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Your search keyword '"Davis, Cuc"' showing total 17 results
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17 results on '"Davis, Cuc"'

1. Correlation of immune fitness with response to teclistamab in relapsed/refractory multiple myeloma in the MajesTEC-1 study

Author

Cortes-Selva, Diana, Perova, Tatiana, Skerget, Sheri, Vishwamitra, Deeksha, Stein, Sarah, Boominathan, Rengasamy, Lau, Onsay, Calara-Nielsen, Karl, Davis, Cuc, Patel, Jaymala, Banerjee, Arnob, Stephenson, Tara, Uhlar, Clarissa, Kobos, Rachel, Goldberg, Jenna, Pei, Lixia, Trancucci, Danielle, Girgis, Suzette, Wang Lin, Shun Xin, Wu, Liviawati S., Moreau, Philippe, Usmani, Saad Z., Bahlis, Nizar J., van de Donk, Niels W. C. J., and Verona, Raluca I.

Published
2024
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3. Teclistamab, a B-Cell Maturation Antigen (BCMA) x CD3 Bispecific Antibody, in Patients with Relapsed/Refractory Multiple Myeloma (RRMM): Correlative Analyses from MajesTEC-1

Author

Cortes-Selva, Diana, Casneuf, Tineke, Vishwamitra, Deeksha, Stein, Sarah, Perova, Tatiana, Skerget, Sheri, Ramos, Elena, van Steenbergen, Laure, De Maeyer, Dries, Boominathan, Rengasamy, Lau, Onsay, Davis, Cuc, Banerjee, Arnob, Stephenson, Tara, Uhlar, Clarissa M., Kobos, Rachel, Goldberg, Jenna D., Pei, Lixia, Trancucci, Danielle, Girgis, Suzette, Wang Lin, Shun Xin, Wu, Liviawati S., Moreau, Philippe, Usmani, Saad, Bahlis, Nizar Jacques, Van De Donk, Niels WCJ, and Verona, Raluca

Published
2022
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5. Biomarker Correlates of Response to Ciltacabtagene Autoleucel in Patients with Relapsed or Refractory Multiple Myeloma from CARTITUDE-1, a Phase 1b/2 Open-Label Study, at the ~3 Year Follow-up

Author

Montes de Oca, Rocio, Gu, Junchen, Zhao, Hao, Zelinsky, Kathy, Wu, Dianna, Davis, Cuc, Patel, Jaymala, Foulk, Brad, Boominathan, Rengasamy, Lau, Onsay, Smirnov, Denis, Lin, Yi, Jagannath, Sundar, Cohen, Adam D., Haddish-Berhane, Nahor, Xu, Jean, Madduri, Deepu, Stevens, An-Sofie, Jackson, Carolyn Chang, Schecter, Jordan M., Banerjee, Arnob, Geng, Dong, Zhu, Jieqing, Xu, Sifan, and Zudaire, Enrique

Published
2023
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7. Longitudinal Correlative Profiles of Responders, Nonresponders, and Those with Relapse on Treatment with Teclistamab in the Phase 1/2 MajesTEC-1 Study of Patients with Relapsed/Refractory Multiple Myeloma

Author

Vishwamitra, Deeksha, Skerget, Sheri, Cortes, Diana, Perova, Tatiana, Lau, Onsay, Davis, Cuc, Guo, Yue, Miao, Xin, Stephenson, Tara, Hodin, Caroline, Uhlar, Clarissa, Trancucci, Danielle, Chastain, Katherine, Bahlis, Nizar J, Van De Donk, Niels W.C.J., and Verona, Raluca

Published
2023
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13. Identification of potential ibrutinib combinations in hematological malignancies using a combination high-throughput screen.

