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21.
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22.
  • Andrén, Ove, 1963-, et al. (författare)
  • MUC-1 gene is associated with prostate cancer death : a 20-year follow-up of a population-based study in Sweden
  • 2007
  • Ingår i: British Journal of Cancer. - London : Harcourt Publishers. - 0007-0920 .- 1532-1827. ; 97:6, s. 730-734
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Anti-adhesion mucins have proven to play an important part in the biology of several types of cancer. Therefore, we test the hypothesis that altered expression of MUC-1 is associated with prostate cancer progression. We retrieved archival tumour tissue from a population-based cohort of 195 men with localised prostate cancer (T1a-b, Nx, M0) that has been followed for up to 20 years with watchful waiting. Semi-automated, quantitative immunohistochemistry was undertaken to evaluate MUC-1 expression. We modelled prostate cancer-specific death as a function of MUC-1 levels accounting for age, Gleason grade and tumour extent, and calculated age-adjusted and multivariate adjusted hazard ratios (HR). Men that had tumours with an MUC-intensity lower or higher than normal tissue had a higher risk of dying in prostate cancer, independent of tumour extent and Gleason score (HR 5.1 and 4.5, respectively). Adjustment for Gleason grade and tumour stage did not alter the results. Men with a Gleason score &gt;=7 and MUC-1 deviating from the normal had a 17 (RR=17.1 95% confidence interval=2.3–128) times higher risk to die in prostate cancer compared with men with Gleason score &lt;7 and normal MUC-1 intensity. In summary, our data show that MUC-1 is an independent prognostic marker for prostate cancer death.</p>
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23.
  • Bergkvist, Leif, et al. (författare)
  • Axillary recurrence rate after negative sentinel node biopsy in breast cancer : three-year follow-up of the Swedish Multicenter Cohort Study
  • 2008
  • Ingår i: Annals of Surgery. - 0003-4932 .- 1528-1140. ; 247:1, s. 150-156
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Sentinel lymph node biopsy is an established staging method in early breast cancer. After a negative biopsy, most institutions will not perform a completion axillary dissection. The present study reports the current axillary recurrence (AR) rate, overall and disease-free survival in the Swedish Multicenter Cohort Study.</p> <p>Methods: From 3534 patients with primary breast cancer ≤3 cm prospectively enrolled in the Swedish multicenter cohort study, 2246 with a negative sentinel node biopsy and no further axillary surgery were selected. Follow-up consisted of annual clinical examination and mammography. Twenty-six hospitals and 131 surgeons contributed to patient accrual.</p> <p>Results: After a median follow-up time of 37 months (0-75), the axilla was the sole initial site of recurrence in 13 patients (13 of 2246, 0.6%). In another 7 patients, axillary relapse occurred after or concurrently with a local recurrence in the breast, and in a further 7 cases, it coincided with distant or extra-axillary lymphatic metastases. Thus, a total of 27 ARs were identified (27 of 2246, 1.2%). The overall 5-year survival was 91.6% and disease-free survival 92.1%.</p> <p>Conclusions: This is the first report from a national multicenter study that covers, not only highly specialized institutions but also small community hospitals with just a few procedures per year. Despite this heterogeneous background, the results lie well within the range of AR rates published internationally (0%-3.6%). The sentinel node biopsy procedure seems to be safe in a multicenter setting. Nevertheless, long-term follow-up data should be awaited before firm conclusions are drawn.</p>
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24.
