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  • 1
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    Abstract 528: A tumor-stroma interaction study in red mammary tumors in green mice with and without enhanced oxygenation
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 528-528
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 528-528
    Abstract: Background: The tumor microenvironment is increasingly recognized as pivotal in tumor progression. Thus, by completely separating tumor cells from stromal cells it enables a thorough elucidation of gene-changes in the two compartments, and thereby offers the possibility to better understand the biological effects in tumors with and without treatment. Since tumor hypoxia is considered to be relevant for several aspects of tumor pathophysiology, including activation of signalling pathways that regulate proliferation, angiogenesis and death, our hypothesis was that a reduction in the hypoxic state of the tumor, might have an inhibitory effect on tumor growth per se. Induction of hyperoxia by hyperbaric oxygen (HBO) exposure, enhance dissolved oxygen in the plasma and thereby the pO2 in the tumor tissue. Methods: The murine mammary dsRed cell line 4T1 was implanted into the mouse mammary fat pad in eGFP expressing NOD/Scid mice. One group was exposed to repeated HBO treatment (2.5 bar, 100% O2, 3 exposures à 90 min), one to daily HBO treatment (2.5bar, 100% O2, 7 exposures à 90 min), whereas the control group was housed under normal atmosphere. Treatment effects were determined by assessment of tumor growth, tumor vascularisation, tumor cell proliferation and cell death. FACS was used to completely separate red tumor cells from green host cells, RNA was extracted and gene expression profiling performed. Results: The model enabled us to completely separate the two compartments (tumor vs stroma), as verified by confocal microscopy and gene expression profiling. Highly upregulated genes in the untreated tumor stroma, included constituents of the ECM and MMP's, as well as genes related to cell-migration and motility. Significant changes in response to treatment between the tumor and stroma was found, especially concerning genes related to cell adhesion and angiogenesis. Furthermore, changes occurring within each of these compartments were found. Tumor growth was significantly inhibited (∼ 50%, after 8 days) after both repeated and daily HBO treatment compared to controls. Repeated HBO treatment showed a significant anti-angiogenic effect, while daily HBO treatment did not. The gene expression confirmed this. Neither morphology, proliferation nor the amount of cell death was significantly changed after the two HBO treatment regimes, despite the significant effect on tumor growth. Conclusion: The present model provides a significant insight into how tumor cells communicate with the stroma, both before any treatment and after enhanced oxygenation. Furthermore, hyperoxia induced a significant inhibitory effect on the 4T1 mammary tumor growth, with a significant anti-angiogenic effect after repeated hyperoxic treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 528. doi:10.1158/1538-7445.AM2011-528
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-528
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 2
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    Gene expression in tumor cells and stroma in dsRed 4T1 tumors in eGFP-expressing mice with and without enhanced oxygenation
    Springer Science and Business Media LLC ; 2012
    In:  BMC Cancer Vol. 12, No. 1 ( 2012-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2012-12)
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/1471-2407-12-21
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2012
    detail.hit.zdb_id: 2041352-X
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  • 3
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    Liquid biopsies and patient-reported outcome measures for integrative monitoring of patients with early-stage breast cancer: a study protocol for the longitudinal observational Prospective Breast Cancer Biobanking (PBCB) study
    BMJ ; 2022
    In:  BMJ Open Vol. 12, No. 4 ( 2022-04), p. e054404-
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    In: BMJ Open, BMJ, Vol. 12, No. 4 ( 2022-04), p. e054404-
    Abstract: Breast cancer is still the most common malignancy among women worldwide. The Prospective Breast Cancer Biobank (PBCB) collects blood and urine from patients with breast cancer every 6 or 12 months for 11 years from 2011 to 2030 at two university hospitals in Western Norway. The project aims to identify new biomarkers that enable detection of systemic recurrences at the molecular level. As blood represents the biological interface between the primary tumour, the microenvironment and distant metastases, liquid biopsies represent the ideal medium to monitor the patient‘s cancer biology for identification of patients at high risk of relapse and for early detection systemic relapse. Including patient-reported outcome measures (PROMs) allows for a vast number of possibilities to compare PROM data with biological information, enabling the study of fatigue and Quality of Life in patients with breast cancer. Methods and analysis A total of 1455 patients with early-stage breast cancer are enrolled in the PBCB study, which has a one-armed prospective observational design. Participants consent to contribute liquid biopsies (i.e., peripheral blood and urine samples) every 6 or 12 months for 11 years. The liquid biopsies are the basis for detection of circulating tumour cells, circulating tumour DNA (ctDNA), exosomal micro-RNA (miRNA), miRNA in Tumour Educated Platelet and metabolomic profiles. In addition, participants respond to 10 PROM questionnaires collected annually. Moreover, a control group comprising 200 women without cancer aged 25–70 years will provide the same data. Ethics and dissemination The general research biobank PBCB was approved by the Ministry of Health and Care Services in 2007, by the Regional Ethics Committee (REK) in 2010 (#2010/1957). The PROM (#2011/2161) and the biomarker study PerMoBreCan (#2015/2010) were approved by REK in 2011 and 2015 respectively. Results will be published in international peer reviewed journals. Deidentified data will be accessible on request. Trial registration number NCT04488614 .
