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  • Larsson, Susanna C., et al. (författare)
  • Meat intake and bladder cancer risk in a Swedish prospective cohort
  • 2009
  • Ingår i: Cancer Causes and Control. - Berlin : Springer. - 0957-5243 .- 1573-7225. ; 20:1, s. 35-40
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background  High meat consumption could potentially increase the risk of bladder cancer, but findings from epidemiologic studies are inconsistent. We prospectively examined the association between meat intake and bladder cancer risk in a population-based cohort study. Methods  We prospectively followed 82,002 Swedish women and men who were free from cancer and completed a food-frequency questionnaire in 1997. Incident cases of bladder cancer were identified in the Swedish cancer registries. Cox proportional hazards models were used to calculate hazard ratios (HR) with 95% confidence intervals (CI), adjusted for age, sex, education, smoking status, pack-years of smoking, and total energy intake. Results  During a mean follow-up of 9.4 years, 485 incident cases of bladder cancer (76 women and 409 men) were ascertained in the cohort. We observed no association between the intake of total or any specific type of meat and the risk of bladder cancer. The multivariate HRs (95% CIs) comparing the highest and the lowest category of intake were 1.05 (0.71–1.55) for total meat, 1.00 (0.71–1.41) for red meat, 1.01 (0.80–1.28) for processed meats, 0.96 (0.70–1.30) for chicken/poultry, and 0.92 (0.65–1.30) for fried meats/fish. The associations did not vary by sex or smoking status. Conclusions  These results do not support the hypothesis that intake of red meat, processed meat, poultry, or fried meats/fish is associated with the risk of developing bladder cancer.</p>
  • Mucci, Lorelei A., et al. (författare)
  • Testing a multigene signature of prostate cancer death in the Swedish Watchful Waiting Cohort
  • 2008
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Philadelphia : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 17:7, s. 1682-1688
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Although prostate cancer is a leading cause of cancer death, most men die with and not from their disease, underscoring the urgency to distinguish potentially lethal from indolent prostate cancer. We tested the prognostic value of a previously identified multigene signature of prostate cancer progression to predict cancer-specific death. The Örebro Watchful Waiting Cohort included 172 men with localized prostate cancer of whom 40 died of prostate cancer. We quantified protein expression of the markers in tumor tissue by immunohistochemistry and stratified the cohort by quintiles according to risk classification. We accounted for clinical variables (age, Gleason, nuclear grade, and tumor volume) using Cox regression and calculated receiver operator curves to compare discriminatory ability. The hazard ratio of prostate cancer death increased with increasing risk classification by the multigene model, with a 16-fold greater risk comparing highest-risk versus lowest-risk strata, and predicted outcome independent of clinical factors (P = 0.002). The best discrimination came from combining information from the multigene markers and clinical data, which perfectly classified the lowest-risk stratum where no one developed lethal disease; using the two lowest-risk groups as reference, the hazard ratio (95% confidence interval) was 11.3 (4.0-32.8) for the highest-risk group and difference in mortality at 15 years was 60% (50-70%). The combined model provided greater discriminatory ability (area under the curve = 0.78) than the clinical model alone (area under the curve = 0.71; P = 0.04). Molecular tumor markers can add to clinical variables to help distinguish lethal and indolent prostate cancer and hold promise to guide treatment decisions. </p>
  • Skirnisdottir, Ingiridur, et al. (författare)
  • Adjuvant chemotherapy with carboplatin and taxane compared with single drug carboplatin in early stage epithelial ovarian carcinoma
  • 2007
  • Ingår i: Oncology Reports. - Athens, Greece : National Hellenic Research Foundation. - 1021-335X .- 1791-2431. ; 18:5, s. 1249-1256
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The objective of the present study was to compare recurrence-free survival (RFS) in early stages (FIGO stages I-II) of epithelial ovarian cancer after adjuvant chemotherapy with carboplatin and a taxane (113 patients) and with carboplatin alone (27 patients). The distribution of clinical and pathological prognostic factors as well as type of primary surgery were comparable in the two groups. Recurrence rate was 21% and RFS was 79% in the series of patients treated with taxane-based chemotherapy and 19% and 81%, respectively, in the series of patients who received single drug carboplatin. Thus, no significant differences were recorded. The major toxicities in the present study were myelosuppression (46%) and neuro-toxicity (26%). Neurotoxicity was more frequently (P=0.007) recorded and of higher grade (P=0.011) for patients in the carboplatin-taxane series compared with patients in the carboplatin series. RFS for patients in FIGO-stage I was 85% and for patients in FIGOstage II only 47%. In a multivariate logistic regression analysis of predictive factors for tumor recurrence in the complete series (n=140) the FIGO stage was the only independent and significant (P=0.0006) predictive factor with an odds ratio of 6.4 (95% CI: 2.2-18.9) for stage II versus IA-C. Age, tumor grade and type of adjuvant chemotherapy (± taxane) were not significant predictive factors. In the present study, although based on a limited number of patients, we could not find any improvement in recurrence rate or recurrence-free survival for patients treated with a carboplatin-taxane combination regimen compared with patients treated with carboplatin monotherapy. The spectrum of side effects was also in favor of the monotherapy regimen. Further, larger randomized studies are needed to give a final and fully conclusive answer to this question.</p>
  • Grundberg, Ida, 1982-, et al. (författare)
  • Diagnostic mutation testing <em>in situ</em> in routine FFPE tissue sections for treatment prediction in clinical oncology
  • ????
