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2. Obinutuzumab plus fludarabine and cyclophosphamide in previously untreated, fit patients with chronic lymphocytic leukemia: a subgroup analysis of the GREEN study

Author

Bosch, Francesc, Cantin, Guy, Cortelezzi, Agostino, Knauf, Wolfgang, Tiab, Mourad, Turgut, Mehmet, Zaritskey, Andrey, Merot, Jean-Louis, Tausch, Eugen, Trunzer, Kerstin, Robson, Susan, Gresko, Ekaterina, Böttcher, Sebastian, Foà, Robin, Stilgenbauer, Stephan, and Leblond, Véronique

Published
2020
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3. Safety and efficacy of vemurafenib in BRAF V600E and BRAF V600K mutation-positive melanoma (BRIM-3): extended follow-up of a phase 3, randomised, open-label study

Author

McArthur, Grant A, Chapman, Paul B, Robert, Caroline, Larkin, James, Haanen, John B, Dummer, Reinhard, Ribas, Antoni, Hogg, David, Hamid, Omid, Ascierto, Paolo A, Garbe, Claus, Testori, Alessandro, Maio, Michele, Lorigan, Paul, Lebbé, Celeste, Jouary, Thomas, Schadendorf, Dirk, O'Day, Stephen J, Kirkwood, John M, Eggermont, Alexander M, Dréno, Brigitte, Sosman, Jeffrey A, Flaherty, Keith T, Yin, Ming, Caro, Ivor, Cheng, Suzanne, Trunzer, Kerstin, and Hauschild, Axel

Subjects
Genetics, Cancer, Clinical Trials and Supportive Activities, Clinical Research, Prevention, Good Health and Well Being, Adult, Aged, Dacarbazine, Disease-Free Survival, Female, Follow-Up Studies, Humans, Indoles, Male, Melanoma, Middle Aged, Mutation, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf, Sulfonamides, Vemurafenib, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

BackgroundIn the BRIM-3 trial, vemurafenib was associated with risk reduction versus dacarbazine of both death and progression in patients with advanced BRAF(V600) mutation-positive melanoma. We present an extended follow-up analysis of the total population and in the BRAF(V600E) and BRAF(V600K) mutation subgroups.MethodsPatients older than 18 years, with treatment-naive metastatic melanoma and whose tumour tissue was positive for BRAF(V600) mutations were eligible. Patients also had to have a life expectancy of at least 3 months, an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, and adequate haematological, hepatic, and renal function. Patients were randomly assigned by interactive voice recognition system to receive either vemurafenib (960 mg orally twice daily) or dacarbazine (1000 mg/m(2) of body surface area intravenously every 3 weeks). Coprimary endpoints were overall survival and progression-free survival, analysed in the intention-to-treat population (n=675), with data censored at crossover. A sensitivity analysis was done. This trial is registered with ClinicalTrials.gov, NCT01006980.Findings675 eligible patients were enrolled from 104 centres in 12 countries between Jan 4, 2010, and Dec 16, 2010. 337 patients were randomly assigned to receive vemurafenib and 338 to receive dacarbazine. Median follow-up was 12·5 months (IQR 7·7-16·0) on vemurafenib and 9·5 months (3·1-14·7) on dacarbazine. 83 (25%) of the 338 patients initially randomly assigned to dacarbazine crossed over from dacarbazine to vemurafenib. Median overall survival was significantly longer in the vemurafenib group than in the dacarbazine group (13·6 months [95% CI 12·0-15·2] vs 9·7 months [7·9-12·8]; hazard ratio [HR] 0·70 [95% CI 0·57-0·87]; p=0·0008), as was median progression-free survival (6·9 months [95% CI 6·1-7·0] vs 1·6 months [1·6-2·1]; HR 0·38 [95% CI 0·32-0·46]; p

Published
2014

4. Safety and efficacy of zinpentraxin alfa as monotherapy or in combination with ruxolitinib in myelofibrosis: stage I of a phase II trial

