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  • 1
    Language: English
    In: memo - Magazine of European Medical Oncology, 2016, Vol.9(2), pp.66-69
    Description: Over the past years immuno-oncology has evolved and become a novel promising strategy for cancer therapy. Immune checkpoint inhibitors such as pembrolizumab or nivolumab, which target the interaction between programmed death receptor 1/programmed death ligand 1 (PD-1/PDL-1) and PDL-2, have been recently approved for the treatment of various malignancies and are currently being investigated in clinical phase III trials for head and neck squamous cell carcinoma (HNSCC). Data available from these trials indicate substantial activity accompanied by a favorable safety and toxicity profile in this patient population. This review article focuses on the molecular background, gives an overview of current clinical data of checkpoint inhibitors in HNSCC, and points out future challenges such as the need for appropriate biomarkers for these novel compounds.
    Keywords: head and neck squamous cell carcinoma ; immunotherapy ; checkpoint inhibitor ; PDL-1 ; PD-1
    ISSN: 1865-5041
    E-ISSN: 1865-5076
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  • 2
    Language: English
    In: memo - Magazine of European Medical Oncology, 2018, Vol.11(2), pp.82-83
    Description: To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1007/s12254-018-0412-2 Byline: Thorsten Fuereder (1) Author Affiliation: (1) 0000 0000 9259 8492, grid.22937.3d, Department of Internal Medicine I & Comprehensive Cancer Center, Division of Clinical Oncology, Medical University of Vienna, Wahringer Gurtel 18--20, 1090, Vienna, Austria Article History: Registration Date: 09/05/2018 Received Date: 04/05/2018 Accepted Date: 09/05/2018 Online Date: 24/05/2018
    Keywords: Cancer – Drug Therapy;
    ISSN: 1865-5041
    E-ISSN: 1865-5076
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  • 3
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.4081-4081
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 4
    Article
    Article
    Language: German
    In: Wiener klinische Wochenschrift Education, 2017, Vol.12(1), pp.17-33
    Description: To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1007/s11812-017-0089-1 Byline: Thorsten Fureder (1) Author Affiliation: (1) Klinische Abteilung fur Onkologie, Universitatsklinik fur Innere Medizin I, Medizinische Universitat Wien, Wahringer Gurtel 18--20, 1090, Wien, Osterreich Article History: Registration Date: 21/11/2017 Online Date: 19/12/2017
    Keywords: Medicine & Public Health ; Medicine/Public Health, General ; Medicine;
    ISSN: 1863-3579
    E-ISSN: 1863-3765
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  • 5
    In: PLoS ONE, 2014, Vol.9(4)
    Description: Background Endothelial progenitor cells (CEPs) and circulating endothelial cells (CECs) are potential biomarkers of response to anti-angiogenic treatment regimens. In the current study, we investigated the effect of docetaxel and sunitinib on CEP/CEC kinetics and clinical response in castration resistant prostate cancer (CRPC) patients. Patients and methods Chemonaive patients with CRPC were enrolled in this study to receive either sunitinib (37.5 mg/d), in combination with docetaxel (75 mg/m 2 ) or docetaxel alone. CEP and CEC kinetics were analyzed for every cycle. The primary objective was to compare CEP/CEC pharmacodynamics between both treatment arms. We also investigated if CEC/CEP spikes, induced by MTD docetaxel, are suppressed by sunitinib in patients treated with docetaxel/sunitinib relative to docetaxel monotherapy. Results A total of 27 patients were enrolled. We observed a significant increase of CEP/CEC (total/viable) counts over time within each cycle (coefficients 0.29233, 0.22092 and 0.26089, respectively; p〈0.001). However, no differences between the treatment groups, in terms of CEP and CEC kinetics, were detected. In the docetaxel monotherapy arm 4 (30%) patients responded to therapy with a 50% PSA decline, while 9 (64%) patients showed a PSA decline in the combination group (n.s.). The median PFS in the docetaxel monotherapy group was 3.1 months (2.6–3.6 months, 95% CI) and 6.2 months (4.9–7.4 months, 95% CI; p = 0.062) in the combination arm. Sunitinib/docetaxel was reasonably well tolerated and toxicity manageable. Conclusion In summary, no significant differences in CEC and CEP kinetics between the treatment arms were observed, although a highly significant increase of CEPs/CECs within each cycle over time was detected. These results mirror the challenge we have to face when employing anti-angiogenic strategies in CRPC. Additional preclinical research is needed to elucidate the underlying molecular mechanisms. However, docetaxel/sunitinib therapy resulted in a better response in terms of PSA decline and a trend towards improved PFS. Trial Registery clinicaltrialsregister.eu EudraCT 2007-003705-27
    Keywords: Research Article ; Medicine And Health Sciences
    E-ISSN: 1932-6203
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  • 6
    Article
    Article
    BMJ Publishing Group Ltd
    Language: English
    In: ESMO Open, 14 August 2017, Vol.2(3)
    Description: Click here to see the linked paper
    Keywords: Medicine
    ISSN: ESMO Open
    E-ISSN: 2059-7029
    E-ISSN: 20597029
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  • 7
    Language: English
    In: ESMO open, 2017, Vol.2(3), pp.e000239
    Keywords: Medicine
    ISSN: 2059-7029
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 8
    Language: English
    In: PLoS ONE, 2012, Vol.7(1), p.e29925
    Description: The phosphoinositide 3-kinase (PI3-kinase) and the mammalian target of rapamycin (mTOR) are two major signaling molecules involved in growth and activation of mast cells (MC) and basophils (BA). We examined the effects of the dual PI3-kinase/mTOR blocker NVP-BEZ235 on growth of normal and neoplastic BA and MC as well as immunoglobulin E (IgE)-dependent cell activation. Growth of MC and BA were determined by measuring 3 H-thymidine uptake and apoptosis. Cell activation was determined in histamine release experiments and by measuring upregulation of CD63 and CD203c after challenging with IgE plus anti-IgE or allergen. We found that NVP-BEZ235 exerts profound inhibitory effects on growth of primary and cloned neoplastic MC. In the MC leukemia cell line HMC-1, NVP-BEZ235 showed similar IC 50 values in the HMC-1.1 subclone lacking KIT D816V (0.025 µM) and the HMC-1.2 subclone expressing KIT D816V (0.005 µM). Moreover, NVP-BEZ235 was found to exert strong growth-inhibitory effects on neoplastic MC in a xenotransplant-mouse model employing NMR1-Foxn1 nu mice. NVP-BEZ235 also exerted inhibitory effects on cytokine-dependent differentiation of normal BA and MC, but did not induce growth inhibition or apoptosis in mature MC or normal bone marrow cells. Finally, NVP-BEZ235 was found to inhibit IgE-dependent histamine release in BA and MC (IC 50 0.5–1 µM) as well as anti-IgE-induced upregulation of CD203c in BA and IgE-dependent upregulation of CD63 in MC. In summary, NVP-BEZ235 produces growth-inhibitory effects in immature neoplastic MC and inhibits IgE-dependent activation of mature BA and MC. Whether these potentially beneficial drug effects have clinical implications is currently under investigation.
