Related Experiment Video
Updated: Apr 27, 2026
12:58
Expression of Exogenous Cytokine in Patient-derived Xenografts via Injection with a Cytokine-transduced Stromal Cell Line
Published on: May 10, 2017
8.7K
Expression and pro-survival function of phospholipase Cγ2 in diffuse large B-cell lymphoma
Minh Q Huynh1, Jennifer Goßmann, Stefan Gattenlöehner
1Department of Hematology, Oncology and Immunology, University Hospital , Marburg , Germany.
Leukemia & Lymphoma
|July 12, 2014
Summary
Phospholipase Cγ2 (PLCγ2) is highly expressed in diffuse large B-cell lymphoma (DLBCL) and may be a therapeutic target. Inhibition of PLCγ2 shows promise for treating DLBCL patients resistant to standard therapies.
Area of Science:
- Hematology
- Oncology
- Molecular Biology
Background:
- Diffuse large B-cell lymphoma (DLBCL) has a cure rate of approximately 60% with current immuno-chemotherapy.
- A significant portion of DLBCL patients either do not achieve remission or experience relapse after initial treatment, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the role of Phospholipase Cγ2 (PLCγ2) in DLBCL pathogenesis.
- To evaluate the therapeutic potential of inhibiting PLCγ2 in DLBCL treatment.
Main Methods:
- Immunohistochemistry was used to assess PLCγ2 expression in DLBCL cases.
- The effects of the PLC inhibitor U73122 on DLBCL cell proliferation, apoptosis, and cell cycle were examined.
- Combination treatments with U73122 and other inhibitors (enzastaurin, pp2) were evaluated.
Main Results:
- PLCγ2 was found to be strongly expressed in 63% of DLBCL cases.
- U73122 demonstrated inhibitory effects on cell proliferation, induced apoptosis, and caused G0/G1 cell cycle arrest.
- Combined treatment with U73122 and enzastaurin or pp2 showed an additive effect on proliferation inhibition compared to U73122 alone.
- Strong PLCγ2 expression unexpectedly correlated with better overall survival.
Conclusions:
- PLCγ2 is frequently expressed in DLBCL and holds prognostic significance.
- Targeting PLCγ2 represents a potential new therapeutic strategy for treating DLBCL, particularly in cases with poor response to standard therapies.
Related Concept Videos
01:31The Intrinsic Apoptotic Pathway
6.2K
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...
6.2K
01:11IP3/DAG Signaling Pathway
12.4K
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
12.4K
01:22Amplifying Signals via Enzymatic Cascade
15.1K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
15.1K
02:23Abnormal Proliferation
4.0K
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...
4.0K
01:15Amplifying Signals via Second Messengers
6.1K
Many receptor binding ligands are hydrophilic; they do not cross the cell membrane but bind to cell-surface receptors. Thus, their message must be relayed by second messengers present in the cell cytoplasm. There are several second messenger pathways, each with its own way of relaying information. For example, the G protein-coupled receptors can activate both phosphoinositol and cyclic AMP (cAMP) second messenger pathways. The phosphoinositol pathway is active when the receptor induces...
6.1K
01:19Interactions Between Signaling Pathways
4.6K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
4.6K