Related Experiment Video
Updated: Mar 19, 2026
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
Toppling high-grade pulmonary neuroendocrine tumors with a DLL3-targeted trojan horse
1Stemcentrx Inc. , 450 East Jamie Court , South San Francisco, CA, USA.
Abstract:
Delta-like protein 3 (DLL3) is a novel and tractable tumor-initiating cell-associated target for the antibody-drug conjugate SC16LD6.5 in high-grade pulmonary neuroendocrine tumors. Elevated expression of DLL3, an inhibitor of Notch pathway activation, marks the second recent observation that impairment of Notch receptor signaling may play a critical role in neuroendocrine tumorigenesis.
Insights
Delta-like protein 3 (DLL3) is a promising target for treating high-grade pulmonary neuroendocrine tumors. Antibody-drug conjugates targeting DLL3 show potential for novel cancer therapies.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Delta-like protein 3 (DLL3) is increasingly recognized as a significant factor in neuroendocrine tumor progression.
- DLL3 acts as an inhibitor of the Notch signaling pathway, a crucial pathway in cell communication and differentiation.
- Aberrant Notch signaling has been implicated in the development of various neuroendocrine tumors.
Purpose of the Study:
- To evaluate DLL3 as a therapeutic target in high-grade pulmonary neuroendocrine tumors.
- To assess the efficacy of the antibody-drug conjugate SC16LD6.5 targeting DLL3.
- To investigate the role of DLL3 and Notch pathway inhibition in neuroendocrine tumorigenesis.
Main Methods:
- Utilized the antibody-drug conjugate SC16LD6.5 for targeted therapy.
- Focused on high-grade pulmonary neuroendocrine tumor models.
- Analyzed DLL3 expression levels and their correlation with tumor characteristics.
Main Results:
- DLL3 was identified as a novel and tractable target associated with tumor-initiating cells.
- SC16LD6.5 demonstrated potential as an antibody-drug conjugate for DLL3-targeted therapy.
- Elevated DLL3 expression was observed, suggesting impaired Notch pathway signaling in neuroendocrine tumors.
Conclusions:
- DLL3 represents a viable therapeutic target for high-grade pulmonary neuroendocrine tumors.
- Targeting DLL3 with antibody-drug conjugates offers a promising strategy for novel cancer treatments.
- The findings reinforce the critical role of Notch receptor signaling impairment in neuroendocrine tumorigenesis.
