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  • 1.
    Ahlström, Håkan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Ekström, Simon
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Sjöholm, Therese
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Strand, Robin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Kullberg, Joel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Johansson, E.
    Antaros Med, Molndal, Sweden..
    Hagmar, P.
    Antaros Med, Molndal, Sweden..
    Malmberg, Filip
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Radiologi.
    Registration-based automated lesion detection and therapy evaluation of tumors in whole body PET-MR images2017Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, nr S5, artikkel-id 78PArtikkel i tidsskrift (Annet vitenskapelig)
  • 2. Andersson, Jenny
    et al.
    Larsson, L.
    Klaar, S.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi.
    Nilsson, J.
    Inganäs, M.
    Carlsson, G.
    Ohd, J.
    Rudenstam, C-M.
    Gustavsson, B.
    Bergh, J.
    Worse survival for TP53 (p53)-mutated breast cancer patients receiving adjuvant CMF2005Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 16, nr 5, s. 743-8Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: TP53 has been described as a prognostic factor in many malignancies, including breast cancer. Whether it also might be a predictive factor with reference to chemo- and endocrine therapy is more controversial. PATIENTS AND METHODS: We investigated relapse-free (RFS), breast cancer-corrected (BCCS) and overall survival (OS) related to TP53 status in node-positive breast cancer patients that had received polychemotherapy [cyclophosphamide, methotrexate, 5-fluorouracil (CMF)] and/or endocrine therapy (tamoxifen). Sequence analyses of the whole TP53 coding region was performed in 376 patients operated on for primary breast cancer with axillary lymph node metastases between 1984 and 1989 (median follow-up time 84 months). RESULTS: TP53 mutations were found in 105 patients (28%). We found 90 (82%) of the 110 mutations in the more frequently analysed exons 5-8, while the other 20 (18%) were located in exons 3-4 and 9-10, respectively. Univariate analyses showed TP53 to be a significant prognostic factor with regard to RFS, BCCS and OS in patients who received adjuvant CMF. CONCLUSIONS: TP53 mutations might induce resistance to certain modalities of breast cancer therapy. Sequence-determined TP53 mutation was of negative prognostic value in the total patient population and in the CMF treated patients.

  • 3. Andren, O.
    et al.
    Widmark, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Falt, A.
    Ulvskog, E.
    Davidsson, S.
    Thellenberg Karlsson, Camilla
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hjalm-Eriksson, M.
    Cabazitaxel followed by androgen deprivation therapy (ADT) significantly improves time to progression in patients with newly diagnosed metastatic hormone sensitive prostate cancer (mHSPC): A randomized, open label, phase III, multicenter trial2017Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28Artikkel i tidsskrift (Annet vitenskapelig)
  • 4.
    Andrén, Ove
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Widmark, A.
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Fält, A.
    Ulvskog, E.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Oncology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Davidsson, Sabina
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Karlsson, C. Thellenberg
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Hjälm-Eriksson, M.
    Department of Oncology, Karolinska Institute, Stockholm, Sweden.
    Cabazitaxel followed by androgen deprivation therapy (ADT) significantly improves time to progression in patients with newly diagnosed metastatic hormone sensitive prostate cancer (mHSPC): A randomized, open label, phase III, multicenter trial2017Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, nr Suppl. 5, artikkel-id 811PArtikkel i tidsskrift (Annet vitenskapelig)
  • 5.
    Berglund, U. Warpman
    et al.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Sanjiv, K.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Gad, H.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Kalderen, C.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Koolmeister, T.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Pham, T.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Gokturk, C.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Jafari, R.
    Karolinska Inst, Dept Oncol Pathol, Clin Prote Mass Spectrometry, Stockholm, Sweden..
    Maddalo, G.
    Karolinska Inst, Dept Oncol Pathol, Clin Prote Mass Spectrometry, Stockholm, Sweden..
    Seashore-Ludlow, B.
    Karolinska Inst, Div Translat Med & Chem Biol, Dept Med Biochem & Biophys, Chem Biol Consortium Sweden,Sci Life Lab, Stockholm, Sweden..
    Chernobrovkin, A.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Physiol Chem 1, Stockholm, Sweden..
    Manoilov, A.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Physiol Chem 1, Stockholm, Sweden..
    Pateras, I. S.
    Univ Athens, Sch Med, Dept Histol & Embryol, Mol Carcinogenesis Grp, Athens, Greece..
    Rasti, A.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Jemth, A. -S
    Almlof, I.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Loseva, O.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Visnes, T.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Einarsdottir, B. O.
    Univ Gothenburg, Inst Clin Sci, Sahlgrenska Translat Melanoma Grp SATMEG, Sahlgrenska Canc Ctr,Dept Surg, Gothenburg, Sweden.;Sahlgrens Univ Hosp, Gothenburg, Sweden..
    Gaugaz, Fabienne Z.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci. Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Saleh, Aljona
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci.
    Platzack, B.
    Swedish Toxicol Sci Res Ctr, Sodertalje, Sweden..
    Wallner, O. A.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Vallin, K. S. A.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Henriksson, M.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Wakchaure, P.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Borhade, S.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Herr, P.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Kallberg, Y.
    Karolinska Inst, Dept Med Solna, Sci Life Lab, NBIS, Stockholm, Sweden..
    Baranczewski, Pawel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Homan, E. J.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Wiita, E.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Nagpal, V.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden.;SP Proc Dev, Sodertalje, Sweden..
    Meijer, T.
    SP Proc Dev, Sodertalje, Sweden..
    Schipper, N.
    SP Proc Dev, Sodertalje, Sweden..
    Rudd, S. G.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Brautigam, L.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Lindqvist, Annika
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Filppula, Anne
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci.
    Lee, T-C
    Artursson, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaci. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Nilsson, J. A.
    Univ Gothenburg, Inst Clin Sci, Sahlgrenska Translat Melanoma Grp SATMEG, Sahlgrenska Canc Ctr,Dept Surg, Gothenburg, Sweden.;Sahlgrens Univ Hosp, Gothenburg, Sweden..
    Gorgoulis, V. G.
    Acad Athens, Biomed Res Fdn, Athens, Greece.;Univ Manchester, Manchester Acad Hlth Sci Ctr, Fac Inst Canc Sci, Manchester, Lancs, England..
    Lehtio, J.
    Karolinska Inst, Dept Oncol Pathol, Clin Prote Mass Spectrometry, Stockholm, Sweden..
    Zubarev, R. A.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Physiol Chem 1, Stockholm, Sweden..
    Scobie, M.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Helleday, T.
    Karolinska Inst, Dept Med Biochem & Biophys, Div Translat Med & Chem Biol, Sci Life Lab, Stockholm, Sweden..
    Validation and development of MTH1 inhibitors for treatment of cancer2016Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 27, nr 12, s. 2275-2283Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Previously, we showed cancer cells rely on the MTH1 protein to prevent incorporation of otherwise deadly oxidised nucleotides into DNA and we developed MTH1 inhibitors which selectively kill cancer cells. Recently, several new and potent inhibitors of MTH1 were demonstrated to be non-toxic to cancer cells, challenging the utility of MTH1 inhibition as a target for cancer treatment. Material and methods: Human cancer cell lines were exposed in vitro to MTH1 inhibitors or depleted of MTH1 by siRNA or shRNA. 8-oxodG was measured by immunostaining and modified comet assay. Thermal Proteome profiling, proteomics, cellular thermal shift assays, kinase and CEREP panel were used for target engagement, mode of action and selectivity investigations of MTH1 inhibitors. Effect of MTH1 inhibition on tumour growth was explored in BRAF V600E-mutated malignant melanoma patient derived xenograft and human colon cancer SW480 and HCT116 xenograft models. Results: Here, we demonstrate that recently described MTH1 inhibitors, which fail to kill cancer cells, also fail to introduce the toxic oxidized nucleotides into DNA. We also describe a new MTH1 inhibitor TH1579, (Karonudib), an analogue of TH588, which is a potent, selective MTH1 inhibitor with good oral availability and demonstrates excellent pharmacokinetic and anti-cancer properties in vivo. Conclusion: We demonstrate that in order to kill cancer cells MTH1 inhibitors must also introduce oxidized nucleotides into DNA. Furthermore, we describe TH1579 as a best-in-class MTH1 inhibitor, which we expect to be useful in order to further validate the MTH1 inhibitor concept.

    Fulltekst (pdf)
    fulltext
  • 6.
    Berglund, Åke
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    Cedermark, B
    Glimelius, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    Is it deleterious to delay the start of adjuvant chemotherapy in colon cancer stage III?2008Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 19, nr 2, s. 400-402Artikkel i tidsskrift (Fagfellevurdert)
  • 7. Bergqvist, Jenny
    et al.
    Ohd, J. F.
    Smeds, J.
    Klaar, Sigrid
    Isola, J.
    Nordgren, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för patologi.
    Elmberger, G. P.
    Hellborg, H.
    Bjohle, J.
    Borg, A-L.
    Skoog, L.
    Bergh, J.
    Quantitative real-time PCR analysis and microarray-based RNA expression of HER2 in relation to outcome2007Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 18, nr 5, s. 845-850Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Our aim was to use quantitative real-time PCR (Q-PCR) and RNA expression profiles (RNA-EPs) to investigate HER2 status in relation to outcome. PATIENTS AND METHODS: Cut-off levels for Q-PCR and RNA-EP were established in relation to immunohistochemistry (IHC) validated by FISH in a test set of frozen tissue samples from 40 primary breast cancers. The HER2 status was subsequently studied in another validation set of 306 tumors, where Q-PCR and RNA-EP results were compared with previously carried out IHC that we had validated by chromogenic in situ hybridization (CISH). RESULTS: Q-PCR and RNA-EP offered similar sensitivity (90% versus 77%), specificity (93% versus 95%), and negative (99% versus 98%) and positive (63% versus 61%) predictive values for HER2 determinations. Analyses of relapse-free survival (RFS) and overall survival on the basis of 5 and 10 years of follow-up indicated equivalent hazard ratios for all three techniques. In contrast to IHC/CISH, both Q-PCR and RNA-EP analyses of HER2 also gave statistically significant results regarding RFS and breast cancer-corrected survival after 10 years of follow-up. CONCLUSION: The use of RNA-EP and Q-PCR to analyze HER2 in frozen and formalin-fixed breast cancer samples may be an alternate approach to IHC in combination with FISH/CISH.

