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Your search keyword '"Grischke, E.M."' showing total 23 results
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23 results on '"Grischke, E.M."'

1. Nab-paclitaxel weekly versus dose-dense solvent-based paclitaxel followed by dose-dense epirubicin plus cyclophosphamide in high-risk HR+/HER2− early breast cancer: results from the neoadjuvant part of the WSG-ADAPT-HR+/HER2− trial

Author

Gluz, O., Kuemmel, S., Nitz, U., Braun, M., Lüdtke-Heckenkamp, K., von Schumann, R., Darsow, M., Forstbauer, H., Potenberg, J., Uleer, C., Grischke, E.M., Aktas, B., Schumacher, C., zu Eulenburg, C., Kates, R., Jóźwiak, K., Graeser, M., Wuerstlein, R., Baehner, R., Christgen, M., Kreipe, H.H., and Harbeck, N.

Published
2023
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5. Electrochemotherapy in the treatment of cutaneous malignancy: Outcomes and subgroup analysis from the cumulative results from the pan-European International Network for Sharing Practice in Electrochemotherapy database for 2482 lesions in 987 patients (2008–2019)

Author

Clover, A.J.P., primary, de Terlizzi, F., additional, Bertino, G., additional, Curatolo, P., additional, Odili, J., additional, Campana, L.G., additional, Kunte, C., additional, Muir, T., additional, Brizio, M., additional, Sersa, G., additional, Pritchard Jones, R., additional, Moir, G., additional, Orlando, A., additional, Banerjee, S.M., additional, Kis, E., additional, McCaul, J.A., additional, Grischke, E.M., additional, Matteucci, P., additional, Mowatt, D., additional, Bechara, F.G., additional, Mascherini, M., additional, Lico, V., additional, Giorgione, R., additional, Seccia, V., additional, Schepler, H., additional, Pecorari, G., additional, MacKenzie Ross, A.D., additional, Bisase, B., additional, and Gehl, J., additional

Published
2020
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6. Patient-reported outcomes and final overall survival results from the randomized phase 3 PENELOPE trial evaluating pertuzumab in low tumor human epidermal growth factor receptor 3 (HER3) mRNA-expressing platinum-resistant ovarian cancer

Author

Lorusso, D., Hilpert, F., Martin, A.G., Rau, J., Ottevanger, P., Greimel, E., Luck, H.J., Selle, F., Colombo, N., Kroep, J.R., Mirza, M.R., Berger, R., Pardo, B., Grischke, E.M., Berton-Rigaud, D., Martinez-Garcia, J., Vergote, I., Redondo, A., Cardona, A., Bastiere-Truchot, L., Bois, A. du, Kurzeder, C., Campo, J.M. del, Bover, I., Barretina-Ginesta, P., Ortega, E., Garcia, Y., Romero, I., Poveda, A., Herrero, A., Vidal, L., Rubio, M.J., Romeo, M., Mendiola, C., Arranz, J.A., Santaballa, A., Liano, A.G. de, Marme, F., Mahner, S., Canzler, U., Zorr, A., Gropp-Meier, M., Cayir, P., Schmalfeldt, B., Rautenberg, B., Meier, W., Belau, A., Gerber, B., Rein, D., Jackisch, C., Janni, W., Heubner, M., Pautier, P., Fabbro, M., Floquet, A., You, B., Favier, L., Joly, F., Weber, B., Hardy-Bessard, A.C., Gadducci, A., Tognon, G., DeCensi, A., Savarese, A., Pisano, C., Sonke, G., Reyners, A., Kristensen, G., Bjurberg, M., Rosenberg, P., Marth, C., PENELOPE Trial Investigators, Lorusso, D, Hilpert, F, Gonzalez Martin, A, Rau, J, Ottevanger, P, Greimel, E, Luck, H, Selle, F, Colombo, N, Kroep, J, Mirza, M, Berger, R, Pardo, B, Grischke, E, Berton-Rigaud, D, Martinez-Garcia, J, Vergote, I, Redondo, A, Cardona, A, Bastiere-Truchot, L, Du Bois, A, Kurzeder, C, Del Campo, J, Bover, I, Barretina-Ginesta, P, Ortega, E, Garcia, Y, Romero, I, Poveda, A, Herrero, A, Vidal, L, Rubio, M, Romeo, M, Mendiola, C, Arranz, J, Santaballa, A, Gomez De Liano, A, Marme, F, Mahner, S, Canzler, U, Zorr, A, Gropp-Meier, M, Cayir, P, Schmalfeldt, B, Rautenberg, B, Meier, W, Belau, A, Gerber, B, Rein, D, Jackisch, C, Janni, W, Heubner, M, Pautier, P, Fabbro, M, Floquet, A, You, B, Favier, L, Joly, F, Weber, B, Hardy-Bessard, A, Gadducci, A, Tognon, G, Decensi, A, Savarese, A, Pisano, C, Sonke, G, Reyners, A, Kristensen, G, Bjurberg, M, Rosenberg, P, Marth, C, Targeted Gynaecologic Oncology (TARGON), and Guided Treatment in Optimal Selected Cancer Patients (GUTS)

