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  • 1
    Language: English
    In: Oncology Research and Treatment, April 2018, Vol.41(5), pp.264-265
    Keywords: Editorial ; Medicine
    ISSN: 2296-5270
    E-ISSN: 2296-5262
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  • 2
    Language: English
    In: International Journal of Cancer, 01 June 2013, Vol.132(11), pp.2548-2556
    Description: This study aimed to investigate the function of toll‐like receptors (TLRs) during oncolytic parvovirus H‐1 (H‐1PV)‐induced human immune responses. First, the role of TLRs in the activation of the NFκB transcription factor was characterized; second, the immunologic effects of H‐1PV‐induced tumor cell lysates (TCL) on human antitumor immune responses were evaluated. A human model was used to study immune responses with dendritic cells (DCs). Human embryonic kidney cells (HEK293) transfected to stably express TLRs were used as potential human DC equivalents to further investigate the role of specific TLRs during immune activation. TLR3 and TLR9 were activated by H‐1PV infection, which correlated with NFκB translocation to the nucleus IκB . Using a TLR‐signaling reporter plasmid (pNiFty‐Luc), NFκB activity was increased following H‐1PV infection. In addition, human DCs coincubated with H‐1PV‐induced TCL demonstrated increased TLR3 and TLR9 expression. These data suggest that H‐1PV‐induced TCL stimulate human DCs at least in part through TLR‐dependent signaling pathways. Thus, DC maturation occurred through exposure to H‐1PV‐induced TCL through TLR‐signaling leading to NFκB‐dependent activation of the adaptive immune system as indicated by the increased expression of CD86, TLR3 and TLR9. Furthermore, the transcription of various cytokines indicates the activation of immune response, therefore the production of the proinflammatory cytokine TNF‐α was determined. Here, H‐1PV‐induced TCL significantly enhanced the TNF‐α level by DCs after coculture. H‐1PV oncolytic virotherapy enhances immune priming by different effects on DCs and generates antitumor immunity. These findings potentially offer a new approach to tumor therapy. What's new? Parvovirus H‐1 (H‐1PV) possesses oncolytic properties and is known to activate dendritic immune cells, though the mechanisms of host cell recognition and immune activation are not well characterized. Here, H‐1PV was found to exert its effects through activation of toll‐like receptor 3 (TLR3) and TLR9, leading to enhanced NFκB expression. In H‐1PV‐infected tumor cell lysates, TLR activation led to dendritic cell maturation and immune stimulation. The findings shed light on mechanisms that could impact the development of novel H‐1PV oncolytic therapies.
    Keywords: Autonomous Parvovirus ; Dendritic Cells ; Toll‐Like Receptors ; Nuclear Factor‐Kappab
    ISSN: 0020-7136
    E-ISSN: 1097-0215
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  • 3
    Language: English
    In: Journal of medicinal chemistry, 26 November 2012, Vol.55(22), pp.9531-40
    Description: Tumor growth and metastasis are highly associated with the overexpression of protein kinases (PKs) regulating cell growth, apoptosis resistance, and prolonged cell survival. This study describes novel azaindolyl-maleimides with significant inhibition of PKs, such as VEGFR, FLT-3, and GSK-3β which are related to carcinogenesis. Furthermore, these compounds exhibit high kinase selectivity and potent inhibition of angiogenesis and cell proliferation, offering versatile options in cancer treatment strategies.
