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  • 1. Braun, M.
    et al.
    Shaikhibrahim, Z.
    Menon, R.
    Offermann, A.
    Queisser, A.
    Boehm, D.
    Vogel, W.
    Ruenauver, K.
    Ruiz, C.
    Zellweger, T.
    Svensson, Maria A.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Kristiansen, G.
    Wernert, N.
    Bubendorf, L.
    Perner, S.
    MED15, Encoding a Subunit of the Mediator Complex, Is Overexpressed at High Frequency in Castration-Resistant Prostate Cancer2014In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 27, p. 219A-219AArticle in journal (Other academic)
  • 2.
    Davidsson, Sabina
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital.
    Ohlson, Anna-Lena
    Dept Urology, Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Meisner, Allison
    School of Public Health, Dept Epidemiology, Harvard University, Boston MA, USA.
    Fiorentino, Michelangelo
    School of Public Health, Dept Epidemiology, Harvard University, Boston MA, USA; Molecular Pathology Lab, Dept Hematological Oncology, Addarii Institute of Oncology, University of Bologna, Bologna, Italy.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital.
    Rider, Jennifer R
    School of Public Health, Dept Epidemiology and School of Medicine, Harvard Univ, Boston MA, USA; Dept Med, Channing Lab, Brigham & Womens Hosp, Boston MA, USA.
    CD4 helper T cells, CD8 cytotoxic T cells, and FOXP3(+) regulatory T cells with respect to lethal prostate cancer2013In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 26, no 3, p. 448-455Article in journal (Refereed)
    Abstract [en]

    Prostate cancer represents a major contributor to cancer mortality, but the majority of men with prostate cancer will die of other causes. Thus, a challenge is identifying potentially lethal disease at diagnosis. Conflicting results have been reported when investigating the relationship between infiltration of lymphocytes and survival in prostate cancer. One of the mechanisms suggested is the recruitment of regulatory T cells (T(regs)), a subpopulation of T cells that have a role in promoting tumor growth. T(regs) counteract tumor rejection through suppressive functions on the anti-immune response but their prognostic significance is still unknown. We report here the results of a conducted case-control study nested in a cohort of men treated with transurethral resection of the prostate and diagnosed incidentally with prostate cancer. Cases are men who died of prostate cancer (n=261) and controls are men who survived >10 years after their diagnosis (n=474). Infiltration of both T(helper) and T(cytotoxic) cells was frequently observed and the majority of the T(regs) were CD4(+). T(helper) or T(cytotoxic) cells were not associated with lethal prostate cancer. However, we found a nearly twofold increased risk of lethal prostate cancer when comparing the highest with the lowest quartile of CD4(+) T(reg) cells (95% confidence interval: 1.3-2.9). Our conclusion is that men with greater numbers of CD4(+) T(regs) in their prostate tumor environment have an increased risk of dying of prostate cancer. Identification of CD4(+) T(regs) in tumor tissue may predict clinically relevant disease at time of diagnosis independently of other clinical factors.Modern Pathology advance online publication, 5 October 2012; doi:10.1038/modpathol.2012.164.

  • 3. Fiorentino, M.
    et al.
    Mucci, L.
    Fall, Katja
    Bailey, D.
    Fiore, C.
    Judson, G.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Loda, M.
    Immunohistochemical Expression of BRCA1 in Prostate Cancer2009In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 22, p. 169A-169A, article id 760Article in journal (Other academic)
    Abstract [en]

    Background: BRCA1 is a multifunctional protein involved in DNA repair, gene transcription and the regulation of cell-cycle check-points. While germline mutations of BRCA1 are rare in prostate cancer and seem to play a limited role in tumor susceptibility, BRCA1 expression has not been investigated to date.

    Design: We analyzed the immunohistochemical expression of BRCA1 in paraffin embedded samples from 524 men with prostate cancer belonging to the Physicians’ Health Study and the Swedish Watchful Waiting cohorts of prostate cancer patients. High density tissue micro-arrays (TMA) including at least three tumor cores for each case were utilized for the immunohistochemical staining with the monoclonal MS110 antibody specific for the N-terminus of the 220 kDa BRCA1 protein. Cases were scored as negative or positive for BRCA1 immunostaining. The Ki67 proliferation index was also assessed on the same TMAs and evaluated by quantitative image analysis.