  • Bill-Axelson, Anna, et al. (författare)
  • Radical prostatectomy versus watchful waiting in localized prostate cancer : the Scandinavian prostate cancer group-4 randomized trial
  • 2008
  • Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 100:16, s. 1144-1154
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: The benefit of radical prostatectomy in patients with early prostate cancer has been assessed in only one randomized trial. In 2005, we reported that radical prostatectomy improved prostate cancer survival compared with watchful waiting after a median of 8.2 years of follow-up. We now report results after 3 more years of follow-up.</p> <p>METHODS: From October 1, 1989, through February 28, 1999, 695 men with clinically localized prostate cancer were randomly assigned to radical prostatectomy (n = 347) or watchful waiting (n = 348). Follow-up was complete through December 31, 2006, with histopathologic review and blinded evaluation of causes of death. Relative risks (RRs) were estimated using the Cox proportional hazards model. Statistical tests were two-sided.</p> <p>RESULTS: During a median of 10.8 years of follow-up (range = 3 weeks to 17.2 years), 137 men in the surgery group and 156 in the watchful waiting group died (P = .09). For 47 of the 347 men (13.5%) who were randomly assigned to surgery and 68 of the 348 men (19.5%) who were not, death was due to prostate cancer. The difference in cumulative incidence of death due to prostate cancer remained stable after about 10 years of follow-up. At 12 years, 12.5% of the surgery group and 17.9% of the watchful waiting group had died of prostate cancer (difference = 5.4%, 95% confidence interval [CI] = 0.2 to 11.1%), for a relative risk of 0.65 (95% CI = 0.45 to 0.94; P = .03). The difference in cumulative incidence of distant metastases did not increase beyond 10 years of follow-up. At 12 years, 19.3% of men in the surgery group and 26% of men in the watchful waiting group had been diagnosed with distant metastases (difference = 6.7%, 95% CI = 0.2 to 13.2%), for a relative risk of 0.65 (95% CI = 0.47 to 0.88; P = .006). Among men who underwent radical prostatectomy, those with extracapsular tumor growth had 14 times the risk of prostate cancer death as those without it (RR = 14.2, 95% CI = 3.3 to 61.8; P &lt; .001).</p> <p>CONCLUSION: Radical prostatectomy reduces prostate cancer mortality and risk of metastases with little or no further increase in benefit 10 or more years after surgery. </p>
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25.
  • Demichelis, F., et al. (författare)
  • TMPRSS2:ERG gene fusion associated with lethal prostate cancer in a watchful waiting cohort
  • 2007
  • Ingår i: Oncogene. - Basingstoke : Nature Publ. Group. - 0950-9232 .- 1476-5594. ; 26:31, s. 4596-4599
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The identification of the <em>TMPRSS2:ERG</em> fusion in prostate cancer suggests that distinct molecular subtypes may define risk for disease progression. In surgical series, <em>TMPRSS2:ERG</em> fusion was identified in 50% of the tumors. Here, we report on a population-based cohort of men with localized prostate cancers followed by expectant (watchful waiting) therapy with 15% (17/111) <em>TMPRSS2:ERG</em> fusion. We identified a statistically significant association between <em>TMPRSS2:ERG</em> fusion and prostate cancer specific death (cumulative incidence ratio=2.7, <em>P</em>&lt;0.01, 95% confidence interval=1.3–5.8). Quantitative reverse-transcription–polymerase chain reaction demonstrated high estrogen-regulated gene (ERG) expression to be associated with <em>TMPRSS2:ERG</em> fusion (<em>P</em>&lt;0.005). These data suggest that <em>TMPRSS2:ERG</em> fusion prostate cancers may have a more aggressive phenotype, possibly mediated through increased ERG expression.</p>
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26.
  • Fall, Katja, et al. (författare)
  • Prostate-specific antigen levels as a predictor of lethal prostate cancer
  • 2007
  • Ingår i: Journal of the National Cancer Institute. - Oxford : Oxford Univ. Press. - 0027-8874 .- 1460-2105. ; 99:7, s. 526-532
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Rates of long-term survival among patients with untreated localized<sup> </sup>prostate cancer are high. To avoid unnecessary treatment, tools<sup> </sup>are needed to identify the small proportion of patients who<sup> </sup>are destined to develop lethal prostate cancer.<sup> </sup></p> <p>Methods: To evaluate the accuracy of early changes in prostate-specific<sup> </sup>antigen (PSA) levels as predictors of prostate cancer outcome,<sup> </sup>we assessed serial measurements of PSA level among 267 men with<sup> </sup>localized prostate cancer in a Scandinavian cohort of men who<sup> </sup>were diagnosed between 1989 and 1999 and who were managed by<sup> </sup>watchful waiting. We then 1) fitted individual regression lines<sup> </sup>to the PSA values assessed for each patient during the first<sup> </sup>2 years of follow-up by using three different models, 2) evaluated<sup> </sup>early PSA curve characteristics as determinants of the cumulative<sup> </sup>incidence of lethal prostate cancer and calculated hazard ratios<sup> </sup>for baseline PSA value and rate of change in PSA level to prostate<sup> </sup>cancer outcome, and 3) plotted time-dependent receiver operating<sup> </sup>characteristic (ROC) curves. All <em>P</em> values are two-sided.<sup> </sup></p> <p>Results: During complete follow-up for a mean of 8.5 years, 34 patients<sup> </sup>(13%) died from prostate cancer, and 18 (7%) developed metastases<sup> </sup>but were still alive at end of follow-up. In a log-linear model,<sup> </sup>both PSA value at baseline (<em>P</em> = .05) and the rate of PSA change<sup> </sup>(<em>P</em>&lt;.001) were associated with the development of lethal prostate<sup> </sup>cancer. In the ROC analysis, however, the accuracy of classifying<sup> </sup>the disease as either indolent or destined to progress was low,<sup> </sup>regardless of the cut point chosen for initial PSA level or<sup> </sup>rate of change in PSA level.<sup> </sup></p> <p>Conclusions: Although baseline PSA value and rate of PSA change are prognostic<sup> </sup>factors for lethal prostate cancer, they are poor predictors<sup> </sup>of lethal prostate cancer among patients with localized prostate<sup> </sup>cancer who are managed by watchful waiting.</p>
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27.
