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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) srt2:(2010-2014)"

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  • Antoniou, A. C., et al. (författare)
  • Common breast cancer susceptibility alleles and the risk of breast cancer for BRCA1 and BRCA2 mutation carriers : Implications for risk prediction
  • 2010
  • Ingår i: Cancer Research. - American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 70:23, s. 9742-9754
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The known breast cancer susceptibility polymorphisms in FGFR2, TNRC9/TOX3, MAP3K1, LSP1, and 2q35 confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. We evaluated the associations of 3 additional single nucleotide polymorphisms (SNPs), rs4973768 in SLC4A7/NEK10, rs6504950 in STXBP4/COX11, and rs10941679 at 5p12, and reanalyzed the previous associations using additional carriers in a sample of 12,525 BRCA1 and 7,409 BRCA2 carriers. Additionally, we investigated potential interactions between SNPs and assessed the implications for risk prediction. The minor alleles of rs4973768 and rs10941679 were associated with increased breast cancer risk for BRCA2 carriers (per-allele HR = 1.10, 95% CI: 1.03-1.18, P = 0.006 and HR = 1.09, 95% CI: 1.01-1.19, P = 0.03, respectively). Neither SNP was associated with breast cancer risk for BRCA1 carriers, and rs6504950 was not associated with breast cancer for either BRCA1 or BRCA2 carriers. Of the 9 polymorphisms investigated, 7 were associated with breast cancer for BRCA2 carriers (FGFR2, TOX3, MAP3K1, LSP1, 2q35, SLC4A7, 5p12, P = 7 × 10-11 - 0.03), but only TOX3 and 2q35 were associated with the risk for BRCA1 carriers (P = 0.0049, 0.03, respectively). All risk-associated polymorphisms appear to interact multiplicatively on breast cancer risk for mutation carriers. Based on the joint genotype distribution of the 7 risk-associated SNPs in BRCA2 mutation carriers, the 5% of BRCA2 carriers at highest risk (i.e., between 95th and 100th percentiles) were predicted to have a probability between 80% and 96% of developing breast cancer by age 80, compared with 42% to 50% for the 5% of carriers at lowest risk. Our findings indicated that these risk differences might be sufficient to influence the clinical management of mutation carriers.</p>
  • Johansson, J., et al. (författare)
  • MiR-155-mediated loss of C/EBP beta shifts the TGF-beta response from growth inhibition to epithelial-mesenchymal transition, invasion and metastasis in breast cancer
  • 2013
  • Ingår i: Oncogene. - Nature Publishing Group. - 0950-9232 .- 1476-5594. ; 32:50, s. 5614-5624
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>During breast cancer progression, transforming growth factor-beta (TGF-beta) switches from acting as a growth inhibitor to become a major promoter of epithelial-mesenchymal transition (EMT), invasion and metastasis. However, the mechanisms involved in this switch are not clear. We found that loss of CCAAT-enhancer binding protein beta (C/EBP beta), a differentiation factor for the mammary epithelium, was associated with signs of EMT in triple-negative human breast cancer, and in invasive areas of mammary tumors in MMTV-PyMT mice. Using an established model of TGF-beta-induced EMT in mouse mammary gland epithelial cells, we discovered that C/EBP beta was repressed during EMT by miR-155, an oncomiR in breast cancer. Depletion of C/EBP beta potentiated the TGF-beta response towards EMT, and contributed to evasion of the growth inhibitory response to TGF-beta. Furthermore, loss of C/EBP beta enhanced invasion and metastatic dissemination of the mouse mammary tumor cells to the lungs after subcutaneous injection into mice. The mechanism by which loss of C/EBP beta promoted the TGF-beta response towards EMT, invasion and metastasis, was traced to a previously uncharacterized role of C/EBP beta as a transcriptional activator of genes encoding the epithelial junction proteins E-cadherin and coxsackie virus and adenovirus receptor. The results identify miR-155-mediated loss of C/EBP beta as a mechanism, which promotes breast cancer progression by shifting the TGF-beta response from growth inhibition to EMT, invasion and metastasis.</p>
  • Tiblom Ehrsson, Ylva, et al. (författare)
