas an inverse association with cancer risk was observed for higher zinc levels (OR = 0.65; 95% CI: 0.43, 0.97; P-trend = 0.07). Consequently, the ratio of copper/zinc was positively associated with CRC (OR = 1.70; 95% CI: 1.20, 2.40; P-trend = 0.0005). In subgroup analyses by follow-up time, the associations remained statistically significant only in those diagnosed within 2 years of blood collection. In conclusion, these data suggest that copper or copper levels in relation to zinc (copper to zinc ratio) become imbalanced in the process of CRC development. Mechanistic studies into the underlying mechanisms of regulation and action are required to further examine a possible role for higher copper and copper/ zinc ratio levels in CRC development and progression.
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