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Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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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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Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

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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...
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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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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Abnormal Proliferation02:23

Abnormal Proliferation

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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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Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
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Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
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Related Experiment Video

Updated: Jun 18, 2025

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
09:16

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

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Oncogenic Enhancers in Leukemia.

Roger Mulet-Lazaro1,2, Ruud Delwel1,2

  • 1Department of Hematology, Erasmus MC Cancer Institute, Rotterdam, the Netherlands.

Blood Cancer Discovery
|August 2, 2024
PubMed
Summary
This summary is machine-generated.

Enhancer dysfunction is a critical driver of leukemia development, complementing traditional gene mutation studies. Understanding these regulatory element alterations is key for developing new targeted therapies for leukemia.

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Area of Science:

  • Oncology
  • Genetics
  • Epigenetics

Background:

  • Leukemogenesis research traditionally focused on protein-coding genes.
  • Emerging evidence highlights the significant role of enhancer dysregulation in cancer development.

Purpose of the Study:

  • To review mechanisms of oncogenic enhancer formation in leukemia.
  • To discuss therapeutic strategies targeting enhancer elements in leukemia.

Main Methods:

  • Review of current literature on leukemogenesis and enhancer biology.
  • Analysis of genetic and epigenetic alterations affecting enhancers.

Main Results:

  • Genetic aberrations like translocations, point mutations, and copy number alterations can create oncogenic enhancers.
  • These dysregulated enhancers drive leukemic transformation by altering gene expression.

Conclusions:

  • Enhancer dysfunction is a crucial, previously underappreciated factor in leukemia.
  • Targeting these regulatory elements offers promising avenues for precision medicine in leukemia treatment.