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Inhibition of Cdk Activity

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...

Positive Regulator Molecules

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M-Cdk Drives Transition Into Mitosis

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

The Retinoblastoma Gene

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Assessing Specificity of Anticancer Drugs In Vitro

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Cyclin D1 in pediatric neuroblastic tumors: A microarray analysis.

Paolo Fagone¹, Ferdinando Nicoletti¹, Giada Maria Vecchio²

¹Department of Biomedical Sciences, School of Medicine, University of Catania, Catania, Italy.

Acta Histochemica

|October 30, 2015

Summary

Neuroblastoma, a common childhood cancer, shows higher cyclin D1 (CCDN1) levels than related tumors. Cyclin D2 may also play a role in neuroblastoma development.

Keywords:

Bioinformatic analysis Cyclin D1 Microarray Neuroblastic tumors Neuroblastoma

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Area of Science:

Pediatric Oncology
Molecular Biology
Developmental Neuroscience

Background:

Neuroblastoma is the most common extracranial solid tumor in children, originating from primitive neuroblasts.
Cyclin D1 (CCDN1) expression in pediatric neuroblastic tumors mirrors its role in peripheral sympathetic nervous system (PSNS) development.

Purpose of the Study:

To compare cyclin D1 expression in neuroblastoma versus ganglioneuroma and ganglioneuroblastoma.
To identify other potential molecular markers or etiological factors in neuroblastoma development.

Main Methods:

Microarray analysis to evaluate gene expression.
Bioinformatic analysis of genes functionally related to cyclin D1.

Main Results:

Confirmed comparable cyclin D1 levels in neuroblastoma and fetal neuroblasts.
Observed significantly higher cyclin D1 levels in neuroblastoma compared to ganglioneuroma and ganglioneuroblastoma.
Identified cyclin D2 as a potential marker and etiological factor in neuroblastoma.

Conclusions:

Neuroblastoma exhibits elevated cyclin D1 expression relative to less malignant counterparts.
Cyclin D2 emerges as a significant factor in neuroblastoma pathogenesis, warranting further investigation.