Related Experiment Video

Updated: Jan 2, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

581

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.

Hematological Oncology
|November 30, 2019
PubMed

Insights

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.
Keywords:
B lymphocytesCK1CK2GSK3lymphomaprotein kinase

More Related Videos

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation09:09

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation

Published on: November 10, 2017

8.7K
Kinase Inhibitor Screening In Self-assembled Human Protein Microarrays13:22

Kinase Inhibitor Screening In Self-assembled Human Protein Microarrays

Published on: October 23, 2019

8.2K

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.5K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.6K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.2K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.0K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.5K