  • Jädersten, Martin, et al. (författare)
  • Erythropoietin and granulocyte-colony stimulating factor treatment associated with improved survival in myelodysplastic syndrome
  • 2008
  • Ingår i: Journal of Clinical Oncology. - New York, N.Y. : Grune & Stratton. - 0732-183X .- 1527-7755. ; 26:21, s. 3607-3613
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>Purpose</strong> To assess the effect of erythropoietin (EPO) plus granulocyte-colony stimulating factor (G-CSF) treatment on survival and leukemic transformation in myelodysplastic syndrome (MDS).</p> <p><strong>Patients and Methods</strong> We compared the long-term outcome of patients with MDS treated with EPO plus G-CSF (n = 121) with untreated patients (n = 237) with MDS using multivariate Cox regression with delayed entry, for the first time adjusting for all major prognostic variables (WHO classification, karyotype, cytopenias, level of transfusion-need, age, and sex).</p> <p><strong>Results</strong> The erythroid response rate to EPO plus G-CSF was 39%, and the median response duration 23 months (range, 3 to 116+). In the multivariate analysis, treatment was associated with improved overall survival (hazard ratio, 0.61; 95% CI, 0.44 to 0.83; <em>P</em> = .002). Interestingly, this positive association was primarily observed in patients requiring fewer than 2 units of RBCs per month. Treatment was not linked to the rate of acute myeloid leukemia in any defined subgroup, including patients with an increase of marrow blasts or an unfavorable karyotype.</p> <p><strong>Conclusion</strong> The inherent risk of leukemic evolution in MDS makes the current investigation highly relevant, in light of the recent reports of potential negative effects of EPO treatment on outcome in patients with cancer. We conclude that treatment of anemia in MDS with EPO plus G-CSF may have a positive impact on outcome in patients with no or low transfusion need, while not affecting the risk of leukemic transformation.</p>
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28.
  • Landgren, Ola, et al. (författare)
  • Personal and family history of autoimmune diabetes mellitus and susceptibility to young-adult-onset Hodgkin lymphoma
  • 2006
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 118:2, s. 449-452
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Young-adult-onset (15-44 years of age) Hodgkin lymphoma (HL) is believed to arise as a consequence of late primary infection in susceptible individuals. The properties of this susceptibility remain little understood. We have previously reported an increased occurrence of HL in patients with rheumatoid arthritis and among their offspring, suggesting that susceptibility to autoimmunity might be of importance also in the pathogenesis of HL. To explore this hypothesis, we assessed the association of personal and family history of diabetes mellitus, with risk of subsequent HL in a population-based case-control study, including as cases all individuals diagnosed with HL above 15 years of age 1964-1999 (n = 6,873) in Sweden, and matched population controls (n = 12,565). First-degree relatives of cases and controls were identified through linkage with the Multi-generation Register. We identified discharges listing diabetes mellitus through linkage with the Inpatient Register (1964-2000). We used odds ratios (OR) as measures of relative risk. Cases with young-adult-onset HL were less likely to have a personal (OR =0.5, 95% CI 0.2-1.1) or family (OR =0.7, 95% CI 0.6-0.8) history of diabetes mellitus. In contrast, HL diagnosed at older ages was neither associated with a personal (OR =1.0) nor family (OR =1.0) history of diabetes mellitus. These findings suggests that characteristics of the immune system associated with conditions such as diabetes mellitus type I are of importance in the pathogenesis of young-adult-onset HL.</p> <p>Copyright 2005 Wiley-Liss, Inc.</p>
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29.
