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Related Concept Videos

Positive Regulator Molecules02:39

Positive Regulator Molecules

5.4K
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.
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M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

5.5K
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...
5.5K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.7K
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...
4.7K
Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
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...
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Separation of Sister Chromatids02:17

Separation of Sister Chromatids

3.6K
At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
3.6K
Negative Regulator Molecules01:23

Negative Regulator Molecules

35.2K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
35.2K

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Related Experiment Video

Updated: Jun 6, 2025

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

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Cyclin D1-negative mantle cell lymphoma.

Chi Young Ok1, L Jeffrey Medeiros1

  • 1Department of Hematopathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.

Human Pathology
|November 21, 2024
PubMed
Summary

Cyclin D1-negative mantle cell lymphoma (MCL) often involves CCND2 or CCND3 translocations, not cyclin D1. This review clarifies diagnostic challenges and proposes specific terminology for rearranged MCL subtypes.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Pathology

Background:

  • Cyclin D1-negative mantle cell lymphoma (MCL) presents diagnostic challenges due to indistinguishable morphology and immunophenotype from typical MCL.
  • Lack of specific diagnostic tools has historically led to confusion regarding this B-cell neoplasm.
  • First identified by gene expression profiling in 2003, cyclin D1-negative MCL lacks cyclin D1 overexpression and the characteristic t(11;14) translocation.

Purpose of the Study:

  • To provide a chronological review of cyclin D1-negative MCL, enhancing understanding of its evolution.
  • To discuss current diagnostic approaches for identifying and classifying these lymphomas.
  • To propose refined terminology for improved diagnostic accuracy.

Main Methods:

  • Review of existing literature and diagnostic criteria for cyclin D1-negative MCL.

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  • Analysis of genetic alterations, particularly CCND2 and CCND3 translocations.
  • Discussion of immunohistochemistry and molecular diagnostic techniques.
  • Main Results:

    • Most cyclin D1-negative MCL cases exhibit translocations involving CCND2 or CCND3 with diverse gene partners.
    • Morphologic and immunophenotypic features are often similar to typical MCL, complicating diagnosis.
    • Gene expression profiling initially identified this distinct entity.

    Conclusions:

    • Refined terminology, such as CCND2-rearranged MCL or CCND3-rearranged MCL, is recommended when the specific translocation is known.
    • The term cyclin D1-negative MCL should be reserved for cases where the rearranged gene remains unidentified.
    • Further development of diagnostic tools is crucial for accurate identification and management.