Author

Verstovsek, Srdan, primary, Foltz, Lynda, additional, Gupta, Vikas, additional, Hasserjian, Robert, additional, Manshouri, Taghi, additional, Mascarenhas, John, additional, Mesa, Ruben, additional, Pozdnyakova, Olga, additional, Ritchie, Ellen, additional, Veletic, Ivo, additional, Gamel, Katia, additional, Hamidi, Habib, additional, Han, Lyrialle, additional, Higgins, Brian, additional, Trunzer, Kerstin, additional, Uguen, Marianne, additional, Wang, Dao, additional, El-Galaly, Tarec Christoffer, additional, Todorov, Boyan, additional, and Gotlib, Jason, additional

Published
2023
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5. Safety and efficacy of zinpentraxin alfa as monotherapy or in combination with ruxolitinib in myelofibrosis:stage I of a phase II trial

Author

Verstovsek, Srdan, Foltz, Lynda, Gupta, Vikas, Hasserjian, Robert, Manshouri, Taghi, Mascarenhas, John, Mesa, Ruben, Pozdnyakova, Olga, Ritchie, Ellen, Veletic, Ivo, Gamel, Katia, Hamidi, Habib, Han, Lyrialle, Higgins, Brian, Trunzer, Kerstin, Uguen, Marianne, Wang, Dao, El-Galaly, Tarec Christoffer, Todorov, Boyan, and Gotlib, Jason

Subjects
Hematology
Abstract

Pentraxin 2 (PTX-2; serum amyloid P component), a circulating endogenous regulator of the inflammatory response to tissue injury and fibrosis, is reduced in patients with myelofibrosis (MF). Zinpentraxin alfa (RO7490677, PRM-151) is a recombinant form of PTX-2 that has shown preclinical antifibrotic activity and no dose-limiting toxicities in phase I trials. We report results from stage 1 of a phase II trial of zinpentraxin alfa in patients with intermediate-1/2 or high-risk MF. Patients (n=27) received intravenous zinpentraxin alfa weekly (QW) or every 4 weeks (Q4W), as monotherapy or an additional therapy for patients on stable-dose ruxolitinib. The primary endpoint was overall response rate (ORR; investigator-assessed) adapted from International Working Group-Myeloproliferative Neoplasms Research and Treatment criteria. Secondary endpoints included modified Myeloproliferative Neoplasm-Symptom Assessment Form Total Symptom Score (MPN-SAF TSS) change, bone marrow (BM) MF grade reduction, pharmacokinetics, and safety. ORR at week 24 was 33% (n=9/27) and varied across individual cohorts (QW: 38% [3/8]; Q4W: 14% [1/7]; QW+ruxolitinib: 33% [2/6]; Q4W+ruxolitinib: 50% [3/6]). Five of 18 evaluable patients (28%) experienced a ≥50% reduction in MPN-SAF TSS, and 6/17 evaluable patients (35%) had a ≥1 grade improvement from baseline in BM fibrosis at week 24. Most treatmentemergent adverse events (AE) were grade 1–2, most commonly fatigue. Among others, anemia and thrombocytopenia were infrequent (n=3 and n=1, respectively). Treatmentrelated serious AE occurred in four patients (15%). Overall, zinpentraxin alfa showed evidence of clinical activity and tolerable safety as monotherapy and in combination with ruxolitinib in this open-label, non-randomized trial. ClinicalTrials.gov Identifier: NCT01981850. Pentraxin 2 (PTX-2; serum amyloid P component), a circulating endogenous regulator of the inflammatory response to tissue injury and fibrosis, is reduced in patients with myelofibrosis (MF). Zinpentraxin alfa (RO7490677, PRM-151) is a recombinant form of PTX-2 that has shown preclinical antifibrotic activity and no dose-limiting toxicities in phase I trials. We report results from stage 1 of a phase II trial of zinpentraxin alfa in patients with intermediate-1/2 or high-risk MF. Patients (n=27) received intravenous zinpentraxin alfa weekly (QW) or every 4 weeks (Q4W), as monotherapy or an additional therapy for patients on stable-dose ruxolitinib. The primary endpoint was overall response rate (ORR; investigator-assessed) adapted from International Working Group-Myeloproliferative Neoplasms Research and Treatment criteria. Secondary endpoints included modified Myeloproliferative Neoplasm-Symptom Assessment Form Total Symptom Score (MPN-SAF TSS) change, bone marrow (BM) MF grade reduction, pharmacokinetics, and safety. ORR at week 24 was 33% (n=9/27) and varied across individual cohorts (QW: 38% [3/8]; Q4W: 14% [1/7]; QW+ruxolitinib: 33% [2/6]; Q4W+ruxolitinib: 50% [3/6]). Five of 18 evaluable patients (28%) experienced a ≥50% reduction in MPN-SAF TSS, and 6/17 evaluable patients (35%) had a ≥1 grade improvement from baseline in BM fibrosis at week 24. Most treatmentemergent adverse events (AE) were grade 1–2, most commonly fatigue. Among others, anemia and thrombocytopenia were infrequent (n=3 and n=1, respectively). Treatmentrelated serious AE occurred in four patients (15%). Overall, zinpentraxin alfa showed evidence of clinical activity and tolerable safety as monotherapy and in combination with ruxolitinib in this open-label, non-randomized trial. ClinicalTrials.gov Identifier: NCT01981850.