  • Larsson, Susanna C., et al. (författare)
  • Cultured milk, yogurt, and dairy intake in relation to bladder cancer risk in a prospective study of Swedish women and men
  • 2008
  • Ingår i: American Journal of Clinical Nutrition. - Bethseda, Md. : American Society for Nutrition. - 0002-9165 .- 1938-3207. ; 88:4, s. 1083-1087
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background:Findings from epidemiologic studies of the effect<sup> </sup>of dairy foods (mainly milk) on the risk of bladder cancer have<sup> </sup>been inconsistent.<sup> </sup></p> <p>Objective:We aimed to examine the association between the intake<sup> </sup>of cultured milk and other dairy foods and the incidence of<sup> </sup>bladder cancer in a prospective, population-based cohort.<sup> </sup></p> <p>Design:We prospectively followed 82 002 Swedish women and men<sup> </sup>who were cancer-free and who completed a 96-item food-frequency<sup> </sup>questionnaire in 1997. Incident cases of bladder cancer were<sup> </sup>identified in the Swedish cancer registries.<sup> </sup></p> <p>Results:During a mean follow-up of 9.4 y, 485 participants (76<sup> </sup>women and 409 men) were diagnosed with bladder cancer. Total<sup> </sup>dairy intake was not significantly associated with risk of bladder<sup> </sup>cancer [<img src="http://www.ajcn.org/math/ge.gif" />7.0 servings/d compared with &lt; 3.5 servings/d: multivariate<sup> </sup>rate ratio (RR) = 0.87; 95% CI: 0.66, 1.15; <em>P</em> for trend = 0.33].<sup> </sup>However, a statistically significant inverse association was<sup> </sup>observed for the intake of cultured milk (sour milk and yogurt).<sup> </sup>The multivariate RRs for the highest category of cultured milk<sup> </sup>intake (<img src="http://www.ajcn.org/math/ge.gif" />2 servings/d) compared with the lowest category (0 serving/d)<sup> </sup>were 0.62 (95% CI: 0.46, 0.85; <em>P</em> for trend = 0.006) in women<sup> </sup>and men combined, 0.55 (95% CI: 0.25, 1.22; <em>P</em> for trend = 0.06)<sup> </sup>in women, and 0.64 (95% CI: 0.46, 0.89; <em>P</em> for trend = 0.03)<sup> </sup>in men. The intake of milk or cheese was not associated with<sup> </sup>bladder cancer risk.<sup> </sup></p>
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30.
  • Larsson, Susanna C., et al. (författare)
  • Fruit and vegetable consumption and risk of bladder cancer : a prospective cohort study
  • 2008
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Baltimore : Waverly Press. - 1055-9965 .- 1538-7755. ; 17:9, s. 2519-2522
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Fruit and vegetable consumption has been inconsistently associated with risk of bladder cancer. We used data from a prospective population-based cohort study of 82,002 Swedish women and men to examine the association between fruit and vegetable consumption and bladder cancer incidence. Diet was assessed with a validated food frequency questionnaire. During a mean follow-up of 9.4 years, 485 incident cases of bladder cancer were identified in the Swedish cancer registries. We found no statistically significant association between intakes of total fruits and vegetables, total fruits, or total vegetables and bladder cancer risk after adjustment for age, sex, education, and cigarette smoking. The multivariate rate ratios (95% confidence intervals) comparing the highest with the lowest quartile of intake were 0.80 (0.60-1.05) for total fruits and vegetables, 0.93 (0.69-1.25) for fruits, and 0.89 (0.67-1.19) for vegetables. Likewise, no associations were observed for citrus fruits, cruciferous vegetables, or green leafy vegetables. The associations did not differ by sex or smoking status. In conclusion, findings from this prospective study suggest that fruit and vegetable intakes are not likely to be appreciably associated with the risk of bladder cancer.</p>
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