Subjects
Oncology, Receptor, ErbB-3, medicine.medical_treatment, Carcinoma, Ovarian Epithelial, Deoxycytidine, 0302 clinical medicine, Antineoplastic Agents, Immunological, Antineoplastic Combined Chemotherapy Protocols, Clinical endpoint, Aged, 80 and over, Ovarian Neoplasms, 0303 health sciences, education.field_of_study, Obstetrics and Gynecology, Middle Aged, Progression-Free Survival, ovarian cancer, patient-reported outcomes, 030220 oncology & carcinogenesis, Female, Pertuzumab, medicine.drug, Adult, medicine.medical_specialty, Paclitaxel, overall survival, Population, Placebo, patient-reported outcome, Antibodies, Monoclonal, Humanized, 03 medical and health sciences, Double-Blind Method, HER3, pertuzumab, Internal medicine, medicine, Humans, Patient Reported Outcome Measures, RNA, Messenger, education, 030304 developmental biology, Aged, Chemotherapy, business.industry, medicine.disease, Gemcitabine, Drug Resistance, Neoplasm, Topotecan, business, Ovarian cancer
Abstract

IntroductionThe PENELOPE trial evaluated pertuzumab added to chemotherapy for biomarker-selected platinum-resistant ovarian cancer. As previously reported, pertuzumab did not statistically significantly improve progression-free survival (primary end point: HR 0.74, 95% CI 0.50 to 1.11), although results in the paclitaxel and gemcitabine cohorts suggested activity. Here, we report final overall survival and patient-reported outcomes.Patients and methodsEligible patients had ovarian carcinoma that progressed during/within 6 months of completing ≥4 platinum cycles, low tumor human epidermal growth factor receptor 3 (HER3) mRNA expression, and ≤2 prior chemotherapy lines. Investigators selected single-agent topotecan, gemcitabine or weekly paclitaxel before patients were randomized to either placebo or pertuzumab (840→420 mg every 3 weeks), stratified by selected chemotherapy, prior anti-angiogenic therapy, and platinum-free interval. Final overall survival analysis (key secondary end point) was pre-specified after 129 deaths. Patient-reported outcomes (secondary end point) were assessed at baseline and every 9 weeks until disease progression.ResultsAt database lock (June 9, 2016), 130 (83%) of 156 randomized patients had died. Median follow-up was 27 months in the pertuzumab arm versus 26 months in the control arm. In the intent-to-treat population there was no overall survival difference between treatment arms (stratified HR 0.90, 95% CI 0.61 to 1.32; p=0.60). Results in subgroups defined by stratification factors indicated heterogeneity similar to previous progression-free survival results. Updated safety was similar to previously published results. Compliance with patient-reported outcomes questionnaire completion was >75% for all validated patient-reported outcomes measures. Pertuzumab demonstrated neither beneficial nor detrimental effects on patient-reported outcomes compared with placebo, except for increased diarrhea symptoms.DiscussionConsistent with the primary results, adding pertuzumab to chemotherapy for low tumor HER3 mRNA-expressing platinum-resistant ovarian cancer did not improve overall survival, but showed trends in some cohorts. Except for increased diarrhea symptoms, pertuzumab had no impact on patient-reported outcomes.ClinicalTrials.gov:ClinicalTrials.gov:NCT01684878.