    Keywords: Angiogenesis Inhibitors -- Pharmacology ; Cell Proliferation -- Drug Effects ; Growth Inhibitors -- Pharmacology ; Maleimides -- Chemistry ; Neoplasms -- Drug Therapy ; Neovascularization, Pathologic -- Drug Therapy ; Protein Kinase Inhibitors -- Pharmacology
    ISSN: 00222623
    E-ISSN: 1520-4804
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  • 4
    Language: English
    In: European Journal of Cancer, May 2016, Vol.59, pp.160-170
    Description: The new therapeutic approach of using immune checkpoint inhibitors as anticancer agents is a landmark innovation. Early studies suggest that immune checkpoint inhibition might also be effective in patients with gastrointestinal cancer. To improve the efficacy of immunotherapy, different strategies are currently under evaluation. This review summarises the discussion during the European Organisation for Research and Treatment of Cancer Gastrointestinal Tract Cancer Translational Research Meeting in Mainz in November 2014 and provides an update on the most recent results of immune therapy in gastrointestinal cancers. Knowledge of potential relationships between tumour cells and their microenvironment including the immune system will be essential in gastrointestinal malignancies. In this context, the density of T cell infiltration within colorectal cancer metastases has been associated with response to chemotherapy, and a high expression of programmed cell death ligand 1 (PD-L1) in advanced gastric cancer has been related with poor prognosis. Effective targets might include neo-antigens encoded from genes carrying tumour-specific somatic mutations. Tailored immunotherapy based on such mutations could enable the effective targeting of an individual patient’s tumour with vaccines produced on demand. Other strategies considering checkpoint inhibitors have shown efficacy by targeting cytotoxic T-lymphocyte-associated protein 4 and PD-1 or PD-L1. DNA mismatch repair-deficient tumours appear to be potentially the best candidates for these therapies. Finally, the combination of oncolytic viruses with immunotherapy might boost antitumour activity as well. Further evaluation of these promising immunological therapeutic approaches will require large prospective clinical studies.
    Keywords: Gastrointestinal Cancer ; Immunotherapy ; Checkpoint Inhibitors ; Medicine
    ISSN: 0959-8049
    E-ISSN: 1879-0852
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  • 5
    Language: German
    In: Karger Kompass Onkologie, October 2017, Vol.4(2), pp.69-70
    Keywords: Editorial
    ISSN: 2296-5416
    E-ISSN: 2296-5386
    Source: Karger Journals (S. Karger AG)
    Source: Karger (S. Karger AG)
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  • 6
    Language: English
    In: Best Practice & Research Clinical Gastroenterology, 2007, Vol.21(6), pp.965-981
    Description: Although radical surgical R0 resections are the basis of cure for gastric cancer, surgery alone only provides long-term survival in 20–30% of patients with advanced-stage disease. Thus, in Western and European countries, advanced gastric cancer has a high risk of recurrence and metachronous metastases. Very recently, multimodal strategies combining different neoadjuvant and/or adjuvant protocols have improved the prognosis of gastric cancer when combined with surgery with curative intent. As used in palliative regimens, the combination of cisplatin with intravenous or oral fluoropyrimidines has been the integral component of such (neo)adjuvant strategies. However, the cytotoxic agents docetaxel, oxaliplatin and irinotecan and new targeted biologicals such as cetuximab, bevacizumab or panitumumab are currently under investigation, with or without irradiation, in multimodal treatment regimens. These studies may further increase R0 resection rates, and prolong disease-free and overall survival times in the treatment of advanced gastric cancer. This article reviews the most relevant literature on multimodal treatment of gastric cancer, and discusses future strategies to improve locoregional failures.
    Keywords: Gastric Cancer ; Chemotherapy ; Radio-Chemotherapy ; Adjuvant ; Neoadjuvant ; Taxanes ; Irinotecan ; Oxaliplatin ; Medicine
    ISSN: 1521-6918
    E-ISSN: 1532-1916
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  • 7
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 24 April 2018, Vol.115(17), pp.E4061-E4070
    Description: Colorectal cancer (CRC) is one of the most common tumor entities, which is causally linked to DNA repair defects and inflammatory bowel disease (IBD). Here, we studied the role of the DNA repair protein poly(ADP-ribose) polymerase-1 (PARP-1) in CRC. Tissue microarray analysis revealed PARP-1 overexpression in human CRC, correlating with disease progression. To elucidate its function in CRC, PARP-1 deficient (PARP-1) and wild-type animals (WT) were subjected to azoxymethane (AOM)/ dextran sodium sulfate (DSS)-induced colorectal carcinogenesis. Miniendoscopy showed significantly more tumors in WT than in PARP-1 mice. Although the lack of PARP-1 moderately increased DNA damage, both genotypes exhibited comparable levels of AOM-induced autophagy and cell death. Interestingly, miniendoscopy revealed a higher AOM/DSS-triggered intestinal inflammation in WT animals, which was associated with increased levels of innate immune cells and proinflammatory cytokines. Tumors in WT animals were more aggressive, showing higher levels of STAT3 activation and cyclin D1 up-regulation. PARP-1 animals were then crossed with -methylguanine-DNA methyltransferase (MGMT)-deficient animals hypersensitive to AOM. Intriguingly, PARP-1/MGMT double knockout (DKO) mice developed more, but much smaller tumors than MGMT animals. In contrast to MGMT-deficient mice, DKO animals showed strongly reduced AOM-dependent colonic cell death despite similar -methylguanine levels. Studies with PARP-1 cells provided evidence for increased alkylation-induced DNA strand break formation when MGMT was inhibited, suggesting a role of PARP-1 in the response to -methylguanine adducts. Our findings reveal PARP-1 as a double-edged sword in colorectal carcinogenesis, which suppresses tumor initiation following DNA alkylation in a MGMT-dependent manner, but promotes inflammation-driven tumor progression.