    Type of Medium: Online Resource
    ISSN: 2044-6055 , 2044-6055
    URL: Article
    DOI: 10.1136/bmjopen-2021-054404
    Language: English
    Publisher: BMJ
    Publication Date: 2022
    detail.hit.zdb_id: 2599832-8
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  • 4
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    Glioma Cell Populations Grouped by Different Cell Type Markers Drive Brain Tumor Growth
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 11 ( 2010-06-01), p. 4274-4279
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 11 ( 2010-06-01), p. 4274-4279
    Abstract: Although CD133 has been proposed as a marker for brain tumor–initiating cells, studies show that a tumorigenic potential exists among CD133− glioma cells as well. However, it is not established whether the ability of CD133− cells to form tumors is a property confined to a small subpopulation, rather than a common trait associated with most glioma cell types. Thus, we used lentiviral vectors expressing green fluorescent protein under lineage-specific promoters to identify CD133− glioma cells expressing Nestin, glial fibrillary acidic protein (GFAP), and neuron-specific enolase (NSE). Flow cytometry analysis showed the presence of CD133− subpopulations expressing these markers in glioma cell lines and in primary cultures from human glioblastoma (GBM) biopsies. Moreover, analysis of cell cycle distribution showed that subgroups expressing Nestin, GFAP, and NSE uniformly contained actively cycling cells, when cultured in serum-containing medium and stem cell medium. These subpopulations were fluorescence-activated cell sorted from CD133− U373 glioma cells and implanted intracerebrally in severe combined immunodeficient mice. Moreover, we implanted Nestin-, GFAP-, and NSE-positive glioma cells sorted from a human GBM biopsy, following removal of CD133-positive cells. All the CD133− subpopulations produced tumors, with no significant differences in survival or tumor take rates. However, there was a trend toward lower take rates for CD133− glioma subpopulations expressing GFAP and NSE. These findings suggest that the ability to form tumors may be a general trait associated with different glioma cell phenotypes, rather than a property limited to an exclusive subpopulation of glioma stem cells. Cancer Res; 70(11); 4274–9. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-3904
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
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    TMIC-35. ASTROCYTE-DEPENDENT ENHANCEMENT OF GLIOBLASTOMA GROWTH AS A CANDIDATE THERAPEUTIC TARGET
    Oxford University Press (OUP) ; 2018
    In:  Neuro-Oncology Vol. 20, No. suppl_6 ( 2018-11-05), p. vi263-vi264
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 20, No. suppl_6 ( 2018-11-05), p. vi263-vi264
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noy148.1094
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2094060-9
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  • 6
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    Abstract 1789: Drug repurposing: Sulfasalazine sensitizes gliomas to gamma knife surgery by blocking cystine uptake through System XC−, leading to gluthatione depletion
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1789-1789
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1789-1789
    Abstract: Glioblastomas (GBMs) are lethal cancers and inherently resistant to radiotherapy. Established treatments including surgery, radio- and chemotherapy have a limited efficacy, and the median survival is approximately 14.6 months. Thus, treatment resistance represents a major challenge in the clinical management of these patients, and new therapies are urgently needed. We hypothesized that the Xc−-inhibitor sulfasalazine (SAS) could potentiate the efficacy of radiotherapy against gliomas. Expression of the catalytic subunit of system Xc−, xCT, was found in a panel of 30 human GBM biopsies. Sections from normal brain tissue displayed only weak immunopositivity, thus our findings therefore suggest that xCT expression is common to most GBMs, which together with its low expression in normal brain tissue could provide a therapeutic window. SAS treatment dramatically reduced cysteine-uptake and glutathione (GSH) levels in glioma cells in vitro and markedly increased the levels of reactive oxygen species (ROS). Furthermore, SAS and radiation synergistically increased DNA double-strand breaks and increased glioma cell death, whereas adding the