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Updated: Feb 14, 2026

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
Published on: May 1, 2015
Targeting HSF1: A Prime Integrator of Proteotoxic Stress Response in Myeloma
1Department of Hematology Oncology, Icahn School of Medicine at Mount Sinai, New York, New York. samir.parekh@mssm.edu.
Abstract:
The HSF1 transcription factor is an integrator of the cellular stress response, and its expression has demonstrated poor prognosis in multiple myeloma. The novel anti-HSF1 small-molecule inhibitors CCT251236 and KRIB11 demonstrate in vitro and in vivo antimyeloma activity, representing a novel approach for targeting the heat shock response in myeloma. Clin Cancer Res; 24(10); 2237-8. ©2018 AACRSee related article by Fok et al., p. 2395.
Insights
New small-molecule inhibitors targeting heat shock factor 1 (HSF1) show promise against multiple myeloma. These compounds demonstrate antimyeloma activity in vitro and in vivo, offering a novel therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cellular Stress Response
Background:
- Heat shock factor 1 (HSF1) is crucial for cellular stress response.
- Elevated HSF1 expression correlates with poor prognosis in multiple myeloma.
Purpose of the Study:
- To investigate the antimyeloma activity of novel small-molecule inhibitors targeting HSF1.
- To evaluate the therapeutic potential of targeting the heat shock response pathway in multiple myeloma.
Main Methods:
- Utilized novel small-molecule inhibitors, CCT251236 and KRIB11, designed to inhibit HSF1.
- Assessed the efficacy of these inhibitors through in vitro and in vivo studies in multiple myeloma models.
Main Results:
- The HSF1 inhibitors CCT251236 and KRIB11 exhibited significant antimyeloma activity.
- Demonstrated effectiveness in both laboratory (in vitro) and living organism (in vivo) settings.
Conclusions:
- Novel anti-HSF1 small-molecule inhibitors represent a promising new therapeutic approach for multiple myeloma.
- Targeting the heat shock response pathway via HSF1 inhibition offers a viable strategy for treating this hematologic malignancy.
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