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Related Concept Videos

Mutations01:39

Mutations

Overview
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...
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...
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
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...
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...

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Related Experiment Video

Updated: May 12, 2026

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells
11:06

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

Published on: February 24, 2014

Leukaemogenesis: more than mutant genes.

Jianjun Chen1, Olatoyosi Odenike, Janet D Rowley

  • 1Department of Medicine, University of Chicago, IL 60637, USA.

Nature Reviews. Cancer
|December 24, 2009
PubMed
Summary
This summary is machine-generated.

Acute leukaemias involve genetic mutations and epigenetic changes like DNA methylation and microRNAs. Targeting these epigenetic factors offers promising new therapeutic strategies for these challenging blood cancers.

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Area of Science:

  • Hematology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Acute leukaemias exhibit characteristic chromosomal aberrations and gene mutations.
  • Epigenetic modifications, including DNA methylation and histone modifications, significantly influence leukaemia cell phenotype.
  • MicroRNAs play a critical role in the pathogenesis of leukaemias through transcriptional regulation.

Purpose of the Study:

  • To explore the role of epigenetic modifications in acute leukaemias.
  • To highlight the pathogenetic significance of microRNAs in leukaemic development.
  • To discuss the therapeutic potential of targeting the epigenetic machinery.

Main Methods:

  • Review of current literature on leukaemia pathogenesis.
  • Analysis of the role of DNA methylation and histone modifications.
  • Investigation of microRNA involvement in gene regulation.

Main Results:

  • Epigenetic alterations are integral to acute leukaemia development.
  • MicroRNAs are key regulators of oncogenes and tumour suppressor genes in leukaemias.
  • Genetic heterogeneity presents therapeutic challenges.

Conclusions:

  • Epigenetic modifications are crucial in acute leukaemias.
  • Targeting epigenetic machinery with pharmacological agents shows therapeutic promise.
  • Further research into epigenetic targets is warranted for effective leukaemia treatment.