Published
2023

6. Supplementary Methods from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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7. Data from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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8. Supplementary Figure 3 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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9. Supplementary Figure 1 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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10. Supplementary Figure 4 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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11. Supplementary Table 3 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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12. Supplementary Table 1 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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13. Supplementary Table 2 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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14. Supplementary Figure 5 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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15. Supplementary Table 4 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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16. Supplementary Figure 2 from Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., primary, Wang, Qiongqing, primary, Yang, Hong, primary, Xu, Lizhong, primary, Higgins, Brian, primary, Kolinsky, Kenneth, primary, Packman, Kathryn, primary, Kim, Min Jung, primary, Trunzer, Kerstin, primary, Lee, Richard J., primary, Schostack, Kathleen, primary, Carter, Jade, primary, Albert, Thomas, primary, Germer, Soren, primary, Rosinski, Jim, primary, Martin, Mitchell, primary, Simcox, Mary Ellen, primary, Lestini, Brian, primary, Heimbrook, David, primary, and Bollag, Gideon, primary

Published
2023
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17. Safety and efficacy of vemurafenib in BRAFV600E and BRAFV600K mutation-positive melanoma (BRIM-3): extended follow-up of a phase 3, randomised, open-label study

Author

McArthur, Grant A, Chapman, Paul B, Robert, Caroline, Larkin, James, Haanen, John B, Dummer, Reinhard, Ribas, Antoni, Hogg, David, Hamid, Omid, Ascierto, Paolo A, Garbe, Claus, Testori, Alessandro, Maio, Michele, Lorigan, Paul, Lebbé, Celeste, Jouary, Thomas, Schadendorf, Dirk, O'Day, Stephen J, Kirkwood, John M., Eggermont, Alexander M, Dréno, Brigitte, Sosman, Jeffrey A, Flaherty, Keith T, Yin, Ming, Caro, Ivor, Cheng, Suzanne, Trunzer, Kerstin, and Hauschild, Axel

Published
2014
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18. Primary results from TAIL: a global single-arm safety study of atezolizumab monotherapy in a diverse population of patients with previously treated advanced non-small cell lung cancer

Author

Ardizzoni, Andrea, primary, Azevedo, Sergio, additional, Rubio-Viqueira, Belen, additional, Rodríguez-Abreu, Delvys, additional, Alatorre-Alexander, Jorge, additional, Smit, Hans J M, additional, Yu, Jinming, additional, Syrigos, Konstantinos, additional, Trunzer, Kerstin, additional, Patel, Hina, additional, Tolson, Jonathan, additional, Cardona, Andres, additional, Perez-Moreno, Pablo D, additional, and Newsom-Davis, Tom, additional

