Author
Peter R. Galle
Other affiliations: Heidelberg University, University Hospital Heidelberg, German Cancer Research Center
Bio: Peter R. Galle is an academic researcher from University of Mainz. The author has contributed to research in topics: Fas receptor & Apoptosis. The author has an hindex of 29, co-authored 44 publications receiving 22582 citations. Previous affiliations of Peter R. Galle include Heidelberg University & University Hospital Heidelberg.
Papers
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University of Barcelona1, University of Pisa2, University of Duisburg-Essen3, Auckland City Hospital4, University of São Paulo5, European University6, Icahn School of Medicine at Mount Sinai7, Goethe University Frankfurt8, University of Bologna9, Hannover Medical School10, University of Mainz11, Aix-Marseille University12, Université catholique de Louvain13, University of Düsseldorf14, Bayer15, Bayer Corporation16
TL;DR: In patients with advanced hepatocellular carcinoma, median survival and the time to radiologic progression were nearly 3 months longer for patients treated with sorafenib than for those given placebo.
Abstract: Background No effective systemic therapy exists for patients with advanced hepatocellular carcinoma. A preliminary study suggested that sorafenib, an oral multikinase inhibitor of the vascular endothelial growth factor receptor, the platelet-derived growth factor receptor, and Raf may be effective in hepatocellular carcinoma. Methods In this multicenter, phase 3, double-blind, placebo-controlled trial, we randomly assigned 602 patients with advanced hepatocellular carcinoma who had not received previous systemic treatment to receive either sorafenib (at a dose of 400 mg twice daily) or placebo. Primary outcomes were overall survival and the time to symptomatic progression. Secondary outcomes included the time to radiologic progression and safety. Results At the second planned interim analysis, 321 deaths had occurred, and the study was stopped. Median overall survival was 10.7 months in the sorafenib group and 7.9 months in the placebo group (hazard ratio in the sorafenib group, 0.69; 95% confidence interval, 0.55 to 0.87; P<0.001). There was no significant difference between the two groups in the median time to symptomatic progression (4.1 months vs. 4.9 months, respectively, P=0.77). The median time to radiologic progression was 5.5 months in the sorafenib group and 2.8 months in the placebo group (P<0.001). Seven patients in the sorafenib group (2%) and two patients in the placebo group (1%) had a partial response; no patients had a complete response. Diarrhea, weight loss, hand-foot skin reaction, and hypophosphatemia were more frequent in the sorafenib group. Conclusions In patients with advanced hepatocellular carcinoma, median survival and the time to radiologic progression were nearly 3 months longer for patients treated with sorafenib than for those given placebo.
10,074 citations
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TL;DR: In patients with unresectable hepatocellular carcinoma, atezolIZumab combined with bevacizumab resulted in better overall and progression-free survival outcomes than sorafenib.
Abstract: Background The combination of atezolizumab and bevacizumab showed encouraging antitumor activity and safety in a phase 1b trial involving patients with unresectable hepatocellular carcinom...
3,085 citations
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TL;DR: A reliable diagnosis of AIH can be made using a very simple diagnostic score proposed, which is the diagnosis of probable AIH at a cutoff point greater than 6 points and definite AIH 7 points or higher.
1,415 citations
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TL;DR: University College, London Cancer Institute, 72 Huntley St.
1,043 citations
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TL;DR: The data suggest that tumor cells can evade immune attack by down–regulation of the CD95 receptor and killing of lymphocytes through expression of CD95L, which is an important mediator of T–cell cytotoxicity.
Abstract: The CD95 (APO-1/Fas) system is an important mediator of T-cell cytotoxicity. We investigated this system in 22 hepatocellular carcinomas (HCCs) from patients. All HCCs had partially or completely lost the expression of the CD95 receptor constitutively expressed by normal liver cells and might thus evade CD95-mediated killing. We also considered a new mechanism of immune evasion, namely, the active destruction of T-lymphocytes by tumor cells expressing CD95 ligand (CD95L). CD95L messenger RNA and protein could be detected in the HCCs. In coculture experiments, HepG2 hepatoblastoma cells, expressing CD95L mRNA after treatment with cytostatic drugs, killed CD95+ Jurkat lymphocytes. Our data suggest that tumor cells can evade immune attack by down-regulation of the CD95 receptor and killing of lymphocytes through expression of CD95L.
936 citations
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TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
8,664 citations
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TL;DR: The following Clinical Practice Guidelines will give up-to-date advice for the clinical management of patients with hepatocellular carcinoma, as well as providing an in-depth review of all the relevant data leading to the conclusions herein.
7,851 citations
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TL;DR: The American Association for the Study of Liver Diseases (AASLD) practice guidelines on the management of hepatocellular carcinoma (HCC) were updated in 2010 as discussed by the authors.
6,964 citations
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TL;DR: Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival.
Abstract: Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival. Certain cells have unique sensors, termed death receptors, on their surface. Death receptors detect the presence of extracellular death signals and, in response, they rapidly ignite the cell's intrinsic apoptosis machinery.
5,968 citations
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TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
5,054 citations