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Related Concept Videos

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...
Abnormal Proliferation02:23

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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...

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Activating ROCK1 somatic mutations in human cancer.

P A Lochhead1, G Wickman, M Mezna

  • 1The Beatson Institute for Cancer Research, Glasgow, Scotland G61 1BD, UK.

Oncogene
|February 9, 2010
PubMed
Summary
This summary is machine-generated.

Somatic mutations in the ROCK1 gene increase its kinase activity, promoting cancer cell migration and decreased adhesion. These ROCK1 mutations are driver mutations, suggesting selective pressure for their acquisition in cancer progression.

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Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells
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Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cancer cells exhibit deregulated growth, survival, and metastasis.
  • Distinguishing driver mutations from passenger mutations is crucial for understanding cancer progression.
  • ROCK1 is a key effector kinase in the Rho GTPase pathway, regulating cell migration.

Purpose of the Study:

  • To investigate the functional consequences of identified somatic mutations in the ROCK1 gene.
  • To determine if these ROCK1 mutations act as driver mutations in cancer.
  • To elucidate the mechanism by which ROCK1 mutations affect its kinase activity and cellular functions.

Main Methods:

  • Analysis of somatic mutations in the ROCK1 gene identified by the Cancer Genome Project.
  • Biochemical assays to measure ROCK1 kinase activity.
  • Cell-based assays to assess actin cytoskeleton rearrangements, cell motility, and adhesion.
  • Structural modeling and mapping of kinase-interacting regions.

Main Results:

  • Three nonsynonymous somatic mutations in ROCK1 were identified.
  • These ROCK1 mutations result in elevated kinase activity.
  • Mutated ROCK1 drives actin cytoskeleton rearrangements, leading to increased cell motility and decreased cell adhesion.
  • Structural analysis provides insights into the regulatory impact of these mutations.

Conclusions:

  • Somatic ROCK1 mutations identified are driver mutations that enhance kinase activity.
  • These mutations contribute to cancer progression by promoting cell motility and reducing adhesion.
  • There is selective pressure for the acquisition of activating ROCK1 mutations in human cancers.