Published
2019

8. Electrochemotherapy in the treatment of cutaneous malignancy; outcomes and subgroup analysis from the cumulative results from the pan- European InspECT Database for 1478 lesions in 691 patients (2008-2018)

Author

Clover, A.J.P., primary, Bertino, G., additional, Curatolo, P., additional, Odili, J., additional, Campana, L., additional, Kunte, C., additional, Muir, T., additional, Brizio, M., additional, Sersa, G., additional, Liew, S.H., additional, Moir, G., additional, Orlando, A., additional, Banerjee, S.M., additional, Kis, E., additional, McCaul, J.A., additional, Grischke, E.M., additional, Matteucci, P., additional, and Gehl, K.J., additional

Published
2019
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11. 1869 Disease characteristics of subgroup patients treated with everolimus + exemestane for <12 months, ≥12 to <18months, and ≥18 months - Results of the 3rd interim analysis of the non-interventional trial BRAWO

Author

Lüftner, D., primary, Grischke, E.M., additional, Fasching, P., additional, Decker, T., additional, Schneeweiss, A., additional, Uleer, C., additional, Foerster, F., additional, Wimberger, P., additional, Kluth-Pepper, B., additional, Schubert, J., additional, Bloch, W., additional, Tesch, H., additional, Schuetz, F., additional, and Jackisch, C., additional

Published
2015
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22. Placenta-derived CD95 ligand causes liver damage in hemolysis, elevated liver enzymes, and low platelet count syndrome

Author

Strand, S., Strand, D., Seufert, R., Mann, A., Lotz, J., Blessing, M., Lahn, M., Wunsch, A., Broering, D.C., Hahn, U., Grischke, E.M., Rogiers, X., Otto, G., Gores, G.J., and Galle, P.R.

Abstract

Background & Aims: The HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome is a life-threatening complication during pregnancy. The associated liver disease may be severe, and maternal hepatic complications may progress to the point that transplantation becomes necessary. CD95 (APO-1, Fas)-mediated apoptosis of liver cells is one of the major pathogenic mechanisms during liver disease. The interaction of CD95 with its ligand, CD95L(FasL), induces apoptosis and thus the source of the death-inducing ligand is critical for understanding the pathomechanism of liver damage involving the CD95-system. Methods: Sera from HELLP patients were analyzed and used in cell culture experiments to study CD95-mediated apoptosis. We established a mouse model for placenta-induced liver damage and used a new therapeutical agent, LY498919, to block CD95 apoptosis. Results: We describe apoptosis in the liver of HELLP patients and cytotoxic activity for primary human hepatocytes in HELLP serum. Blocking of CD95 signaling reduced the cytotoxic activity of HELLP serum. In addition, cytotoxic activity increased as HELLP syndrome developed. Furthermore, CD95L was found to be produced in the placenta and extracts of placenta were cytotoxic for human hepatocytes. Injection of mouse placenta extract in mice induces liver damage that could be prevented by blocking CD95L. Conclusions: Taken together, these data suggest that CD95L derived from the placenta acts systemically and is a primary cause of liver damage in HELLP syndrome. Our results also show that blocking of CD95L can reduce liver cell apoptosis, indicating that such a strategy may have therapeutic advantages.

Published
2004
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