Published
2021
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19. RAS Mutations in Cutaneous Squamous-Cell Carcinomas in Patients Treated with BRAF Inhibitors

Author

Su, Fei, Viros, Amaya, Milagre, Carla, Trunzer, Kerstin, Bollag, Gideon, Spleiss, Olivia, Reis-Filho, Jorge S., Kong, Xiangju, Koya, Richard C., Flaherty, Keith T., Chapman, Paul B., Kim, Min Jung, Hayward, Robert, Martin, Matthew, Yang, Hong, Wang, Qiongqing, Hilton, Holly, Hang, Julie S., Noe, Johannes, Lambros, Maryou, Geyer, Felipe, Dhomen, Nathalie, Niculescu-Duvaz, Ion, Zambon, Alfonso, Niculescu-Duvaz, Dan, Preece, Natasha, Robert, Lídia, Otte, Nicholas J., Mok, Stephen, Kee, Damien, Ma, Yan, Zhang, Chao, Habets, Gaston, Burton, Elizabeth A., Wong, Bernice, Nguyen, Hoa, Kockx, Mark, Andries, Luc, Lestini, Brian, Nolop, Keith B., Lee, Richard J., Joe, Andrew K., Troy, James L., Gonzalez, Rene, Hutson, Thomas E., Puzanov, Igor, Chmielowski, Bartosz, Springer, Caroline J., McArthur, Grant A., Sosman, Jeffrey A., Lo, Roger S., Ribas, Antoni, and Marais, Richard

Published
2012

20. Prognostic value of MRD in CLL patients with comorbidities receiving chlorambucil plus obinutuzumab or rituximab

Author

Langerak, Anton W., Ritgen, Matthias, Goede, Valentin, Robrecht, Sandra, Bahlo, Jasmin, Fischer, Kirsten, Steurer, Michael, Trněný, Marek, Mulligan, Stephen P., Mey, Ulrich J.M., Trunzer, Kerstin, Fingerle-Rowson, Günter, Humphrey, Kathryn, Stilgenbauer, Stephan, Böttcher, Sebastian, Brüggemann, Monika, Hallek, Michael, Kneba, Michael, and van Dongen, Jacques J.M.

Published
2019
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21. A noninterventional, multinational study to assess PD‐L1 expression in cytological and histological lung cancer specimens

Author

Bubendorf, Lukas, primary, Conde, Esther, additional, Cappuzzo, Federico, additional, Langfort, Renata, additional, Schildhaus, Hans‐Ulrich, additional, Votruba, Jiří, additional, Concha‐López, Ángel, additional, Esteban‐Rodriguez, Isabel, additional, Feng, Janine, additional, Devenport, Jenny, additional, Boyiddle, Christine, additional, Morris, Stefanie, additional, Trunzer, Kerstin, additional, and Kerr, Keith M., additional

Published
2020
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22. Obinutuzumab plus fludarabine and cyclophosphamide in previously untreated, fit patients with chronic lymphocytic leukemia: a subgroup analysis of the GREEN study

Author

Bosch, Francesc, primary, Cantin, Guy, additional, Cortelezzi, Agostino, additional, Knauf, Wolfgang, additional, Tiab, Mourad, additional, Turgut, Mehmet, additional, Zaritskey, Andrey, additional, Merot, Jean-Louis, additional, Tausch, Eugen, additional, Trunzer, Kerstin, additional, Robson, Susan, additional, Gresko, Ekaterina, additional, Böttcher, Sebastian, additional, Foà, Robin, additional, Stilgenbauer, Stephan, additional, and Leblond, Véronique, additional