  • Annan publikation (övrigt vetenskapligt)abstract
    • <p><strong>Activating mutations in the <em>KRAS</em> gene are present in different cancer types and are strongly associated with resistance to epidermal growth factor receptor (EGFR) inhibitor therapy. Hence there is a requirement for sensitive <em>KRAS </em>mutation analysis to determine the most suitable treatment for the patients. Also, little is known about the impact of tumor heterogeneity with regard to <em>KRAS</em> mutation status in different sub-clones during tumorigenesis, and if this is important for treatment response and prognosis.</strong> <strong>To improve the diagnostic accuracy, we developed an RNA-based genotyping assay that targets <em>KRAS</em>-mutations in codon 12 and 13 <em>in situ </em>on tissue samples by the use of multiple mutation specific padlock probes and rolling-circle amplification. Thus, the distribution of wild-type (green rolling-circle products) and mutated (red rolling-circle products) <em>KRAS</em> alleles can be determined for single cancer cells in different parts of a heterogeneous tumor without the use of microdissection. We demonstrate reliable detection of <em>KRAS </em>point mutations on cytologic tumor imprints as well as on fresh frozen and formalin-fixed paraffin-embedded tissue sections from colorectal and lung cancer. This <em>in situ</em> method offers single cell mutation detection for diagnostics and holds great promise as a tool to investigate the role of oncogenic mutations in complex tumor tissues.</strong></p>
  • Högberg, Thomas, et al. (författare)
  • Gynekologisk onkologi
  • 2008
  • Ingår i: Onkologi. - 2. - Stockholm : Liber. - 978-91-47-08401-2 ; s. 488-533
  • Bokkapitel (övrigt vetenskapligt)
  • H., Olsson, et al. (författare)
  • Tamoxifen treated patients have a better survival than patients treated with aromatase inhibitors - A population based registry study in Sweden
  • 2015
  • Ingår i: 37th San Antonio Breast Cancer Symposium,San Antonio, Texas, United States,2014-12-09 - 2014-12-13. - American Association for Cancer Research Inc..
  • Konferensbidrag (refereegranskat)abstract
    • Background. Randomised trials suggest that therapy with aromatase inhibitors improves survival in breast cancer compared with tamoxifen therapy in postmenopausal cases with hormone receptor positive breast cancer. Whether these results from randomized studies transform into the general population is unknown. We have therefore compared survival for all breast cancer cases in Sweden diagnosed 2000-2008 (n=54406) who received adjuvant antihormonal therapy. Material and methods. The study includes all women with BC diagnosed in Sweden between 2000 through 2008 (n=54406). The women had no previous cancer diagnosis during the period of 1958-1999. Dates of birth, BC diagnosis and TNM-stage where directly extracted from the cancer registry. The women's antihormonal therapy was gathered from the Swedish Prescription Registry (22213 women were on antihormonal therapy). Information regarding the cause of death and date of death was obtained from the Cause of Death Registry and tbe Swedish Population Register up until the 31st of December 2012 and 31st of December 2013 respectively. The breast cancer death and overall death have been calculated and the survival was compared between tamoxifen and aromatase inhibitor treated breast cancer patients. Analyses were adjusted for TNM-stage and age at diagnosis and restricted to women aged 50 and above. Results. Patients being treated with tamoxifen had a better breast cancer prognosis compared with aromatase inhibitor treated patients (HR 0.54, 95%CI 0.48-0.61). Restricting the analysis to stage 1 disease confirmed a better prognosis for tamoxifen treated women (HR 0.48, 95%CI 0.34-0.66). A better prognosis could be seen in all age strata studies, 50-60.61-70.71-90. The findings for overall survival gave similar results. Conclusion .This population based observational study show that women treated with aromatase inhibitors have a worse overall and breast cancer specific survival compared with tamoxifen treated women regardless of age and tumor stage.
