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Inhibition of Cdk Activity

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Related Experiment Video

Updated: Dec 12, 2025

Bioprinting of Hydrogel Tumor Slices as a 3D Model for Mantle Cell Lymphoma

Bioprinting of Hydrogel Tumor Slices as a 3D Model for Mantle Cell Lymphoma

Published on: September 12, 2025

Targeting CDK4/6 in mantle cell lymphoma.

Christina Lee^1,2, Xiangao Huang¹, Maurizio Di Liberto¹

¹Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA.

Annals of Lymphoma

|August 13, 2020

Summary

Selective CDK4/6 inhibitors, like palbociclib, show promise for mantle cell lymphoma (MCL) therapy by targeting cell cycle dysregulation. Understanding their genomic basis and resistance mechanisms can advance personalized MCL treatment.

Keywords:

CDK4 inhibitor CDK6 inhibitor Mantle cell lymphoma ibrutinib palbociclib

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Last Updated: Dec 12, 2025

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Published on: September 12, 2025

Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma

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Murine Model of CD40-activation of B cells

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Published on: March 5, 2010

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Mantle cell lymphoma (MCL) cells exhibit aberrant cyclin D1 expression and CDK4 dysregulation, driving cell cycle progression.
Historically, cell cycle-targeted cancer therapies lacked selectivity and efficacy.
The development of selective oral CDK4/6 inhibitors has transformed this therapeutic landscape.

Purpose of the Study:

To review the anti-tumor activities and clinical data of selective CDK4/6 inhibitors in MCL.
To summarize the mechanism of action of palbociclib, a specific CDK4/6 inhibitor.
To explore strategies for enhancing clinical responses to palbociclib in combination therapy for MCL.

Main Methods:

Review of existing clinical data and anti-tumor activities of CDK4/6 inhibitors in MCL.
Summary of palbociclib's mechanism of action and specificity.
Discussion of integrative longitudinal functional genomics for biomarker discovery.

Main Results:

Selective CDK4/6 inhibitors demonstrate anti-tumor activity in MCL.
Palbociclib's specificity offers a strategy to improve clinical responses when combined with partner drugs.
Functional genomics can identify biomarkers and immune interactions influencing treatment response.

Conclusions:

Targeting CDK4/6 is a rational approach for MCL therapy.
Understanding the genomic basis and resistance mechanisms of CDK4/6 inhibition is crucial for personalized MCL treatment.
This research may offer insights into drug resistance in other cancer types.