    Results: A positive nuclear immunostaining for BRCA1 was revealed in 62 of 524 (11.9%) patients while normal prostate control cores were all negative. BRCA1 positive tumors were associated with 4 times greater proliferation rate compared to BRCA1 negative tumors (p ∼ 0.0003). In addition, we found a linear trend such that tumors with greater number of TMA cores expressing BRCA1 had stronger extent of proliferation. Men with BRCA1 positive tumors had a slightly higher Gleason’s score (mean 7.5) compared to those negative for BRCA1 (mean 7) No significant correlation was found between BRCA1 staining and cancer-specific death.

    Conclusions: BRCA1 protein is expressed in a small subset of prostate cancers characterized by high proliferation index but not in normal prostate tissue. Expression of BRCA1 might be acquired in selected tumors to prevent DNA damage in actively replicating cells. A different role independent of germline mutations might be disclosed for BRCA1 as cell cycle regulator in prostate canc

  • 4. Offermann, A.
    et al.
    Shaikhibraim, Z.
    Braun, M.
    Menon, R.
    Bohm, D.
    Vogel, W.
    Ruiz, C.
    Zellweger, T.
    Svensson, Maria A.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Kristiansen, G.
    Wernert, N.
    Bubendorf, L.
    Kirfel, J.
    Biskup, S.
    Perner, S.
    MED12 Is a Potential Target for Therapeutic Intervention in Castration Resistant Prostate Cancer2014In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 27, no Suppl. 2, p. 466A-466AArticle in journal (Other academic)
  • 5.
    Offermann, Anne
    et al.
    University Medical Center Schleswig-Holstein, Leibniz Center for Medicine and Biosciences, Lübeck and Borstel, Germany.
    Schneider, Felix
    Klinik am Eicher Alb Fils Kliniken, Goeppingen, Germany.
    Hupe, Marie Christine
    University Hospital Schleswig-Holstein, Lübeck, Germany.
    Hohensteiner, Silke
    Klinik am Eichert Alb Fils Kliniken, Goeppingen, Germany.
    Becker, Finn
    University Medical Center Schleswig-Holstein, Leibniz Center for Medicine and Biosciences, Lübeck and Borstel, Germany.
    Carlsson, Jessica
    Örebro University, School of Medical Sciences. Örebro University Hospital.
    Kirfel, Jutta
    University Hospital Schleswig-Holstein, Leibniz Center for Medicine and Biosciences, Lübeck and Borstel, Germany.
    Svensson, Maria
    Örebro University, School of Medical Sciences. Örebro University Hospital.
    Andrén, Ove
    Örebro University, School of Medical Sciences.
    Merseburger, Axel
    University Hospital Lübeck, Lübeck, Germany.
    Lubczyk, Verena
    Klinik am Eichert Alb Fils Kliniken, Goeppingen, Germany.
    Kuefer, Rainer
    Klinik am Eichert Alb Fils Kliniken, Goeppingen, Germany.
    Sven, Perner
    University Medical Center Schleswig-Holstein, Leibniz Center for Medicine and Biosciences, Lübeck and Borstel, Germany, Lübeck.
    TRIM24 as Independent Prognostic Marker in Prostate Cancer2018In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 31, no Suppl. 2, p. 372-373Article in journal (Other academic)
    Abstract [en]

    Background: Simply applicable biomarkers for prostate cancer (PCa) predicting the clinical course are urgently needed. Recently, TRIM24 has been identified to promote androgen-receptor signaling and to correlate with poor outcome. Based on these data, we validated TRIM24 as a prognostic biomarker for PCa.

    Design: We performed TRIM24 immunohistochemistry on two independent cohorts including a total of 806 primary tumors, 26 locally advanced/recurrent tumors, 30 lymph node metastases, 30 distant metastases and 129 benign prostatic samples from 497 patients. Expression data were correlated with clinic-pathological data including biochemical recurrence free survival (bRFS) as endpoint.

