Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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,...
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Host metabolism can produce many indoles and phenols independently of the microbiome.

Nature metabolism·2026
Same author

Puf3 contributes to changes in mRNA solubility, translation elongation dynamics at rare arginine codons and loss of protein homeostasis in cells lacking Not4.

RNA (New York, N.Y.)·2026
Same author

The PLK4 inhibitor RP-1664 demonstrates potent efficacy in neuroblastoma preclinical models through a dual mechanism of sensitivity.

Nature communications·2026
Same author

Leveraging 13C-Labeling to Assign Molecular Formulas to Unknown Yeast Metabolites.

Journal of the American Society for Mass Spectrometry·2026
Same author

A Liver-Targeted Copper Supplement Reduces Metabolic Dysfunction-Associated Liver Steatosis by Increasing Lipolysis and Fatty Acid Oxidation.

bioRxiv : the preprint server for biology·2026
Same author

Blueprint 2: A self-directed mobile adaptive coping skills intervention to improve psychological distress symptoms among cardiorespiratory failure survivors study protocol.

Contemporary clinical trials·2026
Same journal

Six ways to put the public at the heart of science and policy.

Nature·2026
Same journal

The complex truth about trust in science.

Nature·2026
Same journal

Have people stopped trusting science? The data tell a surprising story.

Nature·2026
Same journal

How FAIR data are helping to build trust in science.

Nature·2026
Same journal

Scientists should recognize their own political biases to build public trust.

Nature·2026
Same journal

Harmonizing standards and resources for the medical genome.

Nature·2026
See all related articles

Related Experiment Video

Updated: May 10, 2026

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells
06:32

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells

Published on: September 1, 2010

16.8K

Reprogramming neuroblastoma by diet-enhanced polyamine depletion.

Sarah Cherkaoui1,2, Christina S Turn3,4, Yuan Yuan1,2,5

  • 1Pediatric Cancer Metabolism Laboratory, Children's Research Center, University of Zurich, Zurich, Switzerland.

Nature
|September 24, 2025
PubMed
Summary
This summary is machine-generated.

Dietary restriction and difluoromethylornithine synergize to treat neuroblastoma. This combined approach depletes polyamine precursors, disrupts oncogenic protein translation, and promotes tumor differentiation, significantly improving survival in a mouse model.

More Related Videos

Zebrafish Model of Neuroblastoma Metastasis
05:20

Zebrafish Model of Neuroblastoma Metastasis

Published on: March 14, 2021

3.2K
Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
09:44

Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases

Published on: May 2, 2025

627

Related Experiment Videos

Last Updated: May 10, 2026

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells
06:32

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells

Published on: September 1, 2010

16.8K
Zebrafish Model of Neuroblastoma Metastasis
05:20

Zebrafish Model of Neuroblastoma Metastasis

Published on: March 14, 2021

3.2K
Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
09:44

Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases

Published on: May 2, 2025

627

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Regulation

Background:

  • Neuroblastoma is a lethal childhood cancer originating from neural crest cells.
  • Cancer growth relies on metabolic pathways, including polyamine biosynthesis, which is crucial for neuroblastoma.
  • Difluoromethylornithine, a polyamine biosynthesis inhibitor, has shown clinical potential.

Purpose of the Study:

  • To investigate if dietary restriction of amino acid substrates can enhance the efficacy of difluoromethylornithine in treating neuroblastoma.
  • To elucidate the molecular mechanisms underlying the combined therapeutic effect.

Main Methods:

  • Utilized the Th-MYCN mouse model of neuroblastoma.
  • Implemented a dietary intervention restricting arginine and proline.
  • Administered difluoromethylornithine.
  • Analyzed polyamine levels, protein translation, and tumor differentiation.

Main Results:

  • An arginine- and proline-free diet decreased ornithine levels, enhancing polyamine depletion by difluoromethylornithine.
  • Polyamine depletion led to ribosome stalling, particularly at adenosine-rich codons.
  • These codons are enriched in cell cycle genes and depleted in neuronal differentiation genes.
  • Combined dietary and pharmacological intervention promoted a pro-differentiation proteome.

Conclusions:

  • Combined dietary restriction and difluoromethylornithine treatment effectively target neuroblastoma.
  • Metabolic stress-induced translational rewiring, via codon usage preferences, can be exploited to promote cancer cell differentiation.
  • This strategy offers a novel approach for treating paediatric cancers like neuroblastoma.