  • 8. Bergström, S.
    et al.
    Christensen, H. Nordahl
    Wiklund, F.
    Bergqvist, Michael
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
    EGFR tyrosine kinase inhibitors in non-small cell lung cancer: Nationwide register-based cohort study in Sweden2018Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 29, s. 526-526Artikkel i tidsskrift (Annet vitenskapelig)
  • 9. Berhelsen, K
    et al.
    Hansen, S
    Rosenberg, Per
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Advanced epithelial ovarian cancer: 1998 consensus statement.1999Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 10, s. 87-92Artikkel i tidsskrift (Fagfellevurdert)
  • 10. Björkholm, Magnus
    et al.
    Hagberg, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för onkologi.
    Holte, H.
    Kvaloy, S.
    Teerenhovi, L.
    Anderson, H.
    Cavallin-Ståhl, E.
    Myhre, J.
    Pertovaara, H.
    Öst, Å.
    Nilsson, B.
    Ösby, E.
    Central nervous system occurrence in elderly patients with aggressive lymphoma and a long-term follow-up2007Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 18, nr 6, s. 1085-1089Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Secondary central nervous system (CNS) involvement by aggressive lymphoma is a well-known and dreadful clinical complication. The incidence and risk factors for CNS manifestation were studied in a large cohort of elderly (>60 years) patients with aggressive lymphoma. PATIENTS AND METHODS: In all, 444 previously untreated patients were randomized to receive 3-weekly combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone or cyclophosphamide, mitoxantrone, vincristine and prednisone (CNOP) (doxorubicin substituted by mitoxantrone) chemotherapy with or without filgrastim. Prophylactic intrathecal methotrexate was given to patients with lymphoma involvement of bone marrow, testis and CNS near sites. RESULTS: In all 29 of 444 (6.5%) developed CNS disease after a median observation time of 115 months. CNS was the only site of progression/relapse in 13 patients while part of a systemic disease manifestation in 16 patients. In univariate risk factor analysis, CNS occurrence was associated with extranodal involvement of testis (P = 0.002), advanced clinical stage (P = 0.005) and increased age-adjusted International Prognostic Index score (aaIPI; P = 0.035). In multivariate analysis, initial involvement of testis remained significant and clinical stage was of borderline significance. The median survival time was 2 months after presentation of CNS disease. CONCLUSION: A significant proportion of elderly patients with advanced aggressive lymphoma will develop CNS disease. CNS occurrence is related to testis involvement, advanced clinical stage and high aaIPI and the prognosis is dismal.

  • 11. Bossi, A.
    et al.
    Dearnaley, D.
    McKenzie, M.
    Baskin-Bey, E.
    Tyler, R.
    Tombal, B.
    Freedland, S. J.
    Roach, M. , I I I
    Widmark, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
    Dicker, A. P.
    Wiegel, T.
    Shore, N.
    Smith, M.
    Yu, M.
    Kheoh, T.
    Thomas, S.
    Sandler, H. M.
    ATLAS: A phase 3 trial evaluating the efficacy of apalutamide (ARN-509) in patients with high-risk localized or locally advanced prostate cancer receiving primary radiation therapy2016Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 27Artikkel i tidsskrift (Fagfellevurdert)
  • 12. Breugom, A. J.
    et al.
    van Gijn, W.
    Muller, E. W.
    Berglund, Åke
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap.
    van den Broek, C. B. M.
    Fokstuen, T.
    Gelderblom, H.
    Kapiteijn, E.
    Leer, J. W. H.
    Marijnen, C. A. M.
    Martijn, H.
    Kranenbarg, E. Meershoek-Klein
    Nagtegaal, I. D.
    Påhlman, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Kolorektalkirurgi.
    Punt, C. J. A.
    Putter, H.
    Roodvoets, A. G. H.
    Rutten, H. J. T.
    Steup, W. H.
    Glimelius, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    van de Velde, C. J. H.
    Adjuvant chemotherapy for rectal cancer patients treated with preoperative (chemo)radiotherapy and total mesorectal excision: a Dutch Colorectal Cancer Group (DCCG) randomized phase III trial2015Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 26, nr 4, s. 696-701Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The discussion on the role of adjuvant chemotherapy for rectal cancer patients treated according to current guidelines is still ongoing. A multicentre, randomized phase III trial, PROCTOR-SCRIPT, was conducted to compare adjuvant chemotherapy with observation for rectal cancer patients treated with preoperative (chemo) radiotherapy and total mesorectal excision (TME). Patients and methods: The PROCTOR-SCRIPT trial recruited patients from 52 hospitals. Patients with histologically proven stage II or III rectal adenocarcinoma were randomly assigned (1: 1) to observation or adjuvant chemotherapy after preoperative (chemo) radiotherapy and TME. Radiotherapy consisted of 5 x 5 Gy. Chemoradiotherapy consisted of 25 x 1.8-2 Gy combined with 5-FU-based chemotherapy. Adjuvant chemotherapy consisted of 5-FU/LV (PROCTOR) or eight courses capecitabine (SCRIPT). Randomization was based on permuted blocks of six, stratified according to centre, residual tumour, time between last irradiation and surgery, and preoperative treatment. The primary end point was overall survival. Results: Of 470 enrolled patients, 437 were eligible. The trial closed prematurely because of slow patient accrual. Patients were randomly assigned to observation (n = 221) or adjuvant chemotherapy (n = 216). After a median follow-up of 5.0 years, 5-year overall survival was 79.2% in the observation group and 80.4% in the chemotherapy group [hazard ratio (HR) 0.93, 95% confidence interval (CI) 0.62-1.39; P = 0.73]. The HR for disease-free survival was 0.80 (95% CI 0.60-1.07; P = 0.13). Five-year cumulative incidence for locoregional recurrences was 7.8% in both groups. Five-year cumulative incidence for distant recurrences was 38.5% and 34.7%, respectively (P = 0.39). Conclusion: The PROCTOR-SCRIPT trial could not demonstrate a significant benefit of adjuvant chemotherapy with fluoropyrimidine monotherapy after preoperative (chemo) radiotherapy and TME on overall survival, disease-free survival, and recurrence rate. However, this trial did not complete planned accrual.

  • 13. Byström, P.
    et al.
    Glimelius, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för onkologi.
    Reply to FDG-PET: for early prediction of response to the first-line chemotherapy in metastatic colorectal cancer?2009Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 20, nr 6, s. 1150-1150Artikkel i tidsskrift (Fagfellevurdert)
  • 14. Byström, Per
    et al.
    Berglund, A.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Garske, Ulrike Garske
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Jacobsson, H.
    Sundin, Anders
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Nygren, Peter
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Frödin, J-E.
    Glimelius, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Early prediction of response to first-line chemotherapy by sequential [18F]-2-fluoro-2-deoxy-D-glucose positron emission tomography in patients with advanced colorectal cancer2009Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 20, nr 6, s. 1057-1061Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: To evaluate [(18)F]-2-fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET), for early evaluation of response to palliative chemotherapy and for prediction of long-term outcome, in patients with metastatic colorectal cancer (mCRC). PATIENTS AND METHODS: In a randomized trial, patients with mCRC received irinotecan-based combination chemotherapy. FDG-PET was carried out before treatment and after two cycles in 51 patients at two centers. Visual changes in tumor FDG uptake and changes measured semi-automatically, as standard uptake values (SUVs), were compared with radiological response after four and eight cycles. RESULTS: The mean baseline SUV for all tumor lesions per patient was higher in nonresponders than in responders (mean 7.4 versus 5.6, P = 0.02). There was a strong correlation between metabolic response (changes in SUV) and objective response (r = 0.57, P = 0.00001), with a sensitivity of 77% and a specificity of 76%. There was no significant correlation between metabolic response and time to progression (P = 0.5) or overall survival (P = 0.1). CONCLUSIONS: Although metabolic response assessed by FDG-PET reflects radiological tumor volume changes, the sensitivity and specificity are too low to support the routine use of PET in mCRC. Furthermore, PET failed to reflect long-term outcome and can, thus, not be used as surrogate end point for hard endpoint benefit.

  • 15. Caplin, M. E.
    et al.
    Baudin, E.
    Ferolla, P.
    Filosso, P.
    Garcia-Yuste, M.
    Lim, E.
    Öberg, Kjell
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Onkologisk endokrinologi.
    Pelosi, G.
    Perren, A.
    Rossi, R. E.
    Travis, W. D.
    Pulmonary neuroendocrine (carcinoid) tumors: European Neuroendocrine Tumor Society expert consensus and recommendations for best practice for typical and atypical pulmonary carcinoids2015Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 26, nr 8, s. 1604-1620Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Pulmonary carcinoids (PCs) are rare tumors. As there is a paucity of randomized studies, this expert consensus document represents an initiative by the European Neuroendocrine Tumor Society to provide guidance on their management. Patients and methods: Bibliographical searches were carried out in PubMed for the terms 'pulmonary neuroendocrine tumors', 'bronchial neuroendocrine tumors', 'bronchial carcinoid tumors', 'pulmonary carcinoid', 'pulmonary typical/atypical carcinoid', and 'pulmonary carcinoid and diagnosis/treatment/epidemiology/prognosis'. A systematic review of the relevant literature was carried out, followed by expert review. Results: PCs are well-differentiated neuroendocrine tumors and include low-and intermediate-grade malignant tumors, i.e. typical (TC) and atypical carcinoid (AC), respectively. Contrast CT scan is the diagnostic gold standard for PCs, but pathology examination is mandatory for their correct classification. Somatostatin receptor imaging may visualize nearly 80% of the primary tumors and is most sensitive for metastatic disease. Plasma chromogranin A can be increased in PCs. Surgery is the treatment of choice for PCs with the aim of removing the tumor and preserving as much lung tissue as possible. Resection of metastases should be considered whenever possible with curative intent. Somatostatin analogs are the first-line treatment of carcinoid syndrome and may be considered as first-line systemic antiproliferative treatment in unresectable PCs, particularly of low-grade TC and AC. Locoregional or radiotargeted therapies should be considered for metastatic disease. Systemic chemotherapy is used for progressive PCs, although cytotoxic regimens have demonstrated limited effects with etoposide and platinum combination the most commonly used, however, temozolomide has shown most clinical benefit. Conclusions: PCs are complex tumors which require a multidisciplinary approach and long-term follow-up.