    Keywords: Research Article ; Biology ; Immunology ; Molecular Biology ; Cell Biology ; Developmental Biology
    E-ISSN: 1932-6203
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  • 9
    In: European Journal of Clinical Investigation, October 2014, Vol.44(10), pp.958-964
    Description: To purchase or authenticate to the full-text of this article, please visit this link: http://onlinelibrary.wiley.com/doi/10.1111/eci.12329/abstract Byline: Thorsten Fuereder, Judith Stift, Irene Kuehrer, Nadja Stranzl, Doris Hoeflmayer, Gabriela Kornek, Werner Scheithauer Keywords: ERCC1; erlotinib; GEMOX ; pancreatic adenocarcinoma Abstract Introduction There are no data about the efficacy of gemcitabine in combination with oxaliplatin (GEMOX) and erlotinib for the treatment of metastatic pancreatic cancer (mPC). Thus, we performed this retrospective analysis in mPC patients to investigate the activity and safety of GEMOX plus erlotinib and correlated the benefit with ERCC1 expression, a potential biomarker for treatment response. Patients and methods Patients with untreated mPC receiving off-protocol GEMOX plus erlotinib were included. Data collection included baseline demographic, response and toxicity data as well as PFS and OS. Additionally, immunohistochemistry was performed to stain for ERCC1 expression. Results A total of 51 patients were included. The median age was 62 years and the median ECOG performance score was 1 (range, 0-1). Objective response or disease stabilization was achieved in 54% of the patients. The median PFS was 4ae4 months (95% CI 4ae4-5ae4) and median OS was 8ae5 months (95% CI 6ae1-10ae9). The 27 patients, who benefited from this regimen, had a median PFS of 6ae7, a median OS of 11ae2 months and an overexpression of ERCC1 (histoscore 10, P [less than or equal to] 0ae05) compared to nonresponders (histoscore 7ae2). Myelosuppression was the most frequent side effect. The most common severe nonhematological toxicities were diarrhoea and skin toxicity in six (12%) patients each. Conclusions These data suggest that the combination of GEMOX plus erlotinib is safe and active in about half of the patients. Patients, who had a higher ERCC1 staining pattern, benefited most from this therapy. Prospective biomarker studies are warranted to confirm these findings.
    Keywords: 1 ; Erlotinib ; Gemox ; Pancreatic Adenocarcinoma
    ISSN: 0014-2972
    E-ISSN: 1365-2362
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  • 10
    Language: English
    In: Arthritis & Rheumatism, August 2010, Vol.62(8), pp.2294-2302
    Description: OBJECTIVE: Activation of the mammalian target of rapamycin (mTOR) pathway is important for immune cell activation and bone metabolism. To date, the contribution of mTOR signaling to joint inflammation and structural bone and cartilage damage is unknown. The aim of this study was to investigate the potential of inhibiting mTOR as a treatment of inflammatory arthritis.METHODS: Human tumor necrosis factor-transgenic mice in which inflammatory arthritis was developing were treated with 2 different mTOR inhibitors, sirolimus or everolimus. The effects of treatment on clinical disease activity, inflammation, and localized joint and cartilage destruction were studied. In addition, the effects of mTOR inhibition on osteoclast survival and expression of key molecules of osteoclast function were analyzed in vitro. Moreover, synovial tissue from patients with rheumatoid arthritis (RA) was assessed for activation of the mTOR pathway.RESULTS: Inhibition of mTOR by sirolimus or everolimus reduced synovial osteoclast formation and protected against local bone erosions and cartilage loss. Clinical signs of arthritis improved after mTOR inhibition, and histologic evaluation showed a decrease in synovitis. In vitro, mTOR inhibition down-regulated the expression of digestive enzymes and led to osteoclast apoptosis. Moreover, mTOR signaling was shown to be active in the synovial membrane of patients with RA, particularly in synovial osteoclasts.CONCLUSION: Signaling through mTOR is an important link between synovitis and structural damage in inflammatory arthritis. Current pharmacologic inhibitors of mTOR could be effective in protecting joints against structural damage.
    Keywords: Medicine;
    ISSN: 0004-3591
    E-ISSN: 1529-0131
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