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Related Concept Videos

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...
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...
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 daughter...

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Related Experiment Video

Updated: May 20, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

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Published on: May 15, 2019

Inhibition of Rac controls NPM-ALK-dependent lymphoma development and dissemination.

A Colomba, S Giuriato, E Dejean

    Blood Cancer Journal
    |July 26, 2012
    PubMed
    Summary
    This summary is machine-generated.

    Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) drives lymphoma by activating Rac1 GTPase. Inhibiting Rac signaling halts cancer progression and metastasis, offering new therapeutic targets for lymphomas.

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    Published on: February 11, 2015

    Area of Science:

    • Oncology
    • Molecular Biology
    • Biochemistry

    Background:

    • Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is a key oncogene in ALK-positive lymphomas.
    • NPM-ALK activates Rac1 GTPase, promoting invadopodia formation and invasiveness in anaplastic large-cell lymphoma (ALCL).

    Purpose of the Study:

    • To investigate the therapeutic potential of inhibiting Rac signaling in ALCL.
    • To validate Rac GTPase as a molecular target in NPM-ALK-driven lymphomas.

    Main Methods:

    • Utilized the Rac inhibitor NSC23766 in vitro and in vivo.
    • Employed xenograft and conditional NPM-ALK transgenic mouse models.
    • Analyzed downstream effectors including Erk1/2, p38, and Akt.

    Main Results:

    • Rac inhibition abrogated NPM-ALK-induced transformation.
    • NSC23766 treatment suppressed disease progression and metastasis in mouse models.
    • Rac signaling regulates key effectors of NPM-ALK transformation.

    Conclusions:

    • Rac GTPase is a critical mediator of NPM-ALK oncogenic activity.
    • Targeting Rac signaling presents a promising therapeutic strategy for ALK-positive lymphomas.
    • Small GTPases and their regulators are viable targets for lymphoma treatment.