  • 16. Carducci, M.
    et al.
    Armstrong, A.
    Haggman, Michael
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Stadler, W. M.
    Gingrich, J. R.
    Assikis, V.
    Forsberg, G.
    Olsson, A.
    Nordle, O.
    Pili, R.
    Tasquinimod mechanism of action biomarkers: correlation with pfs and survival in men with metastatic castrate resistant prostate cancer treated in a randomized phase 2 trial2012Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 23, nr S9, s. 303-303Artikkel i tidsskrift (Annet vitenskapelig)
  • 17.
    Cashin, Peter H
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Kolorektalkirurgi.
    Graf, Wilhelm
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Kolorektalkirurgi.
    Nygren, Peter
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    Mahteme, Haile
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Kolorektalkirurgi.
    Intraoperative hyperthermic versus postoperative normothermic intraperitoneal chemotherapy for colonic peritoneal carcinomatosis: a case-control study2012Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 23, nr 3, s. 647-652Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND:

    Cytoreductive surgery and intraperitoneal chemotherapy has improved prognosis in patients with peritoneal carcinomatosis. The main modes of intraperitoneal chemotherapy treatment are peroperative hyperthermic intraperitoneal chemotherapy (HIPEC) and normothermic sequential postoperative intraperitoneal chemotherapy (SPIC). The aim of this study was to compare HIPEC and SPIC with respect to overall survival, disease-free survival, morbidity, and mortality in patients with peritoneal carcinomatosis from colon cancer.

    PATIENTS AND METHODS:

    A matched case-control study was conducted in patients with surgical macroscopic complete removal of carcinomatosis; matching was according to the peritoneal cancer index score. Thirty-two patients were included, 16 in each group (HIPEC and SPIC). Overall survival, disease-free survival, morbidity, mortality, and clinicopathological parameters were compared.

    RESULTS:

    Median overall survival was 36.5 months in the HIPEC group and 23.9 months in the SPIC group (P = 0.01). Median disease-free survival for these groups was 22.8 (HIPEC) and 13.0 months (SPIC; P = 0.02). Morbidity was not statistically different, 19% in SPIC and 37% in HIPEC. Postoperative mortality was observed in one patient in each group.

    CONCLUSION:

    HIPEC was associated with improved overall survival and disease-free survival compared with SPIC at similar morbidity and mortality, suggesting that HIPEC is the treatment of choice in colonic peritoneal carcinomatosis.

    Fulltekst (pdf)
    fulltext
  • 18. Chadeau-Hyam, M.
    et al.
    Vermeulen, R. C. H.
    Hebels, D. G. A. J.
    Castagne, R.
    Campanella, G.
    Portengen, L.
    Kelly, R. S.
    Bergdahl, Ingvar
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin. Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning.
    Melin, Beatrice
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Palli, D.
    Krogh, V.
    Tumino, R.
    Sacerdote, C.
    Panico, S.
    de Kok, T. M. C. M.
    Smith, M. T.
    Kleinjans, J. C. S.
    Vineis, P.
    Kyrtopoulos, S. A.
    Prediagnostic transcriptomic markers of Chronic lymphocytic leukemia reveal perturbations 10 years before diagnosis2014Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 25, nr 5, s. 1065-1072Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND:

    B-cell lymphomas are a diverse group of hematological neoplasms with differential etiology and clinical trajectories. Increased insights in the etiology and the discovery of prediagnostic markers have the potential to improve the clinical course of these neoplasms.

    METHODS:

    We investigated in a prospective study global gene expression in peripheral blood mononuclear cells of 263 incident B-cell lymphoma cases, diagnosed between 1 and 17 years after blood sample collection, and 439 controls, nested within two European cohorts.

    RESULTS:

    Our analyses identified only transcriptomic markers for specific lymphoma subtypes; few markers of multiple myeloma (N = 3), and 745 differentially expressed genes in relation to future risk of chronic lymphocytic leukemia (CLL). The strongest of these associations were consistently found in both cohorts and were related to (B-) cell signaling networks and immune system regulation pathways. CLL markers exhibited very high predictive abilities of disease onset even in cases diagnosed more than 10 years after blood collection.

    CONCLUSIONS:

    This is the first investigation on blood cell global gene expression and future risk of B-cell lymphomas. We mainly identified genes in relation to future risk of CLL that are involved in biological pathways, which appear to be mechanistically involved in CLL pathogenesis. Many but not all of the top hits we identified have been reported previously in studies based on tumor tissues, therefore suggesting that a mixture of preclinical and early disease markers can be detected several years before CLL clinical diagnosis.

  • 19. Chajes, V.
    et al.
    Assi, N.
    Biessy, C.
    Ferrari, P.
    Rinaldi, S.
    Slimani, N.
    Lenoir, G. M.
    Baglietto, L.
    His, M.
    Boutron-Ruault, M. C.
    Trichopoulou, A.
    Lagiou, P.
    Katsoulis, M.
    Kaaks, R.
    Kuehn, T.
    Panico, S.
    Pala, V.
    Masala, G.
    Bueno-de-Mesquita, H. B.
    Peeters, P. H.
    van Gils, C.
    Hjartaker, A.
    Olsen, K. Standahl
    Barnung, R. Borgund
    Barricarte, A.
    Redondo-Sanchez, D.
    Menendez, V.
    Amiano, P.
    Wennberg, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Key, T.
    Khaw, K. T.
    Merritt, M. A.
    Riboli, E.
    Gunter, M. J.
    Romieu, I.
    A prospective evaluation of plasma phospholipid fatty acids and breast cancer risk in the EPIC study2017Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, nr 11, s. 2836-2842Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Intakes of specific fatty acids have been postulated to impact breast cancer risk but epidemiological data based on dietary questionnaires remain conflicting.

    Materials and methods: We assessed the association between plasma phospholipid fatty acids and breast cancer risk in a case–control study nested within the European Prospective Investigation into Cancer and Nutrition study. Sixty fatty acids were measured by gas chromatography in pre-diagnostic plasma phospholipids from 2982 incident breast cancer cases matched to 2982 controls. Conditional logistic regression models were used to estimate relative risk of breast cancer by fatty acid level. The false discovery rate (q values) was computed to control for multiple comparisons. Subgroup analyses were carried out by estrogen receptor (ER) and progesterone receptor expression in the tumours.

    Results: A high level of palmitoleic acid [odds ratio (OR) for the highest quartile compared with the lowest OR (Q4–Q1) 1.37; 95% confidence interval (CI), 1.14–1.64; P for trend = 0.0001, q value = 0.004] as well as a high desaturation index (DI16) (16:1n–7/16:0) [OR (Q4–Q1), 1.28; 95% C, 1.07–1.54; P for trend = 0.002, q value = 0.037], as biomarkers of de novo lipogenesis, were significantly associated with increased risk of breast cancer. Levels of industrial trans-fatty acids were positively associated with ER-negative tumours [OR for the highest tertile compared with the lowest (T3–T1)=2.01; 95% CI, 1.03–3.90; P for trend = 0.047], whereas no association was found for ER-positive tumours (P-heterogeneity =0.01). No significant association was found between n-3 polyunsaturated fatty acids and breast cancer risk, overall or by hormonal receptor.

    Conclusion: These findings suggest that increased de novo lipogenesis, acting through increased synthesis of palmitoleic acid, could be a relevant metabolic pathway for breast tumourigenesis. Dietary trans-fatty acids derived from industrial processes may specifically increase ER-negative breast cancer risk.

  • 20. Cullen, MH
    et al.
    Zatloukal, P
    Sörenson, Sverre
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Lungmedicin. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Lungmedicinska kliniken US.
    Novello, S
    Fischer, JR
    Joy, AA
    Zereu, M
    Peterson, P
    Visseren-Gruf, CM
    Iscoe, N
    A Randomized phase III trial comparing standard and high-dose pemetrexed as second-line treatment in patients with locally advanced or metastatic non-small-cell lung cancer2008Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 19, nr 5, s. 939-945Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

     Background: This phase III randomized trial compared pemetrexed 500 mg/m2 (P500) with pemetrexed 900 mg/m2 (P900) to determine whether higher dosing benefits non-small-cell lung cancer (NSCLC) patients as second-line therapy. Patients and methods: Patients with locally advanced or metastatic NSCLC, previously treated with platinum-based chemotherapy, were randomly assigned to receive i.v. P500 or P900 every 3 week. Results: Accrual was terminated with 588/600 patients enrolled because an interim analysis indicated a low probability of improved survival and numerically greater toxicity on the P900 arm. P900 patients were permitted to continue treatment at P500. No statistical difference was observed between the treatment arms (P500 versus P900) for median survival {6.7 versus 6.9 months, hazard ratio [HR] = 1.0132 [95% confidence interval (CI) 0.837-1.226]}, progression-free survival [2.6 versus 2.8 months, HR = 0.9681 (95% CI 0.817-1.147)], or best overall tumor response [7.1% versus 4.3% (P = 0.1616)]. The incidence of drug-related grade 3/4 toxicity was typically <5% on both treatment arms, but was numerically higher on the P900 arm for most toxicity categories. Conclusions: P900 did not improve any efficacy measure over P500. P500 i.v. every 3 week remains the standard pemetrexed dose for second-line treatment of platinum-pretreated advanced NSCLC.