Published
2019
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25. Quantitative Analysis of Bone Marrow Features Highlights Heterogeneity in Myelofibrosis Patients Treated with Zinpentraxin Alfa in a Phase II Clinical Study

Author

Ryou, Hosuk, Sirinukunwattana, Korsuk, Wood, Ruby, Aberdeen, Alan, Rittscher, Jens, Weinberg, Olga, Hasserjian, Robert, Pozdnyakova, Olga, Peale, Frank, Higgins, Brian, Lundberg, Pontus, Trunzer, Kerstin, Harrison, Claire N, and Royston, Daniel

Abstract

Quantitative image analysis has potential to transform the interpretation of bone marrow trephine (BMT) samples in myeloproliferative neoplasms (MPN) and improve the evaluation of anti-fibrotic therapies. To investigate the utility of recently developed algorithms evaluating reticulin fibrosis and megakaryocyte features in myelofibrosis (MF), we analysed samples from a multi-center, phase II study of zinpentraxin alfa (ZPN, PRM-151). ZPN is a recombinant form of human pentraxin-2 (PTX2) that has shown clinical activity as monotherapy and in combination with ruxolitinib (RUX) in a phase II trial in patients with Int-1/-2 or high risk MF (NCT01981850). In stage 2 of this study, patients ineligible for, intolerant of, or with an inadequate response to RUX were randomised to receive 0.3, 3.0, or 10.0 mg/kg ZPN on Days 1, 3, and 5 of Cycle 1, and every 4 weeks thereafter for up to 9 cycles. We demonstrate the potential of quantitative image analysis to augment and refine conventional expert histological assessment of MF.

Published
2023
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27. Safety and Efficacy Of Obinutuzumab (GA101) Plus CHOP Chemotherapy In First-Line Advanced Diffuse Large B-Cell Lymphoma: Results From The Phase 2 Gather Study (GAO4915g)

Author

Zelenetz, Andrew D, primary, Mobasher, Mehrdad, additional, Costa, Luciano J, additional, Flinn, Ian, additional, Flowers, Christopher R., additional, Kaminski, Mark S., additional, Sandmann, Thomas, additional, Trunzer, Kerstin, additional, Vignal, Charlotte, additional, and Forero-Torres, Andres, additional

Published
2013
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28. Pharmacodynamic Effects and Mechanisms of Resistance to Vemurafenib in Patients With Metastatic Melanoma

Author

Trunzer, Kerstin, primary, Pavlick, Anna C., additional, Schuchter, Lynn, additional, Gonzalez, Rene, additional, McArthur, Grant A., additional, Hutson, Thomas E., additional, Moschos, Stergios J., additional, Flaherty, Keith T., additional, Kim, Kevin B., additional, Weber, Jeffrey S., additional, Hersey, Peter, additional, Long, Georgina V., additional, Lawrence, Donald, additional, Ott, Patrick A., additional, Amaravadi, Ravi K., additional, Lewis, Karl D., additional, Puzanov, Igor, additional, Lo, Roger S., additional, Koehler, Astrid, additional, Kockx, Mark, additional, Spleiss, Olivia, additional, Schell-Steven, Annette, additional, Gilbert, Houston N., additional, Cockey, Louise, additional, Bollag, Gideon, additional, Lee, Richard J., additional, Joe, Andrew K., additional, Sosman, Jeffrey A., additional, and Ribas, Antoni, additional

Published
2013
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29. Analysis of Dermatologic Events in Vemurafenib-Treated Patients With Melanoma

Author

Lacouture, Mario E., primary, Duvic, Madeleine, additional, Hauschild, Axel, additional, Prieto, Victor G., additional, Robert, Caroline, additional, Schadendorf, Dirk, additional, Kim, Caroline C., additional, McCormack, Christopher J., additional, Myskowski, Patricia L., additional, Spleiss, Olivia, additional, Trunzer, Kerstin, additional, Su, Fei, additional, Nelson, Betty, additional, Nolop, Keith B., additional, Grippo, Joseph F., additional, Lee, Richard J., additional, Klimek, Matthew J., additional, Troy, James L., additional, and Joe, Andrew K., additional

Published
2013
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30. Whole Exome Sequencing of CLL Before Second-Line Treatment with Fludarabine and Cyclophosphamide with or without Rituximab (REACH trial).