  • Explorative study on the predictive value of systematic inflammatory and metabolic markers on weight loss in head and neck cancer patients undergoing radiotherapy
  • 2010
  • Ingår i: Supportive Care in Cancer. - 0941-4355 .- 1433-7339. ; 18:11, s. 1385-1391
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>PURPOSE: This study aimed to explore the predictive value of systematic inflammatory and metabolic markers in head and neck (H&amp;N) cancer patients during radiotherapy (RT). METHODS: Twenty-seven patients were evaluated. The protocol included serial blood tests [highly sensitive C-reactive protein (hsCRP), albumin, insulin-like growth factor 1 (IGF-1), IGF binding protein 1 (IGFBP-1) and ghrelin], measurements of body weight and assessment of oral mucositis. RESULTS: The mean nadir of weight loss was observed at the end of RT. At the time of diagnosis, mean hsCRP was 5.2 +/- 1.0 mg/L. HsCRP significantly increased during RT and decreased during the post-RT period. Mean maximum hsCRP was 35.8 +/- 8.5 mg/L, with seven patients reaching &gt;40 mg/L. A numerical decrease of albumin (by 18.2%) and only small changes in IGF-1, IGFBP-1 and ghrelin levels were observed. None of the metabolic parameters was significantly associated with weight loss. CONCLUSIONS: HsCRP increased in response to RT for H&amp;N cancer as a sign of irradiation-induced inflammation. Weight loss was not preceded by changes of the metabolic parameters, indicating that assessment of the blood markers used in this study is of little value. Regular body weight measurement and assessment of oral mucositis are feasible, cheap and important procedures to control the metabolic homeostasis during RT.</p>
  • Tilling, Kate, et al. (författare)
  • Development of a new method for monitoring prostate-specific antigen changes in men with localised prostate cancer : a comparison of observational cohorts
  • 2010
  • Ingår i: European Urology. - 0302-2838 .- 1873-7560. ; 57:3, s. 446-452
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: Prostate-specific antigen (PSA) measurements are increasingly used to monitor men with localised prostate cancer (PCa), but there is little consensus about the method to use. OBJECTIVE: To apply age-specific predictions of PSA level (developed in men without cancer) to one cohort of men with clinically identified PCa and one cohort of men with PSA-detected PCa. We hypothesise that among men with clinically identified cancer, the annual increase in PSA level would be steeper than in men with PSA-detected cancer. DESIGN, SETTING, AND PARTICIPANTS: The Scandinavian Prostate Cancer Group 4 (SPCG-4) cohort consisted of 321 men assigned to the watchful waiting arm of the SPCG-4 trial. The UK cohort consisted of 320 men with PSA-detected PCa in the Prostate testing for cancer and Treatment (ProtecT) study who opted for monitoring. Multilevel models describing changes in PSA level were fitted to the two cohorts, and average PSA level at age 50, change in PSA level with age, and predicted PSA values were derived. MEASUREMENTS: PSA level. RESULTS AND LIMITATIONS: In the SPCG-4 cohort, mean PSA at age 50 was similar to the cancer-free cohort but with a steeper yearly increase in PSA level (16.4% vs 4.0%). In the UK cohort, mean PSA level was higher than that in the cancer-free cohort (due to a PSA biopsy threshold of 3.0 ng/ml) but with a similar yearly increase in PSA level (4.1%). Predictions were less accurate for the SPCG-4 cohort (median difference between observed and predicted PSA level: -2.0 ng/ml; interquartile range [IQR]: -7.6-0.7 ng/ml) than for the UK cohort (median difference between observed and predicted PSA level: -0.8 ng/ml; IQR: -2.1-0.1 ng/ml). CONCLUSIONS: In PSA-detected men, yearly change in PSA was similar to that in cancer-free men, whereas in men with symptomatic PCa, the yearly change in PSA level was considerably higher. Our method needs further evaluation but has promise for refining active monitoring protocols.</p>
  • Wallin, Åsa, 1976-, et al. (författare)
  • Gene expression profile of colon cancer cell lines treated with SN-38
  • 2010
  • Ingår i: Chemotherapy. - S. Karger AG. - 0009-3157 .- 1421-9794. ; 56:1, s. 17-25