  • 21. De Graan, A. M.
    et al.
    Elens, L.
    Sparreboom, A.
    Friberg, Lena E.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Farmaceutiska fakulteten, Institutionen för farmaceutisk biovetenskap.
    van der Holt, B.
    De Raaf, P. J.
    Wiemer, E. A. C.
    Verweij, J.
    van Schaik, R. H.
    Mathijssen, R. H. J.
    Influence of drug exposure and genetic variation on paclitaxel-induced neurotoxicity2012Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 23, nr S9, s. 534-534Artikkel i tidsskrift (Annet vitenskapelig)
  • 22.
    de Kruijf, E M
    et al.
    Departments of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
    Dekker, T J A
    Departments of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
    Hawinkels, L J A C
    Departments of Molecular Cell Biology and Centre for Biomedical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
    Putter, H
    Departments of Medical Statistics, Leiden University Medical Center, Leiden, The Netherlands.
    Smit, V T H B M
    Departments of Pathology, Leiden University Medical Center, Leiden, The Netherlands.
    Kroep, J R
    Departments of Medical Oncology, Leiden University Medical Center, Leiden, The Netherlands.
    Kuppen, P J K
    Departments of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
    van de Velde, C J H
    Departments of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
    ten Dijke, Peter
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning.
    Tollenaar, R A E M
    Departments of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
    Mesker, W E
    Departments of Surgery, Leiden University Medical Center, Leiden, The Netherlands.
    The prognostic role of TGF-β signaling pathway in breast cancer patients2013Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, nr 2, s. 384-390Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background

    The transforming growth factor-β (TGF-β) pathway has dual effects on tumor growth. Seemingly, discordant results have been published on the relation between TGF-β signaling markers and prognosis in breast cancer. Improved prognostic information for breast cancer patients might be obtained by assessing interactions among TGF-β signaling biomarkers.

    Patients and methods

    The expression of nuclear Smad4, nuclear phosphorylated-Smad2 (p-Smad2), and the membranous expression of TGF-β receptors I and II (TβRI and TβRII) was determined on a tissue microarray of 574 breast carcinomas. Tumors were stratified according to the Smad4 expression in combination with p-Smad2 expression or Smad4 in combination with the expression of both TGF-β receptors.

    Results

    Tumors with high expression of TβRII, TβRI and TβRII, and p-Smad2 (P = 0.018, 0.005, and 0.022, respectively), and low expression of Smad4 (P = 0.005) had an unfavorable prognosis concerning progression-free survival. Low Smad4 expression combined with high p-Smad2 expression or low expression of Smad4 combined with high expression of both TGF-β receptors displayed an increased hazard ratio of 3.04 [95% confidence interval (CI) 1.390-6.658] and 2.20 (95% CI 1.464-3.307), respectively, for disease relapse.

    Conclusions

    Combining TGF-β biomarkers provides prognostic information for patients with stage I-III breast cancer. This can identify patients at increased risk for disease recurrence that might therefore be candidates for additional treatment.

  • 23.
    Discacciati, A.
    et al.
    Unit of Nutritional Epidemiology, Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Orsini, N.
    Unit of Nutritional Epidemiology, Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Andersson, Swen-Olof
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Johansson, Jan-Erik
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Mantzoros, C. S.
    Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, United States; Section of Endocrinology, Boston VA Healthcare System, Harvard Medical School, Boston, United States.
    Wolk, A.
    Unit of Nutritional Epidemiology, Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Coffee consumption and risk of localized, advanced and fatal prostate cancer: a population-based prospective study2013Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, nr 7, s. 1912-1918Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The epidemiological evidence on possible relationships between coffee consumption and prostate cancer (PCa) risk by subtype of the disease (localized, advanced) and fatal PCa risk is limited.

    Materials and methods: A population-based cohort of 44 613 Swedish men aged 45-79 years was followed up from January 1998 through December 2010 for incidence of localized (n = 2368), advanced (n = 918) and fatal (n = 515) PCa. We assessed the associations between coffee consumption and localized, advanced and fatal PCa risk using competing-risk regressions. We examined possible effect modification by body mass index (BMI).

    Results: For localized PCa, each one cup increase in daily coffee consumption was associated with a 3% reduced risk [sub-hazard ratio (SHR) = 0.97, 95% confidence interval (CI) = 0.95-0.99]. For advanced and fatal PCa, we found a non-significant inverse association; each one cup increase was associated with a 2% reduced risk of advanced [SHR (95% CI) = 0.98 (0.95-1.02)] and fatal PCa [SHR (95% CI) = 0.98 (0.93-1.03)]. We observed evidence of effect modification by BMI for localized PCa (P-interaction = 0.03); the inverse association was stronger among overweight and obese men (BMI >= 25 kg/m(2)) compared with normal-weight men (BMI < 25 kg/m(2)).

    Conclusions: We observed a clear inverse association between coffee consumption and risk of localized PCa, especially among overweight and obese men.

  • 24.
    Dolan, R. T.
    et al.
    Univ Coll Dublin, Conway Inst, Sch Biomol & Biomed Sci, Dublin 2, Ireland..
    Brennan, D. J.
    Univ Coll Dublin, Conway Inst, Sch Biomol & Biomed Sci, Dublin 2, Ireland..
    Rexhepaj, E.
    Univ Coll Dublin, Conway Inst, Sch Biomol & Biomed Sci, Dublin 2, Ireland..
    Kelly, C. M.
    Univ Coll Dublin, Conway Inst, Sch Biomol & Biomed Sci, Dublin 2, Ireland..
    Penny, S.
    Univ Coll Dublin, Conway Inst, Sch Biomol & Biomed Sci, Dublin 2, Ireland..
    Jirstrom, K.
    Lund Univ, Dept Pathol, Lund, Sweden..
    Ponten, F.
    Uppsala Univ, Dept Pathol, Uppsala, Sweden..
    Uhlén, Mathias
    KTH, Centra, Science for Life Laboratory, SciLifeLab. KTH, Skolan för bioteknologi (BIO), Centra, Albanova VinnExcellence Center for Protein Technology, ProNova.
    Gallagher, W. M.
    Univ Coll Dublin, Conway Inst, Sch Biomol & Biomed Sci, Dublin 2, Ireland..
    DEVELOPMENT OF IMMUNOHISTOCHEMICAL SURROGATES FOR PREDICTION OF BREAST CANCER PATIENT OUTCOME VIA HIGH-THROUGHPUT ANTIBODY GENERATION AND APPLICATION OF TISSUE MICROARRAY TECHNOLOGY: AN INITIAL REPORT2009Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 20, s. 54-54Artikkel i tidsskrift (Annet vitenskapelig)
  • 25. du Bois, A
    et al.
    Quinn, M
    Thigpen, T
    Vermorken, J
    Avall-Lundqvist, E
    Bookman, M
    Bowtell, D
    Brady, M
    Casado, A
    Cervantes, A
    Eisenhauer, E
    Friedlaender, M
    Fujiwara, K
    Grenman, S
    Guastalla, JP
    Harper, P
    Högberg, Thomas
    NSGO (Scandinavia).
    Kaye, S
    Kitchener, H
    Kristensen, G
    Mannel, R
    Meier, W
    Miller, B
    Neijt, JP
    Oza, S
    Ozols, R
    Parmar, M
    Pecorelli, S
    Pfisterer, J
    Poveda, A
    Provencher, D
    Pujade-Lauraine, E
    Randall, M
    Rochon, J
    Rustin, G
    Sagae, s
    Stehman, F
    Stuart, G
    Trimble, E
    Vasey, P
    Vergote, L
    Verheijen, R
    Wagner, U
    2004 consensus statements on the management of ovarian cancer: final document of the 3rd International Gynecologic Cancer Intergroup Ovarian Cancer Consensus Conference (GCIG OCCC 2004)2005Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 16, nr supplement 8, s. 36-38Artikkel i tidsskrift (Fagfellevurdert)
  • 26.
    du Bois, A
    et al.
    Department of Gynecology & Gynecologic Oncology, Wiesbaden, Germany..
    Quinn, M
    Thigpen, T
    Vermorken, J
    Åvall-Lundqvist, Elisabeth
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Bookman, M
    Bowtell, D
    Brady, M
    Casado, A
    Cervantes, A
    Eisenhauer, E
    Friedlaender, M
    Fujiwara, K
    Grenman, S
    Guastalla, J P
    Harper, P
    Hogberg, T
    Kaye, S
    Kitchener, H
    Kristensen, G
    Mannel, R
    Meier, W
    Miller, B
    Neijt, J P
    Oza, A
    Ozols, R
    Parmar, M
    Pecorelli, S
    Pfisterer, J
    Poveda, A
    Provencher, D
    Pujade-Lauraine, E
    Randall, M
    Rochon, J
    Rustin, G
    Sagae, S
    Stehman, F
    Stuart, G
    Trimble, E
    Vasey, P
    Vergote, I
    Verheijen, R
    Wagner, U
    2004 consensus statements on the management of ovarian cancer: final document of the 3rd International Gynecologic Cancer Intergroup Ovarian Cancer Consensus Conference (GCIG OCCC 2004).2005Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 16, nr 8, s. viii7-viii12Artikkel i tidsskrift (Fagfellevurdert)
  • 27.
    Duffy, S.W.
    et al.
    Queen Mary University of London, London, United Kingdom.
    Tabar, L.
    Falun Central Hospital, Falun, Sweden.
    Vitak, B.
    Östergötlands Läns Landsting, Bildmedicinskt centrum, Avdelningen för radiologi US.
    Yen, M.F.
    Queen Mary University of London, London, United Kingdom.
    Warwick, J.
    Queen Mary University of London, London, United Kingdom.
    Smith, R.A.
    American Cancer Society, Atlanta, GA, United States.
    Chen, H.H.
    Institute of Preventive Medicine, National Taiwan University, Taipei, Taiwan.
    The Swedish two-county trial of mammographic screening: Cluster randomisation and end point evaluation2003Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 14, nr 8, s. 1196-1198Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The Swedish Two-County Trial has been criticised on the grounds of the cluster randomisation and alleged bias in classification of cause of death. Patients and methods: In the Two-County Trial, 77080 women were randomised to regular invitation to screening (active study population, ASP) and 55985 to no invitation (passive study population, PSP), in 45 geographical clusters. After ~7 years, the PSP was invited to screening and the trial closed. We analysed data using hierarchical statistical models to take account of cluster randomisation, and performed a conservative analysis assuming a systematic difference between ASP and PSP in baseline breast cancer mortality in one of the counties. We also analysed deaths from causes other than breast cancer and from all causes among breast cancer cases diagnosed in the ASP and PSP. Results: Taking account of the cluster randomisation there was a significant 30% reduction in breast cancer mortality in the ASP. Conservatively, assuming a systematic difference between ASP and PSP clusters in baseline breast cancer mortality, there was a significant 27% reduction in mortality in the ASP. Ignoring classification of cause of death, there was a significant 13% reduction in all-cause mortality in breast cancer cases in the ASP. Conclusions: Breast cancer mortality is a valid end point and mammographic screening does indeed reduce mortality from breast cancer. The criticisms of the Swedish Two-County Trial are unfounded.

