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Adaptive Mechanisms in Cancer Cells

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,...

Adaptive Mechanisms in Cancer Cells

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.
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Tumor Progression

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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...

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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...

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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...

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Related Experiment Video

Updated: May 13, 2026

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

A Hallmark-Integrated, Agent-Based Framework for Intratumor Heterogeneity in Melanoma Evolution.

Khola Jamshad¹, Trachette L Jackson²

¹Department of Mathematics, University of Michigan, Ann Arbor, MI, United States.

Bulletin of Mathematical Biology

|May 12, 2026

Summary

This study introduces a computational model to explore how cancer hallmarks drive intratumor heterogeneity (ITