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  • 1. Davidsson, Sabina
    et al.
    Sundqvist, Pernilla
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Giunchi, Francesca
    Erlandsson, Ann
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Fiorentiono, Michelangelo
    Carlsson, Jessica
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    M2 macrophages and regulatory T cells as prognostic markers in renal cell carcinoma2019Konferensbidrag (Refereegranskat)
  • 2.
    Erlandsson, Ann
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden; Department of Environmental and Life Sciences/Biology, Karlstad University, Karlstad, Sweden.
    Carlsson, Jessica
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andersson, Sven-Olof
    Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Vyas, Chraig
    Department of Epidemiology, Boston University School of Public Health, Boston MA, USA.
    Wikström, Pernilla
    Department of Medical Biosciences, Umeå University, Umeå, Sweden.
    Andrén, Ove
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Davidsson, Sabina
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Rider, Jennifer R.
    Department of Epidemiology, Boston University School of Public Health, Boston MA, USA.
    High inducible nitric oxide synthase in prostate tumor epithelium is associated with lethal prostate cancer2018Ingår i: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 52, nr 2, s. 129-133Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: The aim of this study was to investigate the role of inducible nitric oxide synthase (iNOS) in lethal prostate cancer (PCa) by studying the iNOS immunoreactivity in tumor tissue from men diagnosed with localized PCa.

    MATERIALS AND METHODS: This study is nested within a cohort of men diagnosed with incidental PCa undergoing transurethral resection of the prostate (the Swedish Watchful Waiting Cohort). To investigate molecular determinants of lethal PCa, men who died from PCa (n = 132) were selected as cases; controls (n = 168) comprised men with PCa who survived for at least 10 years without dying from PCa during follow-up. The immunoreactivity of iNOS in prostate tumor epithelial cells and in cells of the surrounding stroma was scored as low/negative, moderate or high. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) for lethal PCa according to iNOS category.

    RESULTS: There was no association between iNOS immunoreactivity in stroma and lethal disease. However, when comparing high versus low/negative iNOS immunoreactivity in epithelial cells, the OR for lethal PCa was 3.80 (95% CI 1.45-9.97).

    CONCLUSION: Patients with localized PCa have variable outcomes, especially those with moderately differentiated tumors. Identifying factors associated with long-term PCa outcomes can elucidate PCa tumor biology and identify new candidate prognostic markers. These findings support the hypothesis that high iNOS in tumor epithelium of the prostate is associated with lethal disease.

  • 3.
    Erlandsson, Ann
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Carlsson, Jessica
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Lundholm, Marie
    Department of Medical Biosciences, Umeå University, Umeå, Sweden.
    Fält, Anna
    School of Medical Sciences, Örebro University, Örebro, Sweden.
    Andersson, Sven-Olof
    Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Andrén, Ove
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Davidsson, Sabina
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    M2 macrophages and regulatory T cells in lethal prostate cancer2019Ingår i: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 79, nr 4, s. 363-369Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Prostate cancer (PCa) is one of the most frequently diagnosed cancers in the world. Emerging evidence suggests that inflammatory cells such as M2 macrophages and regulatory T cells (Tregs) can contribute to cancer progression by suppressing the anti‐tumor immune response. This study investigated the number of CD163‐positive M2 macrophages in PCa tissue. It also investigated the correlation and interaction of M2 macrophages and Tregs.

    METHODS: were assessed using Spearman's rank-order correlation and a likelihood test, respectively. Logistic regression was used to estimate odds ratios (ORs) for lethal PCa and macrophage counts.

    RESULTS: showed a significant correlation (P < 0.001) but no interactions. The OR for lethal PCa was 1.93 (95%CI: 1.23-3.03) for men with high numbers of M2 macrophages. Also for cases with uncertain outcome (GS categories 3 + 4 and 4 + 3) high numbers of M2 macrophages does predict a poorer prognosis.

    CONCLUSIONS: Our data showed that men with high numbers of M2 macrophages in the prostate tumor environment had increased odds of dying of PCa. It is possible that M2 macrophages, together with other suppressor cells such as Tregs , promote an immunosuppressive environment.