Author

Konstandin, Nikola P, primary, Dufour, Annika, additional, Greif, Philipp A, additional, Ksienzyk, Bianka, additional, Graf, Alexander, additional, Krebs, Stefan, additional, Blum, Helmut, additional, Schneider, Stephanie, additional, Spiekermann, Karsten, additional, Hiddemann, Wolfgang, additional, Trunzer, Kerstin, additional, Weisser, Martin, additional, and Bohlander, Stefan K, additional

Published
2012
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31. Analysis of molecular mechanisms of response and resistance to vemurafenib (vem) in BRAFV600E melanoma.

Author

Sosman, Jeffrey Alan, primary, Pavlick, Anna C., additional, Schuchter, Lynn Mara, additional, Lewis, Karl D, additional, McArthur, Grant A., additional, Cowey, Charles Lance, additional, Moschos, Stergios J, additional, Flaherty, Keith T., additional, Kim, Kevin B., additional, Weber, Jeffrey, additional, Hersey, Peter, additional, Long, Georgina V., additional, Lawrence, Donald P., additional, Kockx, Mark, additional, Spleiss, Olivia, additional, Koehler, Astrid, additional, Bollag, Gideon, additional, Joe, Andrew K., additional, Trunzer, Kerstin, additional, and Ribas, Antoni, additional

Published
2012
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32. Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation

Author

Su, Fei, primary, Bradley, William D., additional, Wang, Qiongqing, additional, Yang, Hong, additional, Xu, Lizhong, additional, Higgins, Brian, additional, Kolinsky, Kenneth, additional, Packman, Kathryn, additional, Kim, Min Jung, additional, Trunzer, Kerstin, additional, Lee, Richard J., additional, Schostack, Kathleen, additional, Carter, Jade, additional, Albert, Thomas, additional, Germer, Soren, additional, Rosinski, Jim, additional, Martin, Mitchell, additional, Simcox, Mary Ellen, additional, Lestini, Brian, additional, Heimbrook, David, additional, and Bollag, Gideon, additional

Published
2012
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33. RASMutations in Cutaneous Squamous-Cell Carcinomas in Patients Treated with BRAF Inhibitors

Author

Su, Fei, primary, Viros, Amaya, additional, Milagre, Carla, additional, Trunzer, Kerstin, additional, Bollag, Gideon, additional, Spleiss, Olivia, additional, Reis-Filho, Jorge S., additional, Kong, Xiangju, additional, Koya, Richard C., additional, Flaherty, Keith T., additional, Chapman, Paul B., additional, Kim, Min Jung, additional, Hayward, Robert, additional, Martin, Matthew, additional, Yang, Hong, additional, Wang, Qiongqing, additional, Hilton, Holly, additional, Hang, Julie S., additional, Noe, Johannes, additional, Lambros, Maryou, additional, Geyer, Felipe, additional, Dhomen, Nathalie, additional, Niculescu-Duvaz, Ion, additional, Zambon, Alfonso, additional, Niculescu-Duvaz, Dan, additional, Preece, Natasha, additional, Robert, Lídia, additional, Otte, Nicholas J., additional, Mok, Stephen, additional, Kee, Damien, additional, Ma, Yan, additional, Zhang, Chao, additional, Habets, Gaston, additional, Burton, Elizabeth A., additional, Wong, Bernice, additional, Nguyen, Hoa, additional, Kockx, Mark, additional, Andries, Luc, additional, Lestini, Brian, additional, Nolop, Keith B., additional, Lee, Richard J., additional, Joe, Andrew K., additional, Troy, James L., additional, Gonzalez, Rene, additional, Hutson, Thomas E., additional, Puzanov, Igor, additional, Chmielowski, Bartosz, additional, Springer, Caroline J., additional, McArthur, Grant A., additional, Sosman, Jeffrey A., additional, Lo, Roger S., additional, Ribas, Antoni, additional, and Marais, Richard, additional

