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

Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
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...

You might also read

Related Articles

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

Sort by
Same author

The Temporal Architecture of Human Cells: Organelle Clocks and Distributed Circadian Time.

BioEssays : news and reviews in molecular, cellular and developmental biology·2026
Same author

Programming the tumor microenvironment through microbiome-driven mechanisms.

Frontiers in cellular and infection microbiology·2026
Same author

From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.

Pathophysiology : the official journal of the International Society for Pathophysiology·2026
Same author

Host-microbiome interactions in breast cancer progression and treatment response.

Frontiers in medicine·2026
Same author

T cell exhaustion landscapes and therapeutic modulation in cancer immunity.

Frontiers in cell and developmental biology·2026
Same author

Mitochondrial drivers of stem cell aging and inflammaging.

npj aging·2026

Related Experiment Video

Updated: Jul 12, 2026

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion
05:23

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion

Published on: July 7, 2023

Metastasis in biological time.

Jhommara Bautista1, Sofía Ojeda-Mosquera1, Camila Beltrán-Flores1

  • 1Cancer Research Group (CRG), Faculty of Medicine, Universidad de Las Américas, Quito, Ecuador.

Frontiers in Cell and Developmental Biology
|July 10, 2026
PubMed
Summary

Metastasis, a major cause of cancer death, is influenced by biological time. Circadian rhythms in tumors, immune cells, and organs affect cancer spread, challenging traditional spatial models.

Keywords:
biological timecircadian immune dynamicscircadian systemmetastasisprecision oncologystromal rhythmstumour-intrinsic clockszeitgebers

More Related Videos

Generation of Organ-conditioned Media and Applications for Studying Organ-specific Influences on Breast Cancer Metastatic Behavior
09:44

Generation of Organ-conditioned Media and Applications for Studying Organ-specific Influences on Breast Cancer Metastatic Behavior

Published on: June 13, 2016

Quantitative Analysis of Cancer Metastasis using an Avian Embryo Model
08:40

Quantitative Analysis of Cancer Metastasis using an Avian Embryo Model

Published on: May 30, 2011

Related Experiment Videos

Last Updated: Jul 12, 2026

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion
05:23

Tracking Tumor Cell Dissemination from Lung Metastases Using Photoconversion

Published on: July 7, 2023

Generation of Organ-conditioned Media and Applications for Studying Organ-specific Influences on Breast Cancer Metastatic Behavior
09:44

Generation of Organ-conditioned Media and Applications for Studying Organ-specific Influences on Breast Cancer Metastatic Behavior

Published on: June 13, 2016

Quantitative Analysis of Cancer Metastasis using an Avian Embryo Model
08:40

Quantitative Analysis of Cancer Metastasis using an Avian Embryo Model

Published on: May 30, 2011

Area of Science:

  • Oncology
  • Chronobiology
  • Cancer Metastasis Research

Background:

  • Metastasis is the primary cause of cancer mortality.
  • Current models often overlook the temporal dimension of cancer progression.
  • Emerging evidence suggests circadian systems influence metastatic processes.

Purpose of the Study:

  • To review how circadian regulation impacts the metastatic cascade.
  • To explore the role of biological time in tumor cell behavior, vascular trafficking, immune interactions, and organ colonization.
  • To integrate temporal dynamics into the understanding of metastasis.

Main Methods:

  • Review of existing literature on circadian biology and cancer metastasis.
  • Analysis of how intrinsic tumor clocks, host rhythms, and external zeitgebers affect metastatic stages.
  • Synthesis of evidence linking biological time to metastatic competence, dissemination, and outgrowth.

Main Results:

  • Circadian clocks within tumor cells modulate invasion and secretion.
  • Host circadian rhythms (e.g., endothelial, immune, organ-specific) create temporal windows for metastasis.
  • Systemic factors like light-dark cycles and feeding patterns influence metastatic progression.

Conclusions:

  • Metastasis is significantly shaped by biological time, not just spatial or genetic factors.
  • Understanding circadian influences can explain metastatic heterogeneity.
  • This temporal framework offers new avenues for precision oncology strategies.