Abstract 1380: Role of cytokine-induced cell death on efficacy of teclistamab-mediated T cell killing of multiple myeloma cells

Abstract Multiple myeloma (MM) is the second most common hematologic malignancy among US adults, characterized by high rates of relapse and refractory disease. Anti-Myeloma T cell immunotherapies, such as chimeric antigen receptors (CAR-Ts) and bispecific T cell engagers (BiTEs), have been able to induce deep responses in the clinic and extending survival for many. However, even these responses are not durable and majority of patients still relapse. MM cell signaling in response to cytokines released by these T cells, such as Tumor Necrosis Factor (TNF) Alpha, and Interferon gamma (IFNγ), may offer additional insight into mechanisms of relapse and resistance as well as avenues of therapeutic manipulation. To evaluate the effects of TNF and IFNγ on MM cell death and proliferation, we obtained human MM cell lines (MMCLs) and stably transduced them with a GFP-NLS reporter. We then monitored these cell lines in the presence of TNF, IFNγ, or TNF+IFNγ and tracked their cell death and growth kinetics over time using DiYO-3 incorporation and GFP count, respectively, via IncuCyteS3 live cell imaging. We next utilized Teclistamab, a B cell maturation antigen (BCMA)-directed BiTE, to co-culture MMCLs with healthy donor derived T cells at various effector to target (E:T) ratios and monitored for T cell mediated death again via IncuCyteS3 live cell imaging. While all MMCLs were able to be killed at high E:T ratios (1:1), only cytokine-sensitive lines remained susceptible to T cell killing at lower E:T ratios (1:10). The addition of TNF and/or IFNγ blocking antibodies confirmed that the increased sensitivity of these lines to T cell killing was indeed mediated by the two cytokines. In summary, were able to show an in vitro model of differential MM cell response to Teclistamab mediated T cell killing, and that this difference in response was predicated on the MM cells’ baseline sensitivity to cytokine mediated cell death via TNF and IFNγ. Thus, further dissecting mechanisms underlying resistance or sensitivity of MM cells to cytokine induced death could suggest therapeutic targets with the potential to enhance the efficacy of anti-MM T cell immunotherapies. Citation Format: Allison Carr, Adrian Ting. Role of cytokine-induced cell death on efficacy of teclistamab-mediated T cell killing of multiple myeloma cells. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 1380.

Authors

Institutions

Publication Details

Journal
Cancer Research
Published
2025-04-21
DOI
https://doi.org/10.1158/1538-7445.am2025-1380
Primary Topic
Multiple Myeloma Research and Treatments
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Abstract 1380: Role of cytokine-induced cell death on efficacy of teclistamab-mediated T cell killing of multiple myeloma cells

Adrian T. Ting, Allison Carr
Cancer Research
Multiple Myeloma Research and Treatments
article

Abstract 1380: Role of cytokine-induced cell death on efficacy of teclistamab-mediated T cell killing of multiple myeloma cells

Adrian T. Ting, Allison Carr
article en

Abstract

Abstract Multiple myeloma (MM) is the second most common hematologic malignancy among US adults, characterized by high rates of relapse and refractory disease. Anti-Myeloma T cell immunotherapies, such as chimeric antigen receptors (CAR-Ts) and bispecific T cell engagers (BiTEs), have been able to induce deep responses in the clinic and extending survival for many. However, even these responses are not durable and majority of patients still relapse. MM cell signaling in response to cytokines released by these T cells, such as Tumor Necrosis Factor (TNF) Alpha, and Interferon gamma (IFNγ), may offer additional insight into mechanisms of relapse and resistance as well as avenues of therapeutic manipulation. To evaluate the effects of TNF and IFNγ on MM cell death and proliferation, we obtained human MM cell lines (MMCLs) and stably transduced them with a GFP-NLS reporter. We then monitored these cell lines in the presence of TNF, IFNγ, or TNF+IFNγ and tracked their cell death and growth kinetics over time using DiYO-3 incorporation and GFP count, respectively, via IncuCyteS3 live cell imaging. We next utilized Teclistamab, a B cell maturation antigen (BCMA)-directed BiTE, to co-culture MMCLs with healthy donor derived T cells at various effector to target (E:T) ratios and monitored for T cell mediated death again via IncuCyteS3 live cell imaging. While all MMCLs were able to be killed at high E:T ratios (1:1), only cytokine-sensitive lines remained susceptible to T cell killing at lower E:T ratios (1:10). The addition of TNF and/or IFNγ blocking antibodies confirmed that the increased sensitivity of these lines to T cell killing was indeed mediated by the two cytokines. In summary, were able to show an in vitro model of differential MM cell response to Teclistamab mediated T cell killing, and that this difference in response was predicated on the MM cells’ baseline sensitivity to cytokine mediated cell death via TNF and IFNγ. Thus, further dissecting mechanisms underlying resistance or sensitivity of MM cells to cytokine induced death could suggest therapeutic targets with the potential to enhance the efficacy of anti-MM T cell immunotherapies. Citation Format: Allison Carr, Adrian Ting. Role of cytokine-induced cell death on efficacy of teclistamab-mediated T cell killing of multiple myeloma cells. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 1380.

Cancer ResearchVol. 85(8_Supplement_1)
Mayo Clinic in Arizona (US)
Openalex Percentile: Top 90%
Multiple Myeloma Research and Treatments
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.