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Updated: Jan 23, 2026

Establishing In Vitro Models of Dorsal Root Ganglia Culture: Complementary Approaches for Investigating Cancer-Nerve Crosstalk
Published on: July 11, 2025
Tracing the roots of cancer evolution
Yanwen Jiang1, Olivier Elemento2
1Institute for Computational Biomedicine, Weill Cornell Medical College, New York, New York. Department of Medicine, Weill Cornell Medical College, New York, New York.
Chronic lymphocytic leukemia (CLL) originates from preleukemic progenitor cells, with early mutations identified. B-cell receptor signaling deregulation is a key hallmark, especially with EGR2 mutations.
Area of Science:
- Hematology
- Oncology
- Genomics
Background:
- Chronic lymphocytic leukemia (CLL) is a heterogeneous B-cell malignancy.
- Understanding the cellular origin and early genetic events in CLL is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the cellular origin of CLL by comparing progenitor and mature cells.
- To identify early genetic mutations associated with CLL development.
- To explore the role of B-cell receptor signaling in CLL pathogenesis.
Main Methods:
- Genomic comparison of progenitor (CD34+) and mature cells from lymphoid and myeloid lineages in CLL patients.
- Analysis of early CLL mutations.
- Investigation of B-cell receptor signaling pathways.
Main Results:
- Confirmed that CLL originates from preleukemic CD34+ progenitor cells.
- Identified specific early CLL mutations linked to these progenitor cells.
- Found that deregulation of B-cell receptor signaling is a hallmark of CLL, particularly in cases with EGR2 mutations.
Conclusions:
- CLL arises from early genetic alterations in CD34+ progenitor cells.
- B-cell receptor signaling dysregulation is a critical feature in CLL pathogenesis.
- EGR2 mutations are associated with B-cell receptor signaling deregulation in CLL.
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