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Positive Regulator Molecules

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

Positive Regulator Molecules

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

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...

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...

Abnormal Proliferation

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...

Anaphase Promoting Complex

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...

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Related Experiment Video

Updated: May 14, 2026

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

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

Published on: March 30, 2018

Cyclin D1-negative mantle cell lymphoma.

¹Aichi Cancer Center Research Institute, Japan.

|February 23, 2013

Summary

This summary is machine-generated.

Mantle cell lymphoma (MCL) lacking Cyclin D1 (CCND1) often shows CCND2 gene rearrangement, particularly with immunoglobulin light chain genes, according to Salaverria et al.

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Last Updated: May 14, 2026

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

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

Published on: March 30, 2018

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

Area of Science:

Hematology
Oncology
Molecular Biology

Background:

Mantle cell lymphoma (MCL) is a B-cell non-Hodgkin lymphoma.
Cyclin D1 (CCND1) expression is a hallmark of classical MCL.
Alternative genetic mechanisms are implicated in CCND1-negative MCL variants.

Purpose of the Study:

To investigate the genetic landscape of CCND1-negative, SOX11-positive MCL.
To identify alternative genetic drivers in this MCL subtype.

Main Methods:

Analysis of gene rearrangements in MCL patient samples.
Focus on CCND1-negative and SOX11-positive cases.
Detection of CCND2 rearrangements and their association with immunoglobulin genes.

Main Results:

Over half of CCND1-negative, SOX11-positive MCL cases exhibited CCND2 gene rearrangement.
CCND2 rearrangement was predominantly observed in conjunction with immunoglobulin (IG) light chain genes.
This suggests an alternative pathway for MCL pathogenesis in a subset of patients.

Conclusions:

CCND2 gene rearrangement is a frequent finding in CCND1-negative, SOX11-positive MCL.
This rearrangement may play a significant role in the pathogenesis of these MCL cases.
Findings highlight the genetic heterogeneity within MCL and potential therapeutic targets.