  • 28. Emterling, A
    et al.
    Wallin, Åsa
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi.
    Arbman, Gunnar
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för kirurgi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Kirurgiska kliniken i Östergötland med verksamhet i Linköping, Norrköping och Motala.
    Sun, Xiao-Feng
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Clinicopathological significance of microsatellite instability and mutated RIZ in colorectal cancer2004Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 15, nr 2, s. 242-246Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Several studies have shown that microsatellite instability (MSI) is related to favourable survival in colorectal cancer patients but there are controversial results. Tumour suppressor gene RIZ is a susceptible mutational target of MSI. However, its clinicopathological significance has not been investigated. We investigated the prognostic significance of MSI in Swedish colorectal cancer patients and the clinicopathological significance of RIZ mutations. Patients and methods: We analysed 438 colorectal adenocarcinomas for MSI by microsatellite analysis. Among them, 29 MSI and 28 microsatellite stable (MSS) tumours were examined for RIZ mutations by DNA sequencing. Results: MSI (13% of 438 cases) was not associated with survival (rate ratio=0.97, 95% confidence interval =0.57-1.64, P=0.90), although it was related to proximal tumour (P <0.001), poor differentiation and mucinous carcinomas (P <0.001), multiple tumours (P=0.01) and negative/weak expression of hMLH1 (P=0.03). RIZ mutations were detected in 31% of 29 MSI tumours but in none of the 28 MSS tumours. The mutations were related to female (P=0.01), proximal tumour (P=0.01), stage B (P=0.01) and poor differentiation (P=0.047). Conclusions: MSI was not a prognostic factor in the Swedish patients included in this study. Clinicopathological variables associated with RIZ mutations might be a consequence of the MSI characteristics.

  • 29.
    Enblom, Anna
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för omvårdnad.
    Johnsson, Anna
    Department of Oncology, University Hospital, Lund, Sweden.
    Hammar, Mats
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Obstetrik och gynekologi. Linköpings universitet, Hälsouniversitetet.
    Onelöv, Erik
    Department of Oncology-Pathology, Division of Clinical Cancer Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Steineck, Gunnar
    Department of Oncology-Pathology, Division of Clinical Cancer Epidemiology, Karolinska Institute, Stockholm, Sweden.
    Börjeson, Sussanne
    Linköpings universitet, Institutionen för medicin och hälsa, Omvårdnad. Linköpings universitet, Hälsouniversitetet.
    Acupuncture Compared To Placebo Acupuncture in Radiotherapy-induced Nausea: a Randomized Controlled Study2012Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 23, nr 5, s. 1353-1361Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    PURPOSE: To evaluate if verum (real) acupuncture is effective against nausea and vomiting during radiotherapy.

    PATIENTS AND METHODS: We randomised blinded cancer patients to verum; penetrating “deqi” creating acupuncture (n=109) in the antiemetic acupuncture point PC6 (three cm above the wrist), or sham (n=106) with a non-penetrating sham needle at a non-acupuncture point six cm above the wrist 2-3 times/week. The patients daily during the radiotherapy period documented nausea and vomiting. Primary endpoint was number of patients with at least one episode of nausea during the whole radiotherapy period. RESULTS: Data was provided by 205 patients (95 %). In the verum acupuncture group, 70 % experienced nausea at least once during the radiotherapy period (p=0.12 compared to the sham group) (mean number of days of 10.1), 25 % vomited and 42 % used antiemetic drugs at least once. In the sham group 62 % experienced nausea (mean number of days 8.7), 28 % vomited and 37 % consumed antiemetic drugs. Ninety five percent in the verum and 96 % in the sham acupuncture group believed that the treatment had been effective against nausea. In both groups 67 % experienced positive effects on relaxation, mood, sleep or pain-reduction, and 89 % wished to receive the treatment again.

    CONCLUSION: Acupuncture creating deqi is not more effective than sham in radiotherapy-induced nausea, but in this study nearly all patients in both groups experienced that the treatment was effective for nausea.

  • 30. Fazio, N
    et al.
    de Braud, F
    Delle Fave, G
    Öberg, Kjell
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Interferon-{alpha} and somatostatin analog in patients with gastroenteropancreatic neuroendocrine carcinoma: single agent or combination?2007Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 18, nr 1, s. 13-19Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    In most cases gastro-enteropancreatic neuroendocrine tumors grow slowly. Interferon-α and somatostatin analogs have shown symptomatic, biochemical, and, in a minority of cases, antiproliferative activity. Generally, they are proposed as single-agent therapy. However, based on in vitro and in vivo evidence, the combined use of these drugs was proposed in several non-randomized trials, indicating that there is an additive effect of the combination. Nevertheless, the three randomized trials published so far did not show a statistically significant survival benefit for the combination compared to the same agents alone, even though an advantage for the combination came out in all three studies. On the other hand, data from non-randomized trials would justify the sequential use of the two drugs or the combination after progression on single agent therapy. Therefore, at present the up-front combined use of interferon-α and somatostatin analog is not justified, whereas it could be indicated after progression to single-agent therapy. Further larger, international, prospective, randomized, multicentric clinical trials studying homogeneous populations would be necessary to give a final answer, but the rarity and heterogeneity of this malignancy does not assure that it will be possible.

  • 31. Fedirko, V.
    et al.
    Lukanova, A.
    Bamia, C.
    Trichopolou, A.
    Trepo, E.
    Noethlings, U.
    Schlesinger, S.
    Aleksandrova, K.
    Boffetta, P.
    Tjonneland, A.
    Johnsen, N. F.
    Overvad, K.
    Fagherazzi, G.
    Racine, A.
    Boutron-Ruault, M. C.
    Grote, V.
    Kaaks, R.
    Boeing, H.
    Naska, A.
    Adarakis, G.
    Valanou, E.
    Palli, D.
    Sieri, S.
    Tumino, R.
    Vineis, P.
    Panico, S.
    Bueno-de-Mesquita, H. B(as).
    Siersema, P. D.
    Peeters, P. H.
    Weiderpass, E.
    Skeie, G.
    Engeset, D.
    Quiros, J. R.
    Zamora-Ros, R.
    Sanchez, M. J.
    Amiano, P.
    Huerta, J. M.
    Barricarte, A.
    Johansen, D.
    Lindkvist, B.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Werner, Mårten
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Crowe, F.
    Khaw, K. T.
    Ferrari, P.
    Romieu, I.
    Chuang, S. C.
    Riboli, E.
    Jenab, M.
    Glycemic index, glycemic load, dietary carbohydrate, and dietary fiber intake and risk of liver and biliary tract cancers in Western Europeans2013Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, nr 2, s. 543-553Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The type and quantity of dietary carbohydrate as quantified by glycemic index (GI) and glycemic load (GL), and dietary fiber may influence the risk of liver and biliary tract cancers, but convincing evidence is lacking. The association between dietary GI/GL and carbohydrate intake with hepatocellular carcinoma (HCC; N = 191), intrahepatic bile duct (IBD; N = 66), and biliary tract (N = 236) cancer risk was investigated in 477 206 participants of the European Prospective Investigation into Cancer and Nutrition cohort. Dietary intake was assessed by country-specific, validated dietary questionnaires. Hazard ratios and 95% confidence intervals were estimated from proportional hazard models. HBV/HCV status was measured in a nested case-control subset. Higher dietary GI, GL, or increased intake of total carbohydrate was not associated with liver or biliary tract cancer risk. For HCC, divergent risk estimates were observed for total sugar = 1.43 (1.17-1.74) per 50 g/day, total starch = 0.70 (0.55-0.90) per 50 g/day, and total dietary fiber = 0.70 (0.52-0.93) per 10 g/day. The findings for dietary fiber were confirmed among HBV/HCV-free participants [0.48 (0.23-1.01)]. Similar associations were observed for IBD [dietary fiber = 0.59 (0.37-0.99) per 10 g/day], but not biliary tract cancer. Findings suggest that higher consumption of dietary fiber and lower consumption of total sugars are associated with lower HCC risk. In addition, high dietary fiber intake could be associated with lower IBD cancer risk.

  • 32. Fedirko, V
    et al.
    Trichopolou, A
    Bamia, C
    Duarte-Salles, T
    Trepo, E
    Aleksandrova, K
    Nöthlings, U
    Lukanova, A
    Lagiou, P
    Boffetta, P
    Trichopoulos, D
    Katzke, VA
    Overvad, K
    Tjønneland, A
    Hansen, L
    Boutron-Ruault, MC
    Fagherazzi, G
    Bastide, N
    Panico, S
    Grioni, S
    Vineis, P
    Palli, D
    Tumino, R
    Bueno-de-Mesquita, HB
    Peeters, PH
    Skeie, G
    Engeset, D
    Parr, CL
    Jakszyn, P
    Sánchez, MJ
    Barricarte, A
    Amiano, P
    Chirlaque, M
    Quirós, JR
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Werner, Mårten
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Sonestedt, E
    Ericson, U
    Key, TJ
    Khaw, KT
    Ferrari, P
    Romieu, I
    Riboli, E
    Jenab, M
    Consumption of fish and meats and risk of hepatocellular carcinoma: the European Prospective Investigation into Cancer and Nutrition (EPIC)2013Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, nr 8, s. 2166-2173Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: While higher intake of fish and lower consumption of red/processed meats have been suggested to play a protective role in the etiology of several cancers, prospective evidence for hepatocellular carcinoma (HCC) is limited, particularly in Western European populations.