  • 4.
    Lindsten, Therése
    et al.
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Hedbrant, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Ramberg, Anna
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden; School of Medical Sciences, Örebro University, Örebro, Sweden.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Solterbeck, Anja
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Eriksson, Margareta
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden; Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Erlandsson, Ann
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Environmental and Life Sciences/Biology, Karlstad University, Karlstad, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Effect of macrophages on breast cancer cell proliferation, and on expression of hormone receptors, uPAR and HER-22017Ingår i: International Journal of Oncology, ISSN 1019-6439, Vol. 51, nr 1, s. 104-114Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Malignant tumors, including breast cancers, are frequently infiltrated with innate immune cells and tumor-associated macrophages (TAMs) represent the major inflammatory component in stroma of many tumors. In this study, we examined the immunoreactivity of the macrophage markers CD68 and CD163 as well as the hormone receptors estrogen receptor alpha (ER alpha), progesterone receptor (PR), estrogen receptor beta 1 (ER beta 1), human epidermal growth factor receptor 2 (HER-2), matrix metalloproteinase 9 (MMP-9), urokinase-type plasminogen activator receptor (uPAR) and the proliferations marker Ki67 in 17 breast cancer biopsies. The quantitative score for CD68(+) and CD163(+) strongly indicate M2 phenotype dominance in the currently investigated biopsies. We found that an increasing level of macrophages was negatively associated with ER alpha or PR, whereas a positive association was observed for Ki-67 or uPAR. No significant association could be seen between the level of macrophage and HER-2, ER beta 1 or MMP-9 expression. Effect of conditioned media (CM) generated from cultured human M1 and M2 macrophage phenotypes were investigated on the proliferation and expression of selected markers in the T47D breast cancer cell line. We found that in contrast to the in vivo situation, in particularly the CM from M1 macrophages decreased the growth and Ki67 expression in T47D, and significantly increased ER beta 1 mRNA levels. Moreover, in accordance to the in vivo situation the CM from the macrophages decreased the expression of ER alpha protein as well as ER alpha or PR mRNA. In conclusion our results show that macrophages alone have the capability to decrease the tumor cell expression of ER alpha and PR in vitro. In the tumor environment in vivo macrophages also contribute to an increase in tumor cell expression of uPAR and Ki67, suggesting that macrophages are involved in impairing the prognosis for breast cancer patients.

  • 5.
    Matikas, A.
    et al.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Lovrot, J.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Ramberg, A.
    Clin Pathol & Cytol, Cent Hosp Karlstad, Karlstad, Sweden.
    Eriksson, M.
    Clin Pathol & Cytol, Cent Hosp Karlstad, Karlstad, Sweden.
    Lindsten, T.
    Clin Pathol & Cytol, Cent Hosp Karlstad, Karlstad, Sweden.
    Lekberg, T.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Hedenfalk, I.
    Oncol Pathol, Lund Univ, Lund, Sweden.
    Loman, N.
    Oncol Pathol, Lund Univ, Lund, Sweden.
    Bergh, J.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Erlandsson, Ann
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hatschek, T.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Foukakis, T.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Immune function and response to neoadjuvant chemotherapy in hormone receptor positive, HER2-negative breast cancer2017Ingår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, nr Suppl. 5, artikel-id 219PArtikel i tidskrift (Övrigt vetenskapligt)
  • 6.
    Matikas, Alexios
    et al.
    Department of Oncology, Karolinska Institutet and University Hospital, Stockholm, Sweden.
    Lövrot, John
    Department of Oncology, Karolinska Institutet and University Hospital, Stockholm, Sweden.
    Ramberg, Anna
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Eriksson, Margareta
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Lindsten, Therese
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Lekberg, Tobias
    Department of Oncology, Karolinska Institutet and University Hospital, Stockholm, Sweden.
    Hedenfalk, Ingrid
    Department of Oncology/Pathology, Lund University, Lund, Sweden.
    Loman, Niklas
    Department of Oncology/Pathology, Lund University, Lund, Sweden.
    Bergh, Jonas
    Department of Oncology, Karolinska Institutet and University Hospital, Stockholm, Sweden.
    Hatschek, Thomas
    Department of Oncology, Karolinska Institutet and University Hospital, Stockholm, Sweden.
    Erlandsson, Ann
    Region Örebro län. Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Biology, Karlstad university, Karlstad, Sweden.
    Foukakis, Theodoros
    Department of Oncology, Karolinska Institutet and University Hospital, Stockholm, Sweden.
    Dynamic evaluation of the immune infiltrate and immune function genes as predictive markers for neoadjuvant chemotherapy in hormone receptor positive, HER2 negative breast cancer2018Ingår i: Oncoimmunology, ISSN 2162-4011, E-ISSN 2162-402X, Vol. 7, nr 9, artikel-id e1466017Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Gene expression (GE) signatures and Tumor Infiltrating Lymphocytes (TIL) enumeration are predictive for response to neoadjuvant chemotherapy in HR- and in HER2+ breast cancer, but data are conflicting in HR+/HER2- disease. This study aimed to explore their predictive value in this subset, measured both at baseline and after short exposure to chemotherapy. Specifically, the PROMIX phase 2 trial enrolled patients with locally advanced HER2- BC to receive six cycles of epirubicin and docetaxel, plus bevacizumab during cycles 3-6. Patients underwent tumor biopsies at baseline and after cycle 2 for GE profiling and enumeration of TIL, FOXP3+ T-cells and CD163+ macrophages. An immune related gene module and the quantification of the immune infiltrate were analyzed for association with pathologic complete response (pCR), decrease in tumor size and disease-free survival (DFS). Of the 150 patients enrolled in PROMIX, 113 were HR+/HER2-. Baseline GE and immune cell enumeration data were available from 71 patients, while data after 2 cycles of chemotherapy were available from 41. At baseline, only GE was statistically significantly associated with higher pCR rates (OR 2.29, 95% CI 1.05 - 5.38, p = 0.037) and decrease in tumor size (r = 0.25, p = 0.047). In contrast, longitudinal data indicate that both GE (r = 0.54, p<0.001) and TIL abundance (p = 0.009) are stronger predictors for the reduction of tumor size, while low FOXP3+ was statistically significantly associated with an improved DFS (p = 0.027). In conclusion, GE analysis, TIL and FOXP3+ enumeration after short-term exposure to chemotherapy carry important predictive information in HR+/HER2- breast cancer at the neoadjuvant setting.