Author

Schaffer, Michael, Chaturvedi, Shalini, Davis, Cuc, Aquino, Regina, Stepanchick, Emily, Balasubramanian, Sriram, Versele, Matthias, Liu, Yang, Yang, Jennifer, and Lu, Rongzhen

Subjects
BCL-2 proteins, DIFFUSE large B-cell lymphomas, MEDICAL screening, COMBINATION drug therapy, PROTEIN-tyrosine kinases
Abstract

Matrix high-throughput screening (HTS) methods are increasingly employed to rapidly define potential therapeutic drug combinations. We used combination HTS to identify compounds showing synergistic anti-proliferative activity with ibrutinib, an irreversible, small-molecule inhibitor of Bruton’s tyrosine kinase. The goal was to identify ibrutinib combinations with maximum synergistic effects in heme malignancy lines, particularly in non-Hodgkin lymphoma including diffuse large B-cell lymphoma (DLBCL). Growth inhibition (GI) was used to measure cell viability; synergy scores characterized strength of synergistic interaction. Single-agent ibrutinib demonstrated varying degrees of activity across 30 cell lines evaluated. In DLBCL lines, TMD8 was the most sensitive to ibrutinib (GI50 = 0.001); combinations with BCL-2 inhibitor ABT-199, and PI3K inhibitors IPI-145 and GDC-0941 showed the strongest synergistic activity. Anti-proliferative synergies were also observed with BET bromodomain inhibitor (+)-JQ1, XPO1 inhibitor selinexor, and IRAK4 inhibitor, and confirmed using apoptosis assay. These findings are intended to inform and advance treatment of B-cell malignancies. [ABSTRACT FROM AUTHOR]

Published
2018
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17. Novel sorafenib-based structural analogues: in-vitro anticancer evaluation of t-MTUCB and t-AUCMB.

Author

Wecksler AT, Hwang SH, Wettersten HI, Gilda JE, Patton A, Leon LJ, Carraway KL 3rd, Gomes AV, Baar K, Weiss RH, and Hammock BD

Subjects
Adamantane pharmacology, Apoptosis drug effects, Apoptosis Inducing Factor metabolism, Autophagy drug effects, Caspases metabolism, Cell Cycle drug effects, Cell Line, Tumor, Drug Screening Assays, Antitumor, Humans, Mitochondrial Membranes physiology, Niacinamide pharmacology, Oxidative Stress, Proteasome Endopeptidase Complex metabolism, Sorafenib, Urea pharmacology, Adamantane analogs & derivatives, Antineoplastic Agents pharmacology, Benzamides pharmacology, Niacinamide analogs & derivatives, Phenylurea Compounds pharmacology, Protein Kinase Inhibitors pharmacology, Urea analogs & derivatives
Abstract

In the current work, we carried out a mechanistic study on the cytotoxicity of two compounds, trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-N-methyl-benzamide (t-AUCMB) and trans-N-methyl-4-{4-[3-(4-trifluoromethoxy-phenyl)-ureido]-cyclohexyloxy}-benzamide (t-MTUCB), that are structurally similar to sorafenib. These compounds show strong cytotoxic responses in various cancer cell lines, despite significant differences in the induction of apoptotic events such as caspase activation and lactate dehydrogenase release in hepatoma cells. Both compounds induce autophagosome formation and LC3I cleavage, but there was little observable effect on mTORC1 or the downstream targets, S6K1 and 4E-binding protein. In addition, there was an increase in the activity of upstream signaling through the IRS1/PI3K/Akt-signaling pathway, suggesting that, unlike sorafenib, both compounds induce mammalian target of rapamycin (mTOR)-independent autophagy. The autophagy observed correlates with mitochondrial membrane depolarization, apoptosis-inducing factor release, and oxidative stress-induced glutathione depletion. However, there were no observable changes in the endoplasmic reticulum-stress markers such as binding immunoglobulin protein, inositol-requiring enzyme-α, phosphorylated eukaryotic initiation factor 2, and the lipid peroxidation marker, 4-hydroxynonenal, suggesting endoplasmic reticulum-independent oxidative stress. Finally, these compounds do not have the multikinase inhibitory activity of sorafenib, which may be reflected in their difference in the ability to halt cell cycle progression compared with sorafenib. Our findings indicate that both compounds have anticancer effects comparable with sorafenib in multiple cell lines, but they induce significant differences in apoptotic responses and appear to induce mTOR-independent autophagy. t-AUCMB and t-MTUCB represent novel chemical probes that are capable of inducing mTOR-independent autophagy and apoptosis to differing degrees, and may thus be potential tools for further understanding the link between these two cellular stress responses.

Published
2014
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