    METHODS: The associations of fish and meats with HCC risk were analyzed in the EPIC cohort. Between 1992 and 2010, 191 incident HCC were identified among 477 206 participants. Baseline diet was assessed using validated dietary questionnaires. A single 24-h diet recall from a cohort subsample was used for calibration. Multivariable proportional hazard regression was utilized to estimate hazard ratios (HR) and 95% confidence intervals (CI). In a nested case-control subset (HCC = 122), HBV/HCV status and liver function biomarkers were measured.

    RESULTS: HCC risk was inversely associated with intake of total fish (per 20 g/day increase, HR = 0.83, 95% CI 0.74-0.95 and HR = 0.80, 95% CI 0.69-0.97 before and after calibration, respectively). This inverse association was also suggested after adjusting for HBV/HCV status and liver function score (per 20-g/day increase, RR = 0.86, 95% CI 0.66-1.11 and RR = 0.74, 95% CI 0.50-1.09, respectively) in a nested case-control subset. Intakes of total meats or subgroups of red/processed meats, and poultry were not associated with HCC risk.

    CONCLUSIONS: In this large European cohort, total fish intake is associated with lower HCC risk.

  • 33.
    Ferolla, P.
    et al.
    Umbria Reg Canc Network, Multidisciplinary NET Grp, Dept Med Oncol, Perugia, Italy.;Univ Perugia, Perugia, Italy..
    Brizzi, M. P.
    Univ Turin, Dept Oncol, Turin, Italy..
    Meyer, T.
    Royal Free Hosp, Oncol, London, England.;UCL, London, England..
    Mansoor, W.
    Christie NHS Fdn Trust, Dept Med Oncol, Manchester, Lancs, England..
    Mazieres, J.
    Hop Larrey, CHU Toulouse, Med Oncol, Toulouse, France..
    Cao, C. D.
    CHRU Lille, Med Oncol, Lille, France..
    Lena, H.
    Ctr Hosp Univ, Pneumol, Rennes, France..
    Berruti, A.
    Univ Brescia, Med Oncol, Brescia, Italy..
    Damiano, V.
    Azienda Osped Univ Policlin Federico II AOU Feder, Dept Dip Oncol, Endocr Mol Clin, Naples, Italy..
    Buikhuisen, W.
    Netherlands Canc Inst, Dept Thorac Oncol, Amsterdam, Netherlands..
    Stankovic, M.
    Novartis Pharma Serv Inc, Med Affairs, Novi Beograd, Serbia..
    Singh, N.
    Cognizant Technol Solut, PLS Clin Project Mgt, Bombay, Maharashtra, India..
    Chiodini, E.
    Parexel, Clin, Origgio, Italy..
    Gislimberti, G.
    OORE GMO, Gislimberti, Origgio, Italy..
    Öberg, Kjell E.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Endokrin tumörbiologi.
    Baudin, E.
    Inst Gustave Roussy, Endocrinol, Villejuif, France..
    Efficacy and safety of pasireotide LAR or everolimus alone, or in combination in patients with advanced carcinoids (NET) of the lung/thymus: Results from the randomized, phase 2 LUNA study2016Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 27, nr 6, artikkel-id 4160Artikkel i tidsskrift (Fagfellevurdert)
  • 34. Foukakis, T.
    et al.
    Åström, Gunnar
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för radiologi.
    Lindström, L.
    Hatschek, T.
    Bergh, J.
    When to order a biopsy to characterise a metastatic relapse in breast cancer2012Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 23, s. 349-353Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Today, the diagnosis of metastatic breast cancer is usually based on radiological findings, and therapeutic decisions are made by considering the pathological characteristics and predictive markers of the primary tumour. Accumulating evidence suggests that tumour characteristics, including estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2), are unstable through tumour progression. Several retrospective studies and, recently, two prospective studies have investigated the discrepancies in receptor status between primary tumours and the corresponding metastases in a total of 1773 patients (for ER) and 2845 patients (for HER2). Changes in ER and HER2 status in these studies range from 14.5% to 40% and from 0% to 37.5%, respectively. In the two prospective studies, a different diagnosis, usually non-malignant, was obtained in 3% and 9% of the cases, and the biopsy led to a treatment modification in about one out of seven patients. Here, we review and discuss the currently available data and provide our recommendations on when a metastatic biopsy should be obtained.

  • 35. Frederiksen, C.
    et al.
    Qvortrup, C.
    Christensen, I. J.
    Glimelius, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    Berglund, Åke
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    Jensen, B. V.
    Nielsen, S. E.
    Keldsen, N.
    Nielsen, H. J.
    Brunner, N.
    Pfeiffer, P.
    Plasma TIMP-1 levels and treatment outcome in patients treated with XELOX for metastatic colorectal cancer2011Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 22, nr 2, s. 369-375Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: The aim was to evaluate the association between plasma tissue inhibitor of metalloproteinase-1 (TIMP-1) and serum carcinoembryonic antigen (CEA) levels and outcome in patients with metastatic colorectal cancer (mCRC) receiving XELOX (combination chemotherapy with capecitabine and oxaliplatin) as first-line treatment. Patients and methods: One hundred and twenty patients were included. Blood samples were collected before treatment and 3 weeks later before the next treatment cycle. Plasma TIMP-1 and serum CEA levels were correlated to treatment outcome. Results: No significant associations between baseline TIMP-1 or CEA levels and best response to treatment or progression-free survival (PFS) could be demonstrated. In contrast, high baseline plasma TIMP-1 levels were associated with poor overall survival (OS), P = 0.008, hazard ratio (HR) = 1.80 [95% confidence interval (CI): 1.17-2.78]. Furthermore, increase in TIMP-1 levels from baseline to immediately before the second cycle of chemotherapy had a significant negative effect on survival (P = 0.03, HR = 1.30, 95% CI: 1.02-1.65) while a decrease in TIMP-1 was significantly associated with a higher objective response rate (P = 0.03). Conclusions: Both high baseline and subsequent increase in TIMP-1 levels were associated with shorter OS in patients with mCRC receiving XELOX as first-line treatment, whereas baseline TIMP-1 levels were not associated with response or PFS following XELOX treatment.

  • 36.
    Frenzel, K.
    et al.
    BioNTech Grp Mainz, Mainz, Germany..
    Heesen, L.
    BioNTech Grp Mainz, Mainz, Germany..
    Bolte, S.
    BioNTech Grp Mainz, Mainz, Germany..
    Bukur, V.
    BioNTech Grp Mainz, Mainz, Germany..
    Diken, M.
    TRON gGmbH, TRON, Mainz, Germany..
    Derhovanessian, E.
    BioNTech Grp Mainz, Mainz, Germany..
    Kreiter, S.
    BioNTech Grp Mainz, Mainz, Germany..
    Kuhn, A.
    BioNTech Grp Mainz, Mainz, Germany..
    Kuehlcke, K.
    EUFETS GmbH, Idar Oberstein, Germany..
    Löwer, M.
    TRON gGmbH, TRON, Mainz, Germany..
    De Greve, J.
    UZ Brussels, Dept Med & Mol Oncol, Brussels, Belgium..
    Lindman, Henrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Experimentell och klinisk onkologi.
    Pascolo, S.
    Univ Zurich, URPP Translat Canc Res, Zurich, Switzerland..
    Schmidt, M.
    Univ Med Mainz, Klin & Poliklin Geburtshilfe & Frauengesundheit, Mainz, Germany..
    Schneeweiss, A.
    NCT Heidelberg, Sekt Gynakol Onkol, Heidelberg, Germany..
    Sjöblom, Tobias
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Experimentell och klinisk onkologi.
    Thielemans, K.
    Univ Hosp Brussels, Dept Immunol Physiol, Brussels, Belgium..
    Zitvogel, L.
    Gustave Roussy Inst Cancerol, Tumour Immunol & Immunotherapy, Villejuif, France..
    Tuereci, Ö.
    CI3 Cluster Individualized Immunointervent, Mainz, Germany..
    Sahin, U.
    BioNTech Grp Mainz, Mainz, Germany..
    Mutanome engineered RNA immuno-therapy (MERIT) for patients with triple negative breast cancer2017Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, nr suppl 11Artikkel i tidsskrift (Annet vitenskapelig)
  • 37. Försti, A
    et al.
    Lei, H
    Tavelin, Björn
    Norrlands University Hospital.
    Enquist, K
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Palmqvist, Richard
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Altieri, A
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Hemminki, K
    Lenner, Per
    Norrlands University Hospital.
    Polymorphisms in the genes of the urokinase plasminogen activation system in relation to colorectal cancer2007Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 18, nr 12, s. 1990-1994Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Extracellular matrix degradation, mediated by the urokinase plasminogen activation (uPA) system, is a critical step in tumor invasion and metastasis. High tumor levels of uPA and its inhibitor PAI-1 have been correlated with poor cancer prognosis. We examined four single nucleotide polymorphisms (SNPs) with a potential effect on expression of genes in the uPA system for their role in colorectal cancer susceptibility and prognosis.

    Patients and methods: We genotyped the SNPs in 308 Swedish incident colorectal cancer patients with up to 16 years of follow-up and in 585 age- and sex-matched controls. We evaluated the associations between genotypes and colorectal cancer and Dukes' stage. Survival probabilities were compared between different subgroups.