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Aim: Colorectal cancer is the third most common form of cancer in the industrialcountries. Due to advances regarding the treatments, primarily development ofimproved surgical methods, and the ability to make the earlier diagnosis, the mortalityhas remained constant during the past decades even though the incidence in fact hasincreased. To improve chemotherapy and enable personalised treatment, the need ofbiomarkers is of great significance. In this study we evaluated the gene expressionprofiles of the colon cancer cell lines treated with SN-38, the active metabolite oftopoisomerase-1 inhibitor irinotecan which leads to cell cycle arrest and apoptosis.Material and Methods: The study included three colon cancer cell lines KM12C,KM12SM and KM12l4a. The three cell lines were treated with SN-38, and sampleswere obtained after 24 and 48 hour treatments. The gene expression analyses wereperformed using oligonucleotide microarrays comprising of ~27,000 spots where theuntreated controls were compared to the SN-38 treated samples. Results: Unsupervisedclustering clearly distinguished the treated cell lines from the untreated. Supervisedanalysis identified 3974 significant genes (p=0.05) differentiating the treated samplesfrom the untreated, majority of which were downregulated after treatment. The toprankeddownregulated genes in the treated cell lines included those related to receptorand kinase activity, signal transduction, apoptosis, RNA processing, protein metabolismand transport, cell cycle and transcription. A smaller number of genes were upregulatedin the cell lines after treatment and included genes involved in apoptosis, transcription,development and differentiation. Conclusions: These results demonstrate that theexpression of the genes involved in cell proliferation and apoptosis as well as RNA,DNA and protein metabolism were affected by SN-38. The impact of certain genes oncolorectal cancer development needs to be further evaluated, however these resultscould serve as a basis for further studies in order to find targets for irinotecan treatment.</p>
  • Brännström, Fredrik, et al. (författare)
  • Surgeon and hospital-related risk factors in colorectal cancer surgery
  • 2011
  • Ingår i: Colorectal Disease. - Wiley-Blackwell. - 1462-8910 .- 1463-1318. ; 13:12, s. 1370-1376
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>AIM</strong>: The aim of this study was to identify surgeon and hospital-related factors in a well-defined population-based cohort; the results of this study could possibly be used to improve outcome in colorectal cancer.</p><p><strong>METHOD</strong>: Data from the colonic (1997-2006) and rectal (1995-2006) cancer registers of the Uppsala/Örebro Regional Oncology Centre were used to assess 1697 patients with rectal and 2692 with colonic cancer. Putative risk factors and their impact on long-term survival were evaluated using the Cox proportional hazard model.</p><p><strong>RESULTS</strong>: The degree of specialization of the operating surgeon had no significant effect on long-term survival. When comparing the surgeons with the highest degree of specialization, noncolorectal surgeons demonstrated a slightly lower long-term survival for rectal cancer stage I and II (HR, 2.03; 95% CI, 1.05-3.92). Surgeons with a high case-load were not associated with better survival in any analysis model. Regional hospitals had a lower survival rate for rectal cancer stage III surgery (HR, 1.47; 95% CI, 1.08-2.00).</p><p><strong>CONCLUSION</strong>: Degree of specialization, surgeon case-load and hospital category could not be identified as important factors when determining outcome in colorectal cancer surgery in this study.</p>
  • Burgu, Berk, et al. (författare)
  • An unusual cause of infantile gynecomastia: sertoli cell tumor.
  • 2011
  • Ingår i: Journal of pediatric hematology/oncology. - 1536-3678. ; 33:3, s. 238-40
  • Tidskriftsartikel (refereegranskat)abstract
    • Prepubertal testicular masses are relatively rare. Sertoli cell tumors account for 2% of prepubertal testicular tumors and very few have occurred in the first decade of life. Gynecomastia can be seen in approximately 5% of patients with testicular mass. We present an 8-month-old boy admitted with bilateral gynecomastia and unilateral testicular mass.