    Keywords: DNA Repair ; Parp-1 ; Colorectal Carcinogenesis ; Intestinal Inflammation ; Mouse Models ; Colorectal Neoplasms -- Enzymology ; Poly (Adp-Ribose) Polymerase-1 -- Metabolism ; Tumor Suppressor Proteins -- Metabolism
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 8
    Language: English
    In: Journal of the National Cancer Institute, 06 November 2013, Vol.105(21), pp.1667-70
    Description: The traditional endpoint for assessing efficacy of chemotherapies for advanced/recurrent gastric cancer is overall survival (OS), but OS requires prolonged follow-up. We investigated whether progression-free survival (PFS) is a valid surrogate for OS. Using individual patient data from the GASTRIC meta-analysis, surrogacy of PFS was assessed through the correlation between the endpoints and through the correlation between the treatment effects on the endpoints. External validation of the prediction based on PFS was also evaluated. Individual data from 4069 patients in 20 randomized trials were analyzed. The rank correlation coefficient between PFS and OS was 0.853 (95% confidence interval [CI] = 0.852 to 0.854). The R (2) between treatment effects on PFS and on OS was 0.61 (95% CI = 0.04 to 1.00). Treatment effects on PFS and on OS were only moderately correlated, and we could not confirm the validity of PFS as a surrogate endpoint for OS in advanced/recurrent gastric cancer.
    Keywords: Neoplasm Recurrence, Local -- Mortality ; Stomach Neoplasms -- Mortality
    ISSN: 00278874
    E-ISSN: 1460-2105
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  • 9
    Language: English
    In: BMC Cancer, Feb 15, 2012, Vol.12, p.70
    Description: Background Our aim was to compare survival of the various treatment modality groups of chemotherapy and/or radiotherapy in relation to SEMS (self-expanding metal stents) in a retrospective case-control study. We have made the hypothesis that the administration of combined chemoradiotherapy improves survival in inoperable esophageal cancer patients. Methods All patients were confirmed histologically as having surgically non- resectable esophageal carcinoma. Included were patients with squamous cell carcinoma, undifferentiated carcinoma as well as Siewert type I--but not type II - esophagogastric junctional adenocarcinoma. The decision to proceed with palliative treatments was taken within the context of a multidisciplinary team meeting and full expert review based on patient's wish, co-morbid disease, clinical metastases, distant metastases, M1 nodal metastases, T4-tumor airway, aorta, main stem bronchi, cardiac invasion, and peritoneal disease. Patients not fit enough to tolerate a radical course of definitive chemo- and/or radiation therapy were referred for self-expanding metal stent insertion. Our approach to deal with potential confounders was to match subjects according to their clinical characteristics (contraindications for surgery) and tumor stage according to diagnostic work-up in four groups: SEMS group (A), Chemotherapy group (B), Radiotherapy group (C), and Chemoradiotherapy group (D). Results Esophagectomy was contraindicated in 155 (35.5%) out of 437 patients presenting with esophageal cancer to the Department of General and Abdominal Surgery of the University Hospital of Mainz, Germany, between November 1997 and November 2007. There were 133 males and 22 females with a median age of 64.3 (43-88) years. Out of 155 patients, 123 were assigned to four groups: SEMS group (A) n = 26, Chemotherapy group (B) n = 12, Radiotherapy group (C) n = 23 and Chemoradiotherapy group (D) n = 62. Mean patient survival for the 4 groups was as follows: Group A: 6.92 [+ -] 8.4 months; Group B: 7.75 [+ -] 6.6 months; Group C: 8.56 [+ -] 9.5 months, and Group D: 13.53 [+ -] 14.7 months. Significant differences in overall survival were associated with tumor histology (P = 0.027), tumor localization (P = 0.019), and type of therapy (P = 0.005), respectively, in univariate analysis. Treatment modality (P = 0.043) was the only independent predictor of survival in multivariate analysis. The difference in overall survival between Group A and Group D was highly significant (P [less than] 0.01) and in favor of Group D. As concerns Group D versus Group B and Group D versus Group C there was a trend towards a difference in overall survival in favor of Group D (P = 0.069 and P = 0.059, respectively). Conclusions The prognosis of inoperable esophageal cancer seems to be highly dependent on the suitability of the induction of patient-specific therapeutic measures and is significantly better, when chemoradiotherapy is applied.