  • Fall, Katja, et al. (författare)
  • Reliability of death certificates in prostate cancer patients
  • 2008
  • Ingår i: Scandinavian Journal of Urology and Nephrology. - 0036-5599 .- 1651-2065. ; 42:4, s. 352-357
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>OBJECTIVE: To evaluate the reliability of cause-of-death diagnoses among prostate cancer patients. MATERIAL AND METHODS: Information from death certificates obtained from the Swedish Death Register was compared with systematically reviewed medical records from the population-based Swedish Regional Prostate Cancer Register, South-East Region. In total, 5675 patients were included who had been diagnosed with prostate cancer between 1987 and 1999 and who had died before 1 January 2003. RESULTS: The proportion of prostate cancer cases classified as having died from prostate cancer was 3% higher in the official death certificates than in the reviewed records [0.03, 95% confidence interval (CI) 0.02 to 0.04]. Overall agreement between the official cause of death and the reviewed data was 86% (95% CI 85 to 87%). A higher accuracy was observed among men with localized disease (88%, 95% CI 87 to 89%), aged 60 years or younger at death (96%, 95% CI 93 to 100%), or who had undergone curative treatment (91%, 95% CI 88 to 95%). This study indicates a relatively high reliability of official cause-of-death statistics of prostate cancer patients in Sweden. CONCLUSION: Mortality data obtained from death certificates may be useful in the evaluation of large-scale prostate cancer intervention programmes, especially among younger patients with localized disease.</p>
  • Johansson, Eva, et al. (författare)
  • Time, Symptom Burden, Androgen Deprivation, and Self-Assessed Quality of Life after Radical Prostatectomy or Watchful Waiting : The Randomized Scandinavian Prostate Cancer Group Study Number 4 (SPCG-4) Clinical Trial
  • 2008
  • Ingår i: European Urology. - 0302-2838 .- 1873-7560. ; 55:2, s. 422-432
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: Quality-of-life outcomes are important in the choice of treatment strategy for men with localized prostate cancer.</p> <p>OBJECTIVE: To evaluate how follow-up time, number of physical symptoms, and presence of androgen deprivation affected quality of life among men randomized to radical prostatectomy or watchful waiting.</p> <p>DESIGN, SETTING, AND PARTICIPANTS: The study group was composed of all 376 living men included in the Swedish part of the Scandinavian Prostate Cancer Group Study Number 4 (SPCG-4) between January 1, 1989, and February 29, 1996. Quality-of-life data were collected after a mean follow-up time of 4.1 yr.</p> <p>INTERVENTION: All patients were randomly assigned to radical prostatectomy or watchful waiting. Forty-five men were androgen deprived.</p> <p>MEASUREMENTS: Data of specific symptoms, symptom-induced stress, sense of well-being, and self-assessed quality of life were obtained by means of a questionnaire. Psychological symptoms were assessed using seven-point visual digital scales.</p> <p>RESULTS AND LIMITATIONS: In analyses stratified on the basis of the numbers of physical symptoms, anxiety and depressed mood were less common, and sense of well-being and self-assessed quality of life were better throughout in the radical prostatectomy group than in the watchful waiting group. As the number of physical symptoms increased, all psychological variables became worse and more prominent in the watchful waiting group. After a follow-up time of 6-8 yr, a significant decrease in quality of life (p=0.03) was seen in the watchful waiting group. Twenty-four percent of androgen-deprived patients assigned to watchful waiting reported high self-assessed quality of life compared with 60% in the radical prostatectomy group. Eighty-eight percent of patients had clinically detected tumors.</p> <p>CONCLUSIONS: Androgen deprivation negatively affected self-assessed quality of life in men assigned to watchful waiting. The number of physical symptoms was associated with the level of quality of life. Quality of life was lower with longer follow-up time in both groups and was statistically significant in the watchful waiting group (p=0.03).</p>