  • Försti, Asta, et al. (författare)
  • Polymorphisms in the transforming growth factor beta 1 pathway in relation to colorectal cancer progression
  • 2010
  • Ingår i: Genes, Chromosomes and Cancer. - New York : Liss. - 1045-2257 .- 1098-2264. ; 49:3, s. 270-281
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Transforming growth factor beta1 (TGFB1) acts as a growth inhibitor of normal colonic epithelial cells, however, as a tumor promoter of colorectal cancer (CRC) cells. To explore the association between genetic polymorphisms in the TGFB1 pathway and CRC susceptibility and clinical outcome, we carried out a case-control study on a Swedish population of 308 CRC cases and 585 age- and gender-matched controls. The cases were sampled prospectively and had up to 16 years follow-up, making the study material particularly suitable for survival analysis. On the basis of their reported or predicted functional effect, nine single-nucleotide polymorphisms (TGFB1: Leu10Pro; TGFBR1: 9A/6A and IVS7G+24A; FURIN: C-229T; THBS1: T+42C; LTBP1L: C-256G; LTBP4: T-893G and Thr750Ala; BAMBI: T-779A) were selected for genotyping. We evaluated the associations between genotypes and CRC and Dukes' stage. Survival probabilities were compared between different subgroups. The observed statistically significant associations included a decreased CRC risk for TGFBR1 IVS7G+24A minor allele carriers (odds ratio (OR): 0.72, 95% confidence interval (CI): 0.53-0.97), less aggressive tumors with Dukes' stage A+B for carriers of LTBP4 Thr750Ala and BAMBI T-779A minor alleles (OR: 0.58, 95%CI: 0.36-0.93 and OR: 0.51, 95%CI: 0.29-0.89, respectively) and worse survival for FURIN C-229T heterozygotes (hazard ratio: 1.63, 95%CI: 1.08-2.46). As this is the first study about the influence of the polymorphisms in the TGFB1 pathway on CRC progression, further studies in large independent cohorts are warranted.</p>
  • Fallbjörk, Ulrika, 1967-, et al. (författare)
  • Differences between women who have and have not undergone breast reconstruction after mastectomy due to breast cancer
  • 2010
  • Ingår i: Acta Oncologica. - Taylor & Francis. - 0284-186X .- 1651-226X. ; 49:2, s. 174-179
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Aim<em>:</em> This study compares potential differences between women with breast cancer who after mastectomy had undergone breast reconstruction with those who had not. Material and methods:<em></em> All women (N=149) in the northern medical region of Sweden who had undergone mastectomy in 2003 received a self-reported questionnaire entitled “Life After Mastectomy (LAM)” that included standardized measures of sociodemographic, decision-making process, breast reconstruction (BR) yes or no, sexuality, and body image. SPSS was used for data processing. Results:<em></em> In total 85% of the women returned the questionnaire and of these 25% had undergone BR. In accordance with previous studies, we found that the mean age of the women in the BR group was significantly lower (52 vs. 64 years), they had a higher education, and a higher proportion were employed, influenced by the physician's opinion regarding BR, sexually active, and rated a negative impact concerning the factors attractiveness and body disclosure. A multiple regression analysis, however, showed that the choice to undergo breast reconstruction or not was only independently associated with age, feeling of attractiveness and sexual interest. Discussion:<em></em> Age explained most differences found between the two groups. When researchers try to identify what differentiates the groups of women who undergo reconstruction between those who do not undergo reconstruction after mastectomy, it is thus necessary to take into consideration that the meanings of mastectomy, body image, attractiveness and similar variables may vary due to the phase of a woman's life. In conclusion, considering the impact of age is of paramount importance in future studies for our understanding of women's experiences.</p>
  • Clendenen, Tess V., et al. (författare)
  • Circulating prolactin levels and risk of epithelial ovarian cancer
  • 2013
  • Ingår i: Cancer Causes and Control. - Springer Netherlands. - 0957-5243 .- 1573-7225. ; 24:4, s. 741-748
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Indirect evidence from experimental and epidemiological studies suggests that prolactin may be involved in ovarian cancer development. However, the relationship between circulating prolactin levels and risk of ovarian cancer is unknown.</p><p>We conducted a nested case-control study of 230 cases and 432 individually matched controls within three prospective cohorts to evaluate whether pre-diagnostic circulating prolactin is associated with subsequent risk of ovarian cancer. We also assessed whether lifestyle and reproductive factors are associated with circulating prolactin among controls.</p><p>Prolactin levels were significantly lower among post- versus pre-menopausal women, parous versus nulliparous women, and past versus never users of oral contraceptives in our cross-sectional analysis of controls. In our nested case-control study, we observed a non-significant positive association between circulating prolactin and ovarian cancer risk (ORQ4vsQ1 1.56, 95 % CI 0.94, 2.63, p trend 0.15). Our findings were similar in multivariate-adjusted models and in the subgroup of women who donated blood a parts per thousand yen5 years prior to diagnosis. We observed a significant positive association between prolactin and risk for the subgroup of women with BMI a parts per thousand yen25 kg/m(2) (ORQ4vsQ1 3.10, 95 % CI 1.39, 6.90), but not for women with BMI &lt; 25 kg/m(2) (ORQ4vsQ1 0.81, 95 % CI 0.40, 1.64).</p><p>Our findings suggest that prolactin may be associated with increased risk of ovarian cancer, particularly in overweight/obese women. Factors associated with reduced risk of ovarian cancer, such as parity and use of oral contraceptives, were associated with lower prolactin levels, which suggests that modulation of prolactin may be a mechanism underlying their association with risk.</p>
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