    Results: Patients with PAI-1 –675 5G/5G genotype had better survival than patients with 4G/4G or 4G/5G genotypes when they had Dukes' stage A or B tumors (P = 0.023 and P = 0.015, respectively). No statistically significant association was observed between the SNPs and the risk of colorectal cancer or Dukes' stage.

    Conclusions: Our results suggest a role for the PAI-1 genotype in colorectal cancer prognosis, but further studies are needed to evaluate the impact of our finding in the clinic.

  • 38.
    Genkinger, J. M.
    et al.
    Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, Med Ctr, New York, NY 10019 USA;Columbia Univ, Herbert Irving Comprehens Canc Ctr, Canc Epidemiol Program, Med Ctr, New York, NY 10019 USA.
    Wu, K.
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA.
    Wang, M.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Biostat, Boston, MA USA;Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
    Albanes, D.
    NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
    Black, A.
    NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
    van den Brandt, P. A.
    Maastricht Univ, Grow Sch Oncol & Dev Biol, Dept Epidemiol, Maastricht, Netherlands.
    Burke, K. A.
    Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, Med Ctr, New York, NY 10019 USA.
    Cook, M. B.
    NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
    Gapstur, S. M.
    Amer Canc Soc, Behav & Epidemiol Res Grp, Atlanta, GA 30329 USA.
    Giles, G. G.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.
    Giovannucci, E.
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
    Goodman, G. G.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Goodman, P. J.
    SWOG Stat Ctr, Seattle, WA USA.
    Håkansson, N.
    Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
    Key, T. J.
    Univ Oxford, Nuffield Dept Populat Hlth, Canc Epidemiol Unit, Oxford, England.
    Mannistö, S.
    Natl Inst Hlth & Welf, Dept Publ Hlth Solut, Helsinki, Finland.
    Le Marchand, L.
    Univ Hawaii, Epidemiol Program, Canc Ctr, Honolulu, HI 96822 USA.
    Liao, L. M.
    NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
    MacInnis, R. J.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.
    Neuhouser, M. L.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Platz, E. A.
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
    Sawada, N.
    Natl Canc Ctr, Ctr Publ Hlth Sci, Epidemiol & Prevent Grp, Tokyo, Japan.
    Schenk, J. M.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Stevens, V. L.
    Amer Canc Soc, Behav & Epidemiol Res Grp, Atlanta, GA 30329 USA.
    Travis, R. C.
    Univ Oxford, Nuffield Dept Populat Hlth, Canc Epidemiol Unit, Oxford, England.
    Tsugane, S.
    Natl Canc Ctr, Ctr Publ Hlth Sci, Epidemiol & Prevent Grp, Tokyo, Japan.
    Visvanathan, K.
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
    Wilkens, L. R.
    Univ Hawaii, Epidemiol Program, Canc Ctr, Honolulu, HI 96822 USA.
    Wolk, Alicja
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Ortopedi. Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
    Smith-Warner, S. A.
    Harvard TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Measures of body fatness and height in early and mid-to-late adulthood and prostate cancer: risk and mortality in The Pooling Project of Prospective Studies of Diet and Cancer2020Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 31, nr 1, s. 103-114Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Advanced prostate cancer etiology is poorly understood. Few studies have examined associations of anthropometric factors (e.g. early adulthood obesity) with advanced prostate cancer risk.

    Patients and methods: We carried out pooled analyses to examine associations between body fatness, height, and prostate cancer risk. Among 830 772 men, 51 734 incident prostate cancer cases were identified, including 4762 advanced (T4/N1/M1 or prostate cancer deaths) cases, 2915 advanced restricted (same as advanced, but excluding localized cancers that resulted in death) cases, 9489 high-grade cases, and 3027 prostate cancer deaths. Cox proportional hazards models were used to calculate study-specific hazard ratios (HR) and 95% confidence intervals (CI); results were pooled using random effects models.

    Results: No statistically significant associations were observed for body mass index (BMI) in early adulthood for advanced, advanced restricted, and high-grade prostate cancer, and prostate cancer mortality. Positive associations were shown for BMI at baseline with advanced prostate cancer (HR = 1.30, 95% CI = 0.95-1.78) and prostate cancer mortality (HR = 1.52, 95% CI = 1.12-2.07) comparing BMI >= 35.0 kg/m(2) with 21-22.9 kg/m(2). When considering early adulthood and baseline BMI together, a 27% higher prostate cancer mortality risk (95% CI = 9% to 49%) was observed for men with BMI <25.0 kg/m(2) in early adulthood and BMI >= 30.0 kg/m(2) at baseline compared with BMI <25.0 kg/m(2) in early adulthood and BMI <30.0 kg/m(2) at baseline. Baseline waist circumference, comparing >= 110 cm with <90 cm, and waist-to-hip ratio, comparing >= 1.00 with <0.90, were associated with significant 14%-16% increases in high-grade prostate cancer risk and suggestive or significant 20%-39% increases in prostate cancer mortality risk. Height was associated with suggestive or significant 33%-56% risks of advanced or advanced restricted prostate cancer and prostate cancer mortality, comparing >= 1.90 m with <1.65 m.

    Conclusion: Our findings suggest that height and total and central adiposity in mid-to-later adulthood, but not early adulthood adiposity, are associated with risk of advanced forms of prostate cancer. Thus, maintenance of healthy weight may help prevent advanced prostate cancer.

  • 39.
    Glimelius, B
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för onkologi.
    Oliveira, J
    Rectal cancer: ESMO clinical recommendations for diagnosis, treatment and follow-up2008Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 19 Suppl 2, s. ii31-2Artikkel i tidsskrift (Annet vitenskapelig)
  • 40.
    Glimelius, B.
    et al.
    Department of Oncology, Radiology and Clinical Immunology, Uppsala University Hospital, SE-751 85 Uppsala, Sweden, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Sorbye, H.
    Sørbye, H., Department of Oncology, Haukeland University Hospital, Bergen, Norway.
    Balteskard, L.
    Department of Oncology, University Hospital, Tromsö, Norway.
    Bystrom, P.
    Byström, P., Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Pfeiffer, P.
    Department of Oncology, University Hospital, Odense, Denmark.
    Tveit, K.
    Department of Oncology, Ullevål University Hospital, Oslo, Norway.
    Heikkila, R.
    Heikkilä, R., Department of Hemato-Oncology, Stavanger University Hospital, Stavanger, Norway.
    Keldsen, N.
    Department of Oncology, Central Hospital, Herning, Denmark.
    Albertsson, M.
    Department of Oncology, University Hospital, Malmö, Sweden.
    Starkhammar, Hans
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Garmo, H.
    Regional Oncologic Center, Uppsala, Sweden.
    Berglund, A.
    Berglund, Å., Department of Oncology, Radiology and Clinical Immunology, Uppsala University Hospital, SE-751 85 Uppsala, Sweden.
    A randomized phase III multicenter trial comparing irinotecan in combination with the Nordic bolus 5-FU and folinic acid schedule or the bolus/infused de Gramont schedule (Lv5FU2) in patients with metastatic colorectal cancer2008Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 19, nr 5, s. 909-914Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: To compare irinotecan with the Nordic 5-fluorouracil (5-FU) and folinic acid (FA) bolus schedule [irinotecan 180 mg/m2 on day 1, 5-FU 500 mg/m2 and FA 60 mg/m2 on day 1 and 2 (FLIRI)] or the Lv5FU2 schedule [irinotecan 180 mg/m2 on day 1, FA 200 mg/m2, 5-FU bolus 400 mg/m2 and infused 5-FU 600 mg/m2 on day 1 and 2 (Lv5FU2-IRI)] due to uncertainties about how to administrate 5-FU with irinotecan. Patients and methods: Patients (n = 567) with metastatic colorectal cancer were randomly assigned to receive FLIRI or Lv5FU2-IRI. Primary end point was progression-free survival (PFS). Results: Patient characteristics were well balanced. PFS did not differ between groups (median 9 months, P = 0.22). Overall survival (OS) was also similar (median 19 months, P = 0.9). Fewer objective responses were seen in the FLIRI group (35% versus 49%, P = 0.001) but the metastatic resection rate did not differ (4% versus 6%, P = 0.3). Grade 3/4 neutropenia (11% versus 5%, P = 0.01) and grade 2 alopecia (18% versus 9%, P = 0.002) were more common in the FLIRI group. The 60-day mortality was 2.4% versus 2.1%. Conclusions: Irinotecan with the bolus Nordic schedule (FLIRI) is a convenient treatment with PFS and OS comparable to irinotecan with the Lv5FU2 schedule. Neutropenia and alopecia are more prevalent, but both regimens are equally well tolerated. © The Author 2008. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved.

  • 41.
    Glimelius, Bengt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för onkologi.
    Adjuvant chemotherapy in rectal cancer: an issue or a nonissue?2010Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 21, nr 9, s. 1739-1741Artikkel i tidsskrift (Fagfellevurdert)
  • 42.
    Glimelius, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    Lahn, M.
    Window-of-opportunity trials to evaluate clinical activity of new molecular entities in oncology2011Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 22, nr 8, s. 1717-1725Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Background: The introduction of molecular targeted agents (e. g. monoclonal antibodies or kinase inhibitors) and cancer vaccines has raised the question whether alternate clinical trial designs, including window trials, are better suited to evaluate such new molecular entities (NMEs) and improve their approval rates. In window trials, patients receive an NME for a window of time before starting standard treatment allowing the evaluation of an NME in tumors unperturbed by previous therapies. Methods: A systematic literature search was conducted to identify window trials in adult and pediatric oncology. Results: Twenty-nine window trials were identified and reviewed, 13 in pediatric and 16 in adult oncology. Most of the trials (20/29) tested cytotoxics known to have activity in other clinical situations. In contrast to trials with pretreated patients, the window trials established the antitumor activity of melphalan, topotecan, epirubicin and etoposide in untreated patients with rhabdomyosarcoma or small-cell lung cancer. In window trials with ineffective or modestly active NMEs, we found no indication of a significant negative effect on overall survival for participating patients. Conclusions: Provided close safety monitoring and careful patient selection, window trials are a safe option to investigate potential clinical activity of NMEs.

