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Centrosome Duplication

Centrosome Duplication

The primary microtubule organizing center (MTOC) in animal cells is the centrosome. A centrosome has two cylindrical centrioles at its core. Each centriole consists of nine sets of three microtubules held together by proteins. The centrioles are positioned at right angles to each other and surrounded by a shapeless protein cloud called the pericentriolar matrix, or pericentriolar material (PCM).
To ensure that each daughter cell receives a centrosome after cell division, centrosome duplication...

Centrosome Duplication

Centrosome Duplication

The primary microtubule organizing center (MTOC) in animal cells is the centrosome. A centrosome has two cylindrical centrioles at its core. Each centriole consists of nine sets of three microtubules held together by proteins. The centrioles are positioned at right angles to each other and surrounded by a shapeless protein cloud called the pericentriolar matrix, or pericentriolar material (PCM).
To ensure that each daughter cell receives a centrosome after cell division, centrosome duplication...

Centrioles and Centrosomes

Centrioles and Centrosomes

Most animal cells comprise a pair of centrioles together called a centrosome. The cell duplicates its centrosome and contains two centrosomes side-by-side, which begin to move apart during the prophase. As the centrosomes migrate to two different sides of the cell, microtubules start extending from each centrosome toward the other end. The mitotic spindle is composed of the centrosomes and their emerging microtubules.
Near the end of the prophase, also called late prophase or "prometaphase,"...

Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...

Cancer

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.

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Related Experiment Video

Updated: Jun 21, 2026

Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations

Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations

Published on: September 20, 2019

Cancer: CINful centrosomes.

Samuel F Bakhoum¹, Duane A Compton

¹Department of Biochemistry, Dartmouth Medical School, Hanover, NH 03755, USA.

Current Biology : CB

|August 14, 2009

Summary

Centrosome number regulation is often lost in tumors, leading to extra centrosomes and chromosomal instability. New research explains how these extra centrosomes drive chromosome mis-segregation in cancer cells.

Area of Science:

Cell Biology
Cancer Biology
Genetics

Background:

Centrosome number dysregulation is a hallmark of many cancers.
An increased number of centrosomes is linked to chromosomal instability and tumorigenesis.

Purpose of the Study:

To elucidate the mechanisms by which supernumerary centrosomes induce chromosome mis-segregation in tumor cells.
To understand the link between centrosome amplification and cancer progression.

Main Methods:

Utilized advanced microscopy techniques to observe centrosome behavior in cancer cells.
Employed genetic manipulation to alter centrosome numbers and assess chromosomal integrity.

Main Results:

Demonstrated that extra centrosomes lead to multipolar spindle formation.

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Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Published on: March 3, 2016

Related Experiment Videos

Last Updated: Jun 21, 2026

Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations

Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations

Published on: September 20, 2019

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Published on: March 3, 2016

Showed that multipolar spindles are the direct cause of chromosome mis-segregation in the studied tumor cells.

Conclusions:

The findings provide a mechanistic link between centrosome amplification and aneuploidy in cancer.
Understanding this process may offer new therapeutic targets for cancer treatment.