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Related Concept Videos

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...
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...
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...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...

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Related Experiment Video

Updated: Jul 2, 2026

Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

c-Myc, Genomic Instability and Disease.

F Kuttler1, S Mai

  • 1Manitoba Institute of Cell Biology, CancerCare Manitoba, University of Manitoba, Winnipeg, Canada.

Genome Dynamics
|August 30, 2008
PubMed
Summary

The proto-oncogene c-Myc (Myc) drives tumor formation by destabilizing the genome. This review explores Myc's role in genomic instability and cancer progression, highlighting its function beyond transcription.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The proto-oncogene c-Myc is implicated in numerous cancers, but its precise role in tumorigenesis remains unclear.
  • Deregulation of c-Myc protein is a common feature in various cancer types, suggesting a critical involvement in disease.
  • While known to target multiple pathways, c-Myc's exact mechanisms in cancer initiation and promotion require further elucidation.

Purpose of the Study:

  • To review the role of the c-Myc protein in inducing genomic instability.
  • To explore the link between c-Myc-induced genomic instability and cancer development.
  • To discuss c-Myc's function beyond classical transcription factors, focusing on its impact on genome stability.

Main Methods:

  • Literature review of studies on c-Myc, genomic instability, and cancer.

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  • Analysis of c-Myc binding partners and downstream targets.
  • Examination of c-Myc's role in human and mouse cancer models concerning genomic instability.

    • Main Results:

    • c-Myc is a multifunctional protein that significantly impacts overall genome stability.
    • c-Myc triggers a complex network of genomic instability, contributing to cancer initiation.
    • Evidence suggests c-Myc affects nuclear organization and acts as a structural modifier of the genome.

    Conclusions:

    • c-Myc is a key driver of genomic instability, promoting cancer development.
    • The protein's function extends beyond transcriptional regulation, influencing genome structure and stability.
    • c-Myc's role in genomic instability positions it as a critical molecule in tumor progression.