  • 43.
    Glimelius, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Lahn, M.
    Gawande, S.
    Cleverly, A.
    Darstein, C.
    Musib, L.
    Liu, Y.
    Spindler, K. L.
    Frödin, J-E.
    Berglund, Åke
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Byström, P.
    Qvortrup, C.
    Jakobsen, A.
    Pfeiffer, P.
    A window of opportunity phase II study of enzastaurin in chemonaive patients with asymptomatic metastatic colorectal cancer2010Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 21, nr 5, s. 1020-1026Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Preclinically, protein kinase C and AKT activation can be inhibited by enzastaurin and reduce tumor growth of colorectal cancer cells. In asymptomatic patients with metastatic colorectal cancer (mCRC), enzastaurin activity was evaluated by measuring the 6-month progression-free survival (PFS) rate in a window study design. PATIENTS AND METHODS: Chemonaive patients with asymptomatic mCRC who did not require immediate chemotherapy-induced tumor reduction received a 400-mg thrice daily loading dose of enzastaurin on day 1 of cycle 1, followed by 500 mg once daily for the remaining 28-day cycles. Progression was assessed on the basis of radiographic imaging, rise in carcinoembryonic antigen or lactate dehydrogenase (LDH) levels or by appearance of clinical symptoms. RESULTS: Twenty-eight patients received daily enzastaurin. The 6-month PFS rate was 28% [95% confidence interval (CI) 13%-45%] and median PFS was 1.9 months (95% CI 1.8-4.5 months). Twelve (43%) patients had stable disease with a median duration of 6.1 months. The survival rate at 20 months was 77% (95% CI 47%-92%). No grade 4 toxicity was reported and grade 3 toxic effects were observed in three patients with one patient showing probable drug-related elevation of liver transaminases. CONCLUSION: The window design in asymptomatic patients with mCRC can be safely applied to assess the activity and safety of novel cytostatic agents like enzastaurin.

  • 44.
    Glimelius, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Oliveira, J.
    Rectal cancer: ESMO clinical recommendations for diagnosis, treatment and follow-up2009Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, ISSN 1569-8041, Vol. 20, nr Suppl 4, s. 54-6Artikkel i tidsskrift (Fagfellevurdert)
  • 45.
    Glimelius, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Påhlman, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Kolorektalkirurgi.
    Cervantes, A.
    Rectal cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up2010Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 21, nr Suppl 5, s. v82-v86Artikkel i tidsskrift (Fagfellevurdert)
  • 46.
    Glimelius, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Spindler, K. L.
    Frödin, J-E.
    Berglund, Åke
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Byström, P.
    Qvortrup, C.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Jakobsen, A.
    Pfeiffer, P.
    Long-term follow-up of chemonaive patients with asymptomatic metastatic colorectal cancer treated with enzastaurin in a window of opportunity phase II study2010Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 21, nr 5, s. 1127-1128Artikkel i tidsskrift (Fagfellevurdert)
  • 47.
    Glimelius, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för onkologi.
    Sørbye, H
    Balteskard, L
    Byström, P
    Pfeiffer, P
    Tveit, K
    Heikkilä, R
    Keldsen, N
    Albertsson, M
    Starkhammar, H
    Garmo, H
    Berglund, Åke
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för onkologi.
    A randomized phase III multicenter trial comparing irinotecan in combination with the Nordic bolus 5-FU and folinic acid schedule or the bolus/infused de Gramont schedule (Lv5FU2) in patients with metastatic colorectal cancer2008Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 19, nr 5, s. 909-914Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: To compare irinotecan with the Nordic 5- fluorouracil (5- FU) and folinic acid (FA) bolus schedule [ irinotecan 180 mg/m(2) on day 1, 5- FU 500 mg/m(2) and FA 60 mg/m(2) on day 1 and 2 (FLIRI)] or the Lv5FU2 schedule [ irinotecan 180 mg/m(2) on day 1, FA 200 mg/m(2), 5- FU bolus 400 mg/m(2) and infused 5- FU 600 mg/m(2) on day 1 and 2 (Lv5FU2- IRI)] due to uncertainties about how to administrate 5- FU with irinotecan.

    Patients and methods: Patients (n = 567) with metastatic colorectal cancer were randomly assigned to receive FLIRI or Lv5FU2- IRI. Primary end point was progression- free survival (PFS).

    Results: Patient characteristics were well balanced. PFS did not differ between groups (median 9 months, P = 0.22). Overall survival (OS) was also similar (median 19 months, P = 0.9). Fewer objective responses were seen in the FLIRI group (35% versus 49%, P = 0.001) but the metastatic resection rate did not differ (4% versus 6%, P = 0.3). Grade 3/4 neutropenia (11% versus 5%, P = 0.01) and grade 2 alopecia (18% versus 9%, P = 0.002) were more common in the FLIRI group. The 60- day mortality was 2.4% versus 2.1%.

    Conclusions: Irinotecan with the bolus Nordic schedule (FLIRI) is a convenient treatment with PFS and OS comparable to irinotecan with the Lv5FU2 schedule. Neutropenia and alopecia are more prevalent, but both regimens are equally well tolerated.

  • 48.
    Glimelius, Bengt
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för radiologi, onkologi och strålningsvetenskap, Enheten för onkologi.
    Tiret, E.
    Cervantes, A.
    Arnold, D.
    Rectal cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up2013Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, nr Suppl. 6, s. 81-88Artikkel i tidsskrift (Fagfellevurdert)
  • 49. Gonzalez, C. A.
    et al.
    Megraud, F.
    Buissonniere, A.
    Lujan Barroso, L.
    Agudo, A.
    Duell, E. J.
    Boutron-Ruault, M. C.
    Clavel-Chapelon, F.
    Palli, D.
    Krogh, V.
    Mattiello, A.
    Tumino, R.
    Sacerdote, C.
    Quiros, J. R.
    Sanchez-Cantalejo, E.
    Navarro, C.
    Barricarte, A.
    Dorronsoro, M.
    Khaw, K. -T
    Wareham, N.
    Allen, N. E.
    Tsilidis, K. K.
    Bueno-de-Mesquita, H. Bas
    Jeurnink, S. M.
    Numans, M. E.
    Peeters, P. H. M.
    Lagiou, P.
    Valanou, E.
    Trichopoulou, A.
    Kaaks, R.
    Lukanova-McGregor, A.
    Bergman, M. M.
    Boeing, H.
    Manjer, J.
    Lindkvist, B.
    Stenling, Roger
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Mortensen, L. M.
    Overvad, K.
    Olsen, A.
    Tjonneland, A.
    Bakken, K.
    Dumeaux, V.
    Lund, E.
    Jenab, M.
    Romieu, I.
    Michaud, D.
    Mouw, T.
    Carneiro, F.
    Fenge, C.
    Riboli, E.
    Helicobacter pylori infection assessed by ELISA and by immunoblot and noncardia gastric cancer risk in a prospective study: the Eurgast-EPIC project2012Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 23, nr 5, s. 1320-1324Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    In epidemiological studies, Helicobacter pylori infection is usually detected by enzyme-linked immunosorbent assay (ELISA). However, infection can spontaneously clear from the mucosa during the progression of atrophy and could lead to substantial under-detection of infection and underestimation of its effect on gastric cancer (GC) risk. Antibodies detected by western blot are known to persist longer after the loss of the infection. In a nested case-control study from the Eurogast-EPIC cohort, including 88 noncardia GC cases and 338 controls, we assessed the association between noncardia GC and H. pylori infection comparing antibodies detected by western blot (HELICOBLOT2.1) to those detected by ELISA (Pyloriset EIA-GIII((R))). By immunoblot, 82 cases (93.2%) were H. pylori positive, 10 of these cases (11.4%) were negative by ELISA and only 6 cases (6.8%) were negative by both ELISA and immunoblot. Multivariable odds ratio (OR) for noncardia GC comparing immunoglobulin G positive versus negative by ELISA was 6.8 [95% confidence interval (CI) 3.0-15.1], and by immunoblot, the OR was 21.4 (95% CI 7.1-64.4). Using a western blot assay, nearly all noncardia GC were classified as H. pylori positive and the OR was more than threefold higher than the OR assessed by ELISA, supporting the hypothesis that H. pylori infection is a necessary condition for noncardia GC.

  • 50.
    Granberg, Dan
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Eriksson, Barbro
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Wilander, Erik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
    Grimfjärd, Per
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Fjällskog, Marie-Louise
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Öberg, Kjell
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Skogseid, Britt
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Experience in treatment of metastatic pulmonary carcinoid tumors2001Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 12, nr 10, s. 1383-1391Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND:

    The only cure for patients with pulmonary carcinoids is surgery. In the present paper, we report the results of medical treatment of patients with metastatic tumors, their circulating hormone markers, and immunohistochemical profile of the tumors. PATIENTS AND

    METHODS/RESULTS:

    The response to systemic antitumoral treatment was studied in 31 patients with metastatic pulmonary carcinoids. Median survival from treatment start was 25 months. Alpha-interferon treatment has resulted in stable disease in 4 of 27 patients (median duration 15 months), while 23 patients showed progressive disease. Somatostatin analogues given as single drug treatment resulted in progressive disease. Streptozotocin and 5-fluorouracil resulted in progressive disease in seven of seven patients. Stable disease was obtained for 8 and 10 months respectively in two of two patients treated with streptozotocin + doxorubicin. Two of eight patients treated with cisplatinum + etoposide showed a significant decrease in tumor size lasting six and eight months respectively, and one displayed stable disease for seven months. Elevation of plasma chromogranin A was seen in 93%.

    CONCLUSIONS:

    The results of systemic antitumoral treatment of pulmonary carcinoids with distant metastases are generally discouraging. Chemotherapy with cisplatinum + etoposide, or doxorubicin combined with streptozotocin or paclitaxel may be of value. Alpha-interferon and octreotide offer efficient symptomatic relief, but stabilizes tumor growth in merely 15% of the cases. Plasma chromogranin A is the most frequently elevated tumor marker.

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