    Results: Benign samples show no/low TRIM24 expression in 94%, while tumors demonstrate significantly higher levels. Strongest expression is observed in metastatic tumors. In multivariate analyses, TRIM24 up-regulation correlates with shorter bRFS independent of other prognostic parameters. 5-(10-) year bRFS rates for TRIM24 negative, low, medium and high expressing tumors are 93.1(93.1)%, 75.4(68.5)%, 54.9(47.5)% and 43.1(32.3)%, respectively. Of interest, tumors diagnosed as indolent disease, TRIM24 expression stratifies patients into specific risk groups. Increased TRIM24 expression associates with higher Grade Group, positive nodal status and extraprostatic tumor growth.

    Conclusions: Using two large independent cohorts, we found that TRIM24 expression predicts patients’ risk to develop disease recurrence with high accuracy and independently from other established prognostic markers. To our knowledge, TRIM24 is the first prognostic biomarker to be independent, accurate and reproducible on three different primary PCa cohorts. Thus, we strongly suggest introducing TRIM24 in clinical routine as a simple immunohistochemical test.

  • 6.
    Ricci, Costantino
    et al.
    S.Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy.
    Dorofte, Luiza
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine.
    Franceschini, Tania
    Bologna, Italy.
    Riefolo, Mattia
    S.Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy.
    Giunchi, Francesca
    S.Orsola-Malpighi Hospital, Bologna, Italy.
    Fiorentino, Michelangelo
    Department of Pathology, Sant’Orsola-Malpighi University Hospital, University of Bologna, Bologna, Italy.
    Davidsson, Sabina
    Örebro University, School of Medical Sciences. Örebro University Hospital.
    Lillsunde-Larsson, Gabriella
    Örebro University, School of Health Sciences.
    HPV Status and World Health Organization 2016 Classification of Penile Squamous Cell Carcinoma and Penile Intraepithelial Neoplasia: 206 Cases from a Single, Contemporary, Western Cohort of Patients with Emphasis on the "Discordant Cases"2020In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 33, no Suppl 2, p. 960-961Article in journal (Other academic)
    Abstract [en]

    Background: Penile squamous cel carcinoma (pSCC) cancer has been considered a rare tumour in the western world. Although some conflicting results, the most recent meta-analyses report an increase in its incidence and in the percentage of HPV(+) cases in numerous western countries. This scenario mirrors what observed for HPV(+) oropharynx cancer and could be explained by changes in sexual practice and in exposure of men to HPV. In this study, we analyzed pathological features and HPV-DNA prevalence in a contemporary, western pSCC cohort.

    Design: This study enrolled 206 patients with pSCC from Örebro University. DNA was extracted from paraffin-embedded tumor tissue samples, and HPV-DNA genotyping were performed using PCR method Anyplex II HPV28. In a subset of cases, HPV-DNA was also assessed in penile intraepithelial neoplasia (PeIN), lymph node metastasis (LnM) or both (51%, 11.6% and 18.9%). All the cases have been histologically re-classified according to the WHO 2016 classification of pSCC.

    Results: HPV -DNA was detected in 92/206 (44.7%) pSCC, 78/141 (55.3%) PeIN and 28/61 LnM (45.9%), respectively. HPV16 was the predominant type, representing 78.3% for pSCC, 79.5% for PeIN and 96.4% for LnM. In 7.8% of the cases, more than a HPV genotype has been detected in the same specimen or in different specimens of the same patients. Curiously, we found 8.5% of cases (14/164) with discordance of HPV-DNA detection in different specimens from the same patient (pSCC, PeIN and/or /LnM). In HPV(+) pSCC the predominant histologic subtype was “warty” (41.3%); in HPV(-) pSCC it was “usual” (65.8%). For PeIN, “warty” was the predominant subtype in HPV(+) PeIN (39.7%) and “differentiated” in HPV(-) PeIN (79.4%). For pSCC, we observed disagreement between histology and HPV status in 23.8% of cases: 13.1% HPV(+)/Non-HPV -related histology and 10.7% HPV(-)/HPV-related histology.

