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Your search keyword '"Michels S"' showing total 23 results
Start Over Author "Michels S" Publisher elsevier b.v.
23 results on '"Michels S"'

6. 1336P Small cell transformation in EGFR-mutated non-small cell lung cancer (EGFR+ NSCLC): Efficacy of immune checkpoint inhibitors or tyrosine kinase inhibitors combined with platinum-based chemotherapy.

Author

Saalfeld, F.C., Möller, J., Michels, S., Grohe, C., Wiesweg, M., Schubart, C., Alt, J., Griesinger, F., Kauffmann-Guerrero, D., Kulhavy, J., Overbeck, T.R., Pelusi, N., Rohde, G., Wesseler, C., Vathiotis, I., Veluswamy, R., Illini, O.M., Rothschild, S.I., Christopoulos, P., and Wermke, M.

Subjects
*PROTEIN-tyrosine kinase inhibitors, *NON-small-cell lung carcinoma, *IMMUNE checkpoint inhibitors, *CELL transformation, *PEMETREXED, *IPILIMUMAB, *CANCER chemotherapy
Published
2023
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9. 52P ROS1 aberrations in non-small cell lung cancer patients without rearrangements: Clinical and molecular characteristics.

Author

Glaser, M., von Levetzow, C., Michels, S., Nogova, L., Katzenmeier, M., Wömpner, C., Schmitz, J., Bitter, E., Terjung, I., Passmann, E., Schaufler, D., Eisert, A., Fischer, R., Riedel, R., Weber, J-P., Hahne, S., Merkelbach-Bruse, S., Büttner, R., Wolf, J., and Scheffler, M.

Subjects
*NON-small-cell lung carcinoma, *REARRANGEMENTS (Chemistry), *CANCER patients
Published
2022
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10. 1308P Molecular and clinical characteristics of patients with non-small cell lung cancer (NSCLC) harboring KRAS Q61 mutations.

Author

Ruge, L.V., John, F., Scharpenseel, H., Siemanowski-Hrach, J., Fassunke, J., Riedel, R., Fischer, R.N., Michels, S., Eisert, A., Rasokat, A., Kron, A., Serke, M., Kappes, J., Kambartel, K., Siebolts, U., Merkelbach-Bruse, S., Büttner, R., Nogova, L., Wolf, J., and Scheffler, M.

Subjects
*NON-small-cell lung carcinoma, *RAS oncogenes, *GENETIC mutation
Published
2024
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14. Impact of TP53 mutation status on systemic treatment outcome in ALK-rearranged non-small-cell lung cancer.

Author

Kron, A, Alidousty, C, Scheffler, M, Merkelbach-Bruse, S, Seidel, D, Riedel, R, Ihle, M A, Michels, S, Nogova, L, and Fassunke, J

Subjects
*NON-small-cell lung carcinoma, *CANCER treatment, *GENETIC mutation, *CANCER chemotherapy, *DRUG efficacy
Abstract

Background We analyzed whether co-occurring mutations influence the outcome of systemic therapy in ALK -rearranged non-small-cell lung cancer (NSCLC). Patients and methods ALK -rearranged stage IIIB/IV NSCLC patients were analyzed with next-generation sequencing and fluorescence in situ hybridization analyses on a centralized diagnostic platform. Median progression-free survival (PFS) and overall survival (OS) were determined in the total cohort and in treatment-related sub-cohorts. Cox regression analyses were carried out to exclude confounders. Results Among 216 patients with ALK -rearranged NSCLC, the frequency of pathogenic TP53 mutations was 23.8%, while other co-occurring mutations were rare events. In ALK/TP53 co-mutated patients, median PFS and OS were significantly lower compared with TP53 wildtype patients [PFS 3.9 months (95% CI: 2.4–5.6) versus 10.3 months (95% CI: 8.6–12.0), P < 0.001; OS 15.0 months (95% CI: 5.0–24.9) versus 50.0 months (95% CI: 22.9–77.1), P = 0.002]. This difference was confirmed in all treatment-related subgroups including chemotherapy only [PFS first-line chemotherapy 2.6 months (95% CI: 1.3–4.1) versus 6.2 months (95% CI: 1.8–10.5), P = 0.021; OS 2.0 months (95% CI: 0.0–4.6) versus 9.0 months (95% CI: 6.1–11.9), P = 0.035], crizotinib plus chemotherapy [PFS crizotinib 5.0 months (95% CI: 2.9–7.2) versus 14.0 months (95% CI: 8.0–20.1), P < 0.001; OS 17.0 months (95% CI: 6.7–27.3) versus not reached, P = 0.049] and crizotinib followed by next-generation ALK-inhibitor [PFS next-generation inhibitor 5.4 months (95% CI: 0.1–10.7) versus 9.9 months (95% CI: 6.4–13.5), P = 0.039; OS 7.0 months versus 50.0 months (95% CI: not reached), P = 0.001). Conclusions In ALK -rearranged NSCLC co-occurring TP53 mutations predict an unfavorable outcome of systemic therapy. Our observations encourage future research to understand the underlying molecular mechanisms and to improve treatment outcome of the ALK/TP53 co-mutated subgroup. [ABSTRACT FROM AUTHOR]

Published
2018
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15. Economic burden of clinical trials in lung cancer in a German Comprehensive Cancer Center.

