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Related Concept Videos

Nondisjunction01:21

Nondisjunction

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold sister...
Nondisjunction01:29

Nondisjunction

During meiosis, chromosomes occasionally separate improperly. This occurs due to failure of homologous chromosome separation during meiosis I or failed sister chromatid separation during meiosis II. In some species, notably plants, nondisjunction can result in an organism with an entire additional set of chromosomes, which is called polyploidy. In humans, nondisjunction can occur during male or female gametogenesis and the resulting gametes possess one too many or one too few chromosomes.
Nondisjunction01:29

Nondisjunction

During meiosis, chromosomes occasionally separate improperly. This occurs due to failure of homologous chromosome separation during meiosis I or failed sister chromatid separation during meiosis II. In some species, notably plants, nondisjunction can result in an organism with an entire additional set of chromosomes, which is called polyploidy. In humans, nondisjunction can occur during male or female gametogenesis and the resulting gametes possess one too many or one too few chromosomes.
Cancers Originate from Somatic Mutations in a Single Cell02:21

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 Cell02:21

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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
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Aneuploidy and cancer.

Ya-Hui Chi1, Kuan-Teh Jeang

  • 1Molecular Virology Section, Laboratory of Molecular Microbiology, The National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0460, USA.

Journal of Cellular Biochemistry
|July 31, 2007
PubMed
Summary

Aneuploidy, or abnormal chromosome number, can arise from defects in the spindle assembly checkpoint (SAC), centrosome cycle, and cytokinesis. This review explores how these cellular mechanisms link to aneuploidy and human cancers.

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Area of Science:

  • Cell Biology
  • Genetics
  • Cancer Research

Background:

  • Cellular euploidy is crucial for normal function and is maintained by mechanisms like the spindle assembly checkpoint (SAC), centrosome cycle, and cytokinesis.
  • Dysregulation of these processes, particularly SAC function, centrosome cycle, and cytokinesis, is implicated in the development of aneuploidy in mammalian cells.
  • Aneuploidy is a common feature of human cancers, with altered expression of SAC genes frequently observed.

Purpose of the Study:

  • To review the mechanisms contributing to cellular aneuploidy.
  • To provide a perspective on the relationship between aneuploidy and human cancers.
  • To highlight the role of the spindle assembly checkpoint (SAC) in maintaining genomic stability.

Main Methods:

  • Literature review of studies on cellular aneuploidy mechanisms.
  • Analysis of experimental mouse models linking SAC function to tumorigenesis.
  • Examination of gene expression alterations in SAC genes in human cancers.

Main Results:

  • Defects in SAC, centrosome cycle, and cytokinesis can lead to aneuploidy.
  • Weakened SAC function is linked to in vivo tumorigenesis in experimental models.
  • Human cancers frequently exhibit aneuploidy and altered SAC gene expression.

Conclusions:

  • Aneuploidy arises from multiple cellular mechanisms, including SAC, centrosome cycle, and cytokinesis.
  • The SAC plays a critical role in preventing aneuploidy and may act as a tumor suppressor.
  • Understanding the link between aneuploidy and cancer is vital for developing new therapeutic strategies.