  • Mucci, Lorelei A., et al. (författare)
  • Nine-gene molecular signature is not associated with prostate cancer death in a watchful waiting cohort
  • 2008
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Baltimore : Waverly Press. - 1055-9965 .- 1538-7755. ; 17:1, s. 249-251
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Tumor molecular markers hold promise to distinguish potentially lethal from indolent prostate cancer and to guide treatment choices. A previous study identified a nine-gene molecular signature in tumors associated with prostate-specific antigen relapse after prostatectomy. We examined this molecular model in relation to prostate cancer death among 172 men with initially localized disease. We quantified protein expression of the nine genes in tumors to classify progression risk. Accounting for clinical prognostic factors, the nine-gene model did not provide discrimination to predict lethal and indolent prostate cancer.</p>
  • Setlur, Sunita R., et al. (författare)
  • Estrogen-dependent signaling in a molecularly distinct subclass of aggressive prostate cancer
  • 2008
  • Ingår i: Journal of the National Cancer Institute. - Oxford : Oxford univ. press. - 0027-8874 .- 1460-2105. ; 100:11, s. 815-825
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: The majority of prostate cancers harbor gene fusions of the 5'-untranslated region of the androgen-regulated transmembrane protease serine 2 (TMPRSS2) promoter with erythroblast transformation-specific transcription factor family members. The common fusion between TMPRESS2 and v-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG) is associated with a more aggressive clinical phenotype, implying the existence of a distinct subclass of prostate cancer defined by this fusion. METHODS: We used complementary DNA-mediated annealing, selection, ligation, and extension to determine the expression profiles of 6144 transcriptionally informative genes in archived biopsy samples from 455 prostate cancer patients in the Swedish Watchful Waiting cohort (1987-1999) and the United States-based Physicians(') Health Study cohort (1983-2003). A gene expression signature for prostate cancers with the TMPRSS2-ERG fusion was determined using partitioning and classification models and used in computational functional analysis. Cell proliferation and TMPRSS2-ERG expression in androgen receptor-negative (NCI-H660) prostate cancer cells after treatment with vehicle or estrogenic compounds were assessed by viability assays and quantitative polymerase chain reaction, respectively. All statistical tests were two-sided. RESULTS: We identified an 87-gene expression signature that distinguishes TMPRSS2-ERG fusion prostate cancer as a discrete molecular entity (area under the curve = 0.80, 95% confidence interval [CI] = 0.792 to 0.81; P &lt; .001). Computational analysis suggested that this fusion signature was associated with estrogen receptor (ER) signaling. Viability of NCI-H660 cells decreased after treatment with estrogen (viability normalized to day 0, estrogen vs vehicle at day 8, mean = 2.04 vs 3.40, difference = 1.36, 95% CI = 1.12 to 1.62) or ERbeta agonist (ERbeta agonist vs vehicle at day 8, mean = 1.86 vs 3.40, difference = 1.54, 95% CI = 1.39 to 1.69) but increased after ERalpha agonist treatment (ERalpha agonist vs vehicle at day 8, mean = 4.36 vs 3.40, difference = 0.96, 95% CI = 0.68 to 1.23). Similarly, expression of TMPRSS2-ERG decreased after ERbeta agonist treatment (fold change over internal control, ERbeta agonist vs vehicle at 24 hours, NCI-H660, mean = 0.57- vs 1.0-fold, difference = 0.43-fold, 95% CI = 0.29- to 0.57-fold) and increased after ERalpha agonist treatment (ERalpha agonist vs vehicle at 24 hours, mean = 5.63- vs 1.0-fold, difference = 4.63-fold, 95% CI = 4.34- to 4.92-fold). CONCLUSIONS: TMPRSS2-ERG fusion prostate cancer is a distinct molecular subclass. TMPRSS2-ERG expression is regulated by a novel ER-dependent mechanism.</p>
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