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Updated: Jan 2, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
Published on: June 6, 2025
New responsibilities for aged kinases in B-lymphomas.
Francesco Piazza1,2, Sabrina Manni1,2, Arash Arjomand1,2
1Department of Medicine, Hematology and Clinical Immunology Branch, University of Padova, Padova, Italy.
Novel therapies targeting specific kinases like CK1, CK2, and GSK3 show promise for treating B-cell non-Hodgkin lymphoma (B-NHL). These kinases are crucial for malignant lymphocyte survival and signaling, offering new therapeutic avenues.
Area of Science:
- Hematology
- Oncology
- Molecular Biology
Background:
- Recent advances in understanding B-cell non-Hodgkin lymphoma (B-NHL) pathogenesis have revealed key molecular abnormalities.
- Therapies targeting B-cell receptor signaling (BTK, PI3K, SYK inhibitors) and apoptosis (BH3-mimetics) are now available.
- Malignant B-cell growth is sustained by oncogene mutations and addiction to non-oncogene molecules.
Purpose of the Study:
- To review the role of Ser/Thr kinases CK1, CK2, and GSK3 in B-NHL.
- To summarize evidence supporting these kinases as therapeutic targets in B-NHL.
- To propose future research directions for kinase-directed therapies.
Main Methods:
- Review of accumulated knowledge on B-NHL pathogenesis over the last decade.
- Examination of the main features of CK1, CK2, and GSK3 kinases.
- Summary of data supporting CK1, CK2, and GSK3 as therapeutic targets in B-NHL.
Main Results:
- CK1, CK2, and GSK3 kinases are involved in malignant lymphocyte biology.
- These kinases act as pro-survival and signaling-boosting molecules in B-cell tumors.
- Significant experimental and clinical groundwork exists for developing therapies targeting these kinases.
Conclusions:
- CK1, CK2, and GSK3 are suitable therapeutic targets for B-NHL.
- Targeting these kinases offers new perspectives for novel anti-lymphoma/leukemia therapies.
- Further research can advance the development of CK1-, CK2-, and GSK3-directed treatments.
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