Published
2012
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34. Prospective Molecular Marker Analyses of EGFR and KRAS From a Randomized, Placebo-Controlled Study of Erlotinib Maintenance Therapy in Advanced Non–Small-Cell Lung Cancer

Author

Brugger, Wolfram, primary, Triller, Nadja, additional, Blasinska-Morawiec, Maria, additional, Curescu, Stefan, additional, Sakalauskas, Raimundas, additional, Manikhas, Georgy Moiseevich, additional, Mazieres, Julien, additional, Whittom, Renaud, additional, Ward, Carol, additional, Mayne, Karen, additional, Trunzer, Kerstin, additional, and Cappuzzo, Federico, additional

Published
2011
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36. Resistance to Selective BRAF Inhibition Can Be Mediated by Modest Upstream Pathway Activation.

Author

Fei Su, Bradley, William D., Qiongqing Wang, Hong Yang, Lizhong Xu, Higgins, Brian, Kolinsky, Kenneth, Packman, Kathryn, Min Jung Kim, Trunzer, Kerstin, Lee, Richard J., Schostack, Kathleen, Carter, Jade, Albert, Thomas, Germer, Soren, Rosinski, Jim, Martin, Mitchell, Simcox, Mary Ellen, Lestini, Brian, and Heimbrook, David

Subjects
*MELANOMA, *PHOSPHORYLATION, *CHEMICAL reactions, *ONCOGENES, *CANCER genes
Abstract

A high percentage of patients with BRAFV600E mutant melanomas respond to the selective RAF inhibitor vemurafenib (RG7204, PLX4032) but resistance eventually emerges. To better understand the mechanisms of resistance, we used chronic selection to establish BRAFV600E melanoma clones with acquired resistance to vemurafenib. These clones retained the V600E mutation and no second-site mutations were identified in the BRAF coding sequence. Further characterization showed that vemurafenib was not able to inhibit extracellular signal-regulated kinase phosphorylation, suggesting pathway reactivation. Importantly, resistance also correlated with increased levels of RAS-GTP, and sequencing of RAS genes revealed a rare activating mutation in KRAS, resulting in a K117N change in the KRAS protein. Elevated levels of CRAF and phosphorylated AKT were also observed. In addition, combination treatment with vemurafenib and either a MAP/ERK kinase (MEK) inhibitor or an AKT inhibitor synergistically inhibited proliferation of resistant cells. These findings suggest that resistance to BRAFV600E inhibition could occur through several mechanisms, including elevated RAS-GTP levels and increased levels of AKT phosphorylation. Together, our data implicate reactivation of the RAS/RAF pathway by upstream signaling activation as a key mechanism of acquired resistance to vemurafenib, in support of clinical studies in which combination therapy with other targeted agents are being strategized to combat resistance. [ABSTRACT FROM AUTHOR]

Published
2012
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37. A randomized, double-blind study of zinpentraxin alfa in patients with myelofibrosis who were previously treated with or ineligible for ruxolitinib: stage 2 of a phase II trial.

Author

Verstovsek S, Talpaz M, Wadleigh M, Isidori A, Te Boekhorst P, Savona MR, Bose P, Pozdnyakova O, Mesa R, El-Galaly TC, O'Sullivan J, Gamel K, Higgins B, Katakam S, Todorov B, Trunzer K, and Harrison CN

Subjects
Aged, Female, Humans, Male, Middle Aged, Double-Blind Method, Treatment Outcome, Nitriles therapeutic use, Primary Myelofibrosis drug therapy, Pyrazoles therapeutic use, Pyrimidines therapeutic use
Published
2024
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