antioxidant N-acetyl-L-cysteine (NAC) reversed cell death. Moreover, SAS and gamma knife radiosurgery (GKRS) synergistically prolonged survival in nude rats harboring human GBM xenografts, compared to controls or either treatment alone. In conclusion, SAS effectively blocks cystine uptake in glioma cells in vitro, leading to GSH depletion and increased ROS levels, DNA damage and cell death. Moreover, it potentiates the anti-tumor efficacy of GKRS in rats with human GBM xenografts, providing a survival benefit. Thus, SAS may have a role as a radiosensitizer to enhance the efficacy of current radiotherapies for glioma patients. We are currently preparing a clinical trial for patients with GBM recurrences combining pre-treatment with SAS and GKRS. Citation Format: Linda Sleire, Bente Sandvei Skeie, Inger Anne Netland, Hilde Elise Førde, Ernest Dodoo, Frode Selheim, Lina Leiss, Jian Wang, Jan Heggdal, Paal-Henning Pedersen, Per Øyvind Enger. Drug repurposing: Sulfasalazine sensitizes gliomas to gamma knife surgery by blocking cystine uptake through System XC−, leading to gluthatione depletion. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1789. doi:10.1158/1538-7445.AM2015-1789
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-1789
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
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    Abstract 1590: Sulfasalazine sensitizes glioblastoma cells to radiation treatment.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1590-1590
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 1590-1590
    Abstract: Glioblastoma (GBM) is a lethal cancer with a limited response to ionizing radiation. Recent studies suggest that Sulfasalazine (SAS), a drug used to treat inflammatory bowel disease, inhibits the Xc− antiporter system in glioma cells, thereby blocking their uptake of cystein. Since the availability of cystein is a rate limiting step in intracellular antioxidant production, we wanted to investigate whether sulfasalazine sensitizes glioma cells to radiation. Expression of xCT, the catalytic subunit of system Xc−, was found in 30 patient GBM biopsies. SAS effect on glioma cell growth was investigated using an electric cell substrate impedance sensing (ECIS) instrument. All glioma cell lines showed altered growth curves in response to SAS treatment. To assess the effect of blocking the antiporter, intracellular levels of the antioxidant glutathione were measured. With increasing doses of SAS, glutathione levels decreased in a dose response manner. In addition, cysteine was added to the medium to see if the toxic effects of SAS could be counteracted. Furthermore, accumulation of reactive oxygen species upon SAS treatment was measured. Glioma cells were also treated with escalating doses of SAS, alone or in combination with radiation (8 Gy). The presence of double stranded breaks increased markedly in the irradiated samples and also somewhat with increasing doses with SAS. In addition, cell death, viability and clonogenicity were investigated using live/dead staining, the MTS assay and the clonogenic assay. All treatment groups exhibited increased rates of cell death compared to untreated controls. A combination of SAS and radiation resulted in higher levels of cell death, than radiation or SAS administered alone. Furthermore we continued with implantation of human GBMs into the brain of Nude rats. These animals were treated with Gamma Knife Radiosurgery alone or in combination with SAS. SAS were administered as a pre-treatment for three days before Radiosurgery. The rats receiving the combination treatment lived significantly longer compared to either treatment alone. Interestingly, the animals only receiving pre-treatment with SAS for three days lived significantly longer compared to the untreated controls, although this was not statistically significant. We are currently preparing a clinical trial for patients with GBM recurrences combining pre-treatment with Sulfasalazine and Gamma Knife Radiosurgery. Citation Format: Linda Sleire, Bente S. Skeie, Inger A. Netland, Jan Heggdal, Paal-Henning Pedersen, Per Ø. Enger. Sulfasalazine sensitizes glioblastoma cells to radiation treatment. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1590. doi:10.1158/1538-7445.AM2013-1590
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-1590
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    Abstract 1456: Sulfasalazine sensitizes glioblastoma cells to radiation treatment
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1456-1456