    Conclusions: HPV -DNA was observed in a relevant portion of pSCC and PeIN in our case series, confirming an increasing role of HPV in the pathogenesis of this disease. These results are particularly relevant, as they reflect the current epidemiological trend in the western world. Future studies are needed to clarify the exact role of HPV in cases with discordance between histology and HPV status and in cases with disagreement of HPV detection in different specimens from the same patient (pSCC, PeIN and/or LnM).

  • 7. Svensson, Maria A.
    et al.
    Nowak, M.
    Vogel, W.
    Carlsson, Jessica
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Perner, S.
    Combination of Multiple Markers Predicts Prostate Cancer Outcome2014In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 27, p. 262A-262AArticle in journal (Other academic)
  • 8.
    Villman, Kenneth
    et al.
    Department of Oncology, Örebro University Hospital, Örebro, Sweden.
    Ståhl, Elisabeth
    2Department of Pathology, Örebro University Hospital, Örebro, Sweden.
    Liljegren, Göran
    Department of Surgery, Örebro University Hospital, Örebro, Sweden.
    Tidefelt, Ulf
    Department of Medicine, Örebro University Hospital, Örebro, Sweden; Karolinska Institute, Stockholm, Sweden.
    Karlsson, Mats G.
    2Department of Pathology, Örebro University Hospital, Örebro, Sweden.
    Topoisomerase II-alpha expression in different cell cycle phases in fresh human breast carcinomas2002In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 15, no 5, p. 486-491Article in journal (Refereed)
    Abstract [en]

    Topoisomerase II-alpha (topo II alpha) is the key target enzyme for the topoisomerase inhibitor class of anti-cancer drugs. In normal cells, topo II alpha is expressed predominantly in the S/G2/M phase of the cell cycle. In malignant cells, in vitro studies have indicated that the expression of topo II alpha is both higher and less dependent on proliferation state in the cell. We studied fresh specimens from 50 cases of primary breast cancer. The expression of topo II alpha in different cell cycle phases was analyzed with two-parameter flow cytometry using the monoclonal antibody SWT3D1 and propidium iodide staining. The expression of topo II alpha was significantly higher in the S/G2/M phase of the cell cycle than in the G0/G1 phase in both DNA diploid and DNA non-diploid tumors. In 18 of 21 diploid tumors, and in 25 of 29 non-diploid tumors, >50% of the topo II alpha-positive cells were in the G0/G1 phase. This significant expression of topo II alpha in the G0/G1 phase of the cell cycle may have clinically important implications for treatment efficacy of topoisomerase II inhibitors.

  • 9. Villman, Kenneth
    et al.
    Ståhl, Elisabeth
    Liljegren, Göran
    Örebro University, School of Health and Medical Sciences.
    Tidefelt, Ulf
    Örebro University, School of Health and Medical Sciences.
    Karlsson, Mats G.
    Örebro University, School of Health and Medical Sciences.
    Topoisomerase II-α expression in different cell cycle phases in fresh human breast carcinomas2002In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 15, no 5, p. 486-491Article in journal (Refereed)
    Abstract [en]

    Topoisomerase II-alfa (topo IIalfa) is the key target enzyme for the topoisomerase inhibitor class of anti-cancer drugs. In normal cells, topo IIalfa is expressed predominantly in the S/G2/M phase of the cell cycle. In malignant cells, in vitro studies have indicated that the expression of topo IIalfa is both higher and less dependent on proliferation state in the cell. We studied fresh specimens from 50 cases of primary breast cancer. The expression of topo IIalfa in different cell cycle phases was analyzed with two-parameter flow cytometry using the monoclonal antibody SWT3D1 and propidium iodide staining. The expression of topo IIalfa was significantly higher in the S/G2/M phase of the cell cycle than in the G0/G1 phase in both DNA diploid and DNA nondiploid tumors. In 18 of 21 diploid tumors, and in 25 of 29 nondiploid tumors, >50% of the topo IIalfa–positive cells were in the G0/G1 phase. This significant expression of topo IIalfa in the G0/G1 phase of the cell cycle may have clinically important implications for treatment efficacy of topoisomerase II inhibitors.

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