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Updated: May 24, 2026

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
Published on: May 3, 2018
Cyclin dependent kinases in cancer: potential for therapeutic intervention
Miriam Canavese1, Loredana Santo, Noopur Raje
1MGH Cancer Center, Boston, MA, USA.
Abstract:
Cell cycle progression through each phase is regulated by heterodimers formed by cyclin-dependent kinases (CDKs) and their regulatory partner proteins, the cyclins. Together they coordinate the cellular events through cell cycle. De-regulation of cell-cycle control due to aberrant CDK activity is a common feature of most cancer types. Intensive research on small molecules that target cell cycle regulatory proteins has led to the identification of many candidate inhibitors that are able to arrest proliferation and induce apoptosis in neoplastic cells as a promising strategy to treat cancer. Interestingly, cyclin-dependent kinases (CDKs) have also been proposed as therapeutic targets for Multiple Myeloma (MM). Overexpression and aberrant expression of the cyclins, specifically the D cyclins is seen in the majority of MM underscoring the value of exploring CDK inhibition in MM which currently remains an incurable neoplastic plasma-cell disorder. It is characterized by clonal proliferation of malignant plasma cells in the bone marrow microenviroment and associated organ dysfunction. Recent preclinical and early clinical data explore several CDK inhibitors in the context of MM. This review will provide an overview of the main classes of CDK inhibitors with a focus on their mechanism of action and discuss clinical and pharmacological implications of CDK inhibitors as possible therapeutic approaches for the treatment of cancer with specific consideration to MM.
Insights
Cyclin-dependent kinases (CDKs) regulate cell cycle progression and are implicated in cancer. CDK inhibitors show promise for treating cancers, including Multiple Myeloma (MM), by halting cancer cell proliferation.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Cell cycle progression is tightly regulated by cyclin-dependent kinases (CDKs) and cyclins.
- Dysregulation of cell-cycle control and aberrant CDK activity are hallmarks of many cancers.
- Multiple Myeloma (MM), a plasma-cell malignancy, exhibits cyclin overexpression, suggesting CDK inhibition as a therapeutic strategy.
Purpose of the Study:
- To review the main classes of CDK inhibitors.
- To focus on their mechanisms of action.
- To discuss the clinical and pharmacological implications of CDK inhibitors for cancer treatment, with a specific focus on MM.
Main Methods:
- Literature review of CDK inhibitors.
- Analysis of preclinical and early clinical data for CDK inhibitors in MM.
- Examination of mechanisms of action and therapeutic potential.
Main Results:
- CDK inhibitors are a promising strategy for cancer treatment, inducing proliferation arrest and apoptosis.
- Specific D cyclins are overexpressed in MM, validating CDK inhibition as a target.
- Several CDK inhibitors are under investigation in preclinical and early clinical studies for MM.
Conclusions:
- CDK inhibitors represent a potential therapeutic approach for various cancers, including the currently incurable Multiple Myeloma.
- Understanding the mechanisms and clinical implications of CDK inhibitors is crucial for advancing cancer therapy.
- Targeting cell-cycle regulatory proteins offers a promising avenue for neoplastic disease treatment.
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