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

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

6.4K
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...
6.4K
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

2.3K
2.3K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

15.5K
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...
15.5K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

3.5K
3.5K
Tumor Progression02:07

Tumor Progression

7.9K
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...
7.9K
Tumor Progression02:07

Tumor Progression

3.6K
3.6K

You might also read

Related Articles

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

Sort by
Same author

Investigational CRISPR-Cas9-edited T cells for metastatic colorectal cancer treatment: Clinical insights for future development.

Molecular therapy. Oncology·2026
Same author

A statistical framework for detecting therapy-induced resistance from drug screens.

NPJ systems biology and applications·2025
Same author

Limit theorems for the site frequency spectrum of neutral mutations in an exponentially growing population.

Stochastic processes and their applications·2025
Same author

Early Circulating Tumor DNA Kinetics as a Dynamic Biomarker of Cancer Treatment Response.

JCO clinical cancer informatics·2025
Same author

Parameter estimation from single patient, single time-point sequencing data of recurrent tumors.

Journal of mathematical biology·2024
Same author

Early ctDNA kinetics as a dynamic biomarker of cancer treatment response.

bioRxiv : the preprint server for biology·2024

Related Experiment Video

Updated: Apr 7, 2026

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma
15:07

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

Published on: December 28, 2015

27.4K

Clonal Diversity at Early Cancer Recurrence.

Kevin Leder1, Zicheng Wang2

  • 1Department of Industrial and Systems Engineering, University of Minnesota, Twin Cities, US.

Bulletin of Mathematical Biology
|April 5, 2026
PubMed
Summary

Cancer therapies can fail due to drug-resistant cells. Our mathematical model shows that recurrent cancer, often linked to early recurrence, suggests high clonal diversity, not a single resistant cell line.

Keywords:
Birth–death processCancer recurrenceClonal diversity

More Related Videos

Advanced Animal Model of Colorectal Metastasis in Liver: Imaging Techniques and Properties of Metastatic Clones
11:43

Advanced Animal Model of Colorectal Metastasis in Liver: Imaging Techniques and Properties of Metastatic Clones

Published on: November 30, 2016

13.7K
Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence
07:54

Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence

Published on: October 25, 2011

19.3K

Related Experiment Videos

Last Updated: Apr 7, 2026

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma
15:07

VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma

Published on: December 28, 2015

27.4K
Advanced Animal Model of Colorectal Metastasis in Liver: Imaging Techniques and Properties of Metastatic Clones
11:43

Advanced Animal Model of Colorectal Metastasis in Liver: Imaging Techniques and Properties of Metastatic Clones

Published on: November 30, 2016

13.7K
Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence
07:54

Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence

Published on: October 25, 2011

19.3K

Area of Science:

  • Mathematical Oncology
  • Evolutionary Biology
  • Cancer Research

Background:

  • Cancer therapies frequently fail due to the development of drug-resistant cell populations.
  • Tumor recurrence after treatment is a significant clinical challenge, driven by the evolution of resistant cancer cells.

Purpose of the Study:

  • To investigate the evolutionary dynamics of cancer recurrence using a mathematical model.
  • To analyze the clonal diversity of drug-resistant cells at the time of cancer recurrence.
  • To determine if early recurrence is associated with low clonal diversity (single mutation) or high clonal diversity (multiple mutations).

Main Methods:

  • Development of a two-type birth-death process mathematical model to simulate drug-sensitive and drug-resistant cancer cell populations.
  • Analysis of clonal diversity indices, including the number of clones and Simpson's Index, at cancer recurrence.
  • Examination of these indices conditioned on early recurrence in a model with a decaying sensitive population.

Main Results:

  • The study calculated the expected values of clonal diversity indices at the time of cancer recurrence.
  • Findings indicate that early cancer recurrence is more likely driven by a high number of resistance mutations (high clonal diversity) rather than a single dominant resistant clone.
  • The time of cancer recurrence was identified as a potential indicator of underlying clonal diversity.

Conclusions:

  • Recurrent cancers, particularly those occurring early, are characterized by high clonal diversity.
  • Mathematical modeling provides valuable insights into the evolutionary mechanisms driving cancer recurrence and drug resistance.
  • Understanding clonal diversity at recurrence can inform future therapeutic strategies and predict treatment outcomes.