  • 7.
    Rider, Jennifer R.
    et al.
    Boston University School of Public Health, Boston, MA, USA.
    Erlandsson, Ann
    Örebro University Hospital, Örebro, Sweden.
    Vyas, Chirag
    Boston University School of Public Health, Boston, MA, USA.
    Davidsson, Sabina
    Örebro University Hospital, Örebro, Sweden.
    Carlsson, Jessica
    Örebro universitet, Institutionen för medicinska vetenskaper. Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Örebro University Hospital, Örebro, Sweden.
    Andren, Ove
    Örebro University Hospital, Örebro, Sweden.
    iNOS expression and lethal prostate cancer in patients with localized disease2017Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, nr 22S, artikel-id B26Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Inducible nitric oxide synthase (iNOS) has demonstrated both tumor-promoting and tumor-inhibiting effects in prostate cancer. However, the relationship between iNOS protein expression and long-term prostate cancer outcomes is unclear. We evaluated iNOS expression in tumor epithelia and stroma in 300 men with localized tumors diagnosed incidentally by transurethral resection of the prostate (TURP) in Sweden. In this extreme case-control design, cases (N=132) died of prostate cancer and controls (N=168) survived at least 8 years following diagnosis without death from prostate cancer or a competing cause. Immunohistochemistry was undertaken with a polyclonal rabbit anti-human NOS2 antibody (Abcam) and the Ventana (Roche) semi-automated staining system. Two observers individually scored the staining according to intensity and number of positive cells from 0-3. The median value across cores in each patient were then categorized as <1, >1-<2, and >2, separately for epithelial and stromal compartments. Odds ratios for lethal prostate cancer were estimated with logistic regression controlling for the matching factors (age, calendar year of diagnosis), as well as tumor stage, Gleason score, and percent tumor. iNOS was expressed by stromal-associated M1 macrophages and fibroblasts, as well as tumor cells. Gleason score was positively associated with both stromal and epithelial iNOS staining. In the stroma, there was no statistically significant association between iNOS expression and lethal prostate cancer after adjustment for clinical covariates. However, the odds of lethal prostate cancer increased with tumor expression of iNOS in the fully adjusted model. Compared to patients with the lowest category of iNOS expression, the odds ratios for lethal prostate cancer were 2.96 (95% CI: 1.26-6.96) for patients in the second category and 3.80 (95% CI: 1.45-9.97) for patients in the top category. These results suggest that iNOS may help to identify patients with aggressive prostate cancer at the time of diagnosis, or may be a therapeutic target. Given previously reported in vitro data suggesting that iNOS promotes proliferation of androgen-independent prostate tumors, future analyses will investigate association between iNOS expression and time to castration-resistant prostate cancer in this patient population.

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