    Keywords: Chemotherapy -- Health Aspects ; Chemotherapy -- Patient Outcomes ; Chemotherapy -- Comparative Analysis ; Esophageal Cancer -- Care And Treatment ; Esophageal Cancer -- Patient Outcomes ; Esophageal Cancer -- Research ; Radiotherapy -- Health Aspects ; Radiotherapy -- Patient Outcomes ; Radiotherapy -- Comparative Analysis
    ISSN: 1471-2407
    Source: Cengage Learning, Inc.
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  • 10
    Language: English
    In: BMC Cancer, Feb 15, 2012, Vol.12, p.70
    Description: Background Our aim was to compare survival of the various treatment modality groups of chemotherapy and/or radiotherapy in relation to SEMS (self-expanding metal stents) in a retrospective case-control study. We have made the hypothesis that the administration of combined chemoradiotherapy improves survival in inoperable esophageal cancer patients. Methods All patients were confirmed histologically as having surgically non- resectable esophageal carcinoma. Included were patients with squamous cell carcinoma, undifferentiated carcinoma as well as Siewert type I--but not type II - esophagogastric junctional adenocarcinoma. The decision to proceed with palliative treatments was taken within the context of a multidisciplinary team meeting and full expert review based on patient's wish, co-morbid disease, clinical metastases, distant metastases, M1 nodal metastases, T4-tumor airway, aorta, main stem bronchi, cardiac invasion, and peritoneal disease. Patients not fit enough to tolerate a radical course of definitive chemo- and/or radiation therapy were referred for self-expanding metal stent insertion. Our approach to deal with potential confounders was to match subjects according to their clinical characteristics (contraindications for surgery) and tumor stage according to diagnostic work-up in four groups: SEMS group (A), Chemotherapy group (B), Radiotherapy group (C), and Chemoradiotherapy group (D). Results Esophagectomy was contraindicated in 155 (35.5%) out of 437 patients presenting with esophageal cancer to the Department of General and Abdominal Surgery of the University Hospital of Mainz, Germany, between November 1997 and November 2007. There were 133 males and 22 females with a median age of 64.3 (43-88) years. Out of 155 patients, 123 were assigned to four groups: SEMS group (A) n = 26, Chemotherapy group (B) n = 12, Radiotherapy group (C) n = 23 and Chemoradiotherapy group (D) n = 62. Mean patient survival for the 4 groups was as follows: Group A: 6.92 [+ -] 8.4 months; Group B: 7.75 [+ -] 6.6 months; Group C: 8.56 [+ -] 9.5 months, and Group D: 13.53 [+ -] 14.7 months. Significant differences in overall survival were associated with tumor histology (P = 0.027), tumor localization (P = 0.019), and type of therapy (P = 0.005), respectively, in univariate analysis. Treatment modality (P = 0.043) was the only independent predictor of survival in multivariate analysis. The difference in overall survival between Group A and Group D was highly significant (P [less than] 0.01) and in favor of Group D. As concerns Group D versus Group B and Group D versus Group C there was a trend towards a difference in overall survival in favor of Group D (P = 0.069 and P = 0.059, respectively). Conclusions The prognosis of inoperable esophageal cancer seems to be highly dependent on the suitability of the induction of patient-specific therapeutic measures and is significantly better, when chemoradiotherapy is applied.
    Keywords: Chemotherapy -- Health Aspects ; Chemotherapy -- Patient Outcomes ; Chemotherapy -- Comparative Analysis ; Esophageal Cancer -- Care And Treatment ; Esophageal Cancer -- Patient Outcomes ; Esophageal Cancer -- Research ; Radiotherapy -- Health Aspects ; Radiotherapy -- Patient Outcomes ; Radiotherapy -- Comparative Analysis
    ISSN: 1471-2407
    Source: Cengage Learning, Inc.
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