Author

Kron, F., Kostenko, A., Scheffler, M., Müller, D., Glossmann, J.-P., Fischer, R., Michels, S., Nogova, L., Hallek, M., Zander, T., and Wolf, J.

Subjects
*LUNG cancer, *LUNG diseases, *DRUGS, *CLINICAL drug trials, *CLINICAL pharmacology
Abstract

Objectives The recent success of individualized lung cancer therapy has triggered fundamental changes in clinical research strategies. To date there is a strong focus on early proof of concept trials in genetically preselected small patient subgroups. This analysis focuses on the economic burden caused by such trials for advanced lung cancer patients in a German Comprehensive Cancer Center (CCC). Methods The profit margins between recruiting groups with ≤3 and >3 patients were compared. Clinical and economic data from clinical trials for advanced lung cancer (LC), pharma-sponsored trials (PhST) as well as investigator initiated trials (IIT), conducted between 2011 and 2015 at the Center for Integrated Oncology (CIO) Cologne, were analyzed using a profit-center calculation model. Results 161 patients were enrolled in 27 clinical trials. The key economic parameter determining costs and payments was the ‘trial visits’. In comparison of the two groups (A ≤ 3; B > 3 patients enrolled) we found negative profit margins for the low recruiting group (€ −1444). Concerning the number of visits significant differences were found between PhST and IIT (p = 0.009). Additionally, sub-analysis show structural differences in cost composition by conducting PhST and IIT. Conclusion Trials with low patient numbers and IIT, do not cover the cost. To ensure adequate, cost-covering compensation by pharmaceutical companies CCCs have to thoroughly calculate the cost of early proof of concept trials. The findings of this study also underline the need for novel structures in public funding for investigator-initiated clinical trials in precision medicine. [ABSTRACT FROM AUTHOR]

Published
2017
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16. 1171P A phase II theranostic study with osimertinib in patients with EGFR-mutated non-small cell lung cancer (NSCLC) progressing on EGFR tyrosine kinase inhibitors (TKI) and undetectable EGFR T790M (THEROS).

Author

Wiesweg, M., Hense, J., Darwiche, K., Michels, S., Hautzel, H., Kobe, C., Metzenmacher, M., Herold, T., Zaun, G., Laue, K., Drzezga, A., Schildhaus, H-U., Wolf, J., Herrmann, K., and Schuler, M.H.H.

Subjects
*NON-small-cell lung carcinoma, *PROTEIN-tyrosine kinase inhibitors, *EPIDERMAL growth factor receptors, *OSIMERTINIB
Published
2022
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17. 1028P BIOLUMA: A phase II trial of nivolumab in combination with ipilimumab to evaluate efficacy and safety in lung cancer and to evaluate biomarkers predictive for response – results from the NSCLC cohort.

Author

Fischer, R.N., George, J., Scheel, A., Schloesser, H., Brossart, P., Engel-Riedel, W., Griesinger, F., Grohé, C., Kern, J.K., Panse, J., Sebastian, M., Serke, M., Wiewrodt, R., Michels, S., Nogova, L., Riedel, R., Weber, J-P., Büttner, R., Thomas, R., and Wolf, J.

Subjects
*TUMOR markers, *LUNG cancer, *NIVOLUMAB, *NON-small-cell lung carcinoma, *IPILIMUMAB
Published
2022
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18. 991P EGFR exon 20 insertions in non-small cell lung cancer (NSCLC): Impact of TP53 mutation status and value of immune checkpoint blockade (ICB).

Author

Kron, A., Scheffler, M., Ihle, M., Michels, S., Süptitz, J., Prang, D., Jakobs, F., Nogova, L., Fischer, R.N., Eisert, A.K., Riedel, R., Kron, F., Hillmer, A., Loges, S., Merkelbach-Bruse, S., Büttner, R., and Wolf, J.

Subjects
*NON-small-cell lung carcinoma, *IMMUNE checkpoint proteins, *IMMUNITY, *EPIDERMAL growth factor receptors, *GENETIC mutation
Published
2022
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