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1456-1456
    Abstract: Glioblastoma (GBM) is a lethal cancer with a limited response to ionizing radiation. Recent studies suggest that Sulfasalazine (SAS), a drug used to treat inflammatory bowel disease, inhibits the Xc- antiporter system in glioma cells, thereby blocking their uptake of cystein. Since the availability of cystein is a rate limiting step in intracellular antioxidant production, we wanted to investigate whether sulfasalazine sensitizes glioma cells to radiation. Expression of xCT, the catalytic subunit of system Xc-, was found in 30 patient GBM biopsies. SAS effect on glioma cell growth was investigated using an electric cell substrate impedance sensing (ECIS) instrument. All glioma cell lines showed altered growth curves in response to SAS treatment. To assess the effect of blocking the antiporter, intracellular levels of the antioxidant glutathione were measured. With increasing doses of SAS, glutathione levels decreased in a dose response manner. In addition, cysteine was added to the medium to see if the cells could survive high doses of SAS. U251 glioma cells were treated with escalating doses of SAS, alone or in combination with radiation (8 Gy). Nuclear integrity was evaluated to estimate cell death following treatment, as well as the presence of double stranded breaks. In addition, cell death and viability were investigated using live/dead staining and the MTS assay. All treatment groups exhibited increased rates of cell death compared to untreated controls. A combination of SAS and radiation resulted in higher levels of cell death, than radiation or SAS administered alone. In order to assess whether this can be exploited therapeutically, we are preparing to treat nude rats harbouring glioblastoma biopsy xenografts with SAS, alone or in combination with gamma knife radiation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1456. doi:1538-7445.AM2012-1456
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-1456
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Establishment of a Novel dsRed NOD/Scid Mouse Strain to Investigate the Host and Tumor Cell Compartments
    Informa UK Limited ; 2013
    In:  Cancer Investigation Vol. 31, No. 4 ( 2013-05), p. 221-230
    Details
    In: Cancer Investigation, Informa UK Limited, Vol. 31, No. 4 ( 2013-05), p. 221-230
    Type of Medium: Online Resource
    ISSN: 0735-7907 , 1532-4192
    URL: Article
    DOI: 10.3109/07357907.2013.780075
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2013
    detail.hit.zdb_id: 2043112-0
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  • 10
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    Gamma Knife Surgery as Monotherapy with Clinically Relevant Doses Prolongs Survival in a Human GBM Xenograft Model
    Hindawi Limited ; 2013
    In:  BioMed Research International Vol. 2013 ( 2013), p. 1-9
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2013 ( 2013), p. 1-9
    Abstract: Object . Gamma knife surgery (GKS) may be used for recurring glioblastomas (GBMs). However, patients have then usually undergone multimodal treatment, which makes it difficult to specifically validate GKS independent of established treatments. Thus, we developed an experimental brain tumor model to assess the efficacy and radiotoxicity associated with GKS. Methods . GBM xenografts were implanted intracerebrally in nude rats, and engraftment was confirmed with MRI. The rats were allocated to GKS, with margin doses of 12 Gy or 18 Gy, or to no treatment. Survival time was recorded, tumor sections were examined, and radiotoxicity was evaluated in a behavioral open field test. Results . In the first series, survival from the time of implantation was 96 days in treated rats and 72 days in controls ( P 〈 0.001 ). In a second experiment, survival was 72 days in the treatment group versus 54 days in controls ( P 〈 0.006 ). Polynuclear macrophages and fibrosis was seen in groups subjected to GKS. Untreated rats with GBM xenografts displayed less mobility than GKS-treated animals in the open field test 4 weeks after treatment ( P = 0.04 ). Conclusion . GKS administered with clinically relevant doses prolongs survival in rats harboring GBM xenografts, and the associated toxicity is mild.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2013/139674
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2013
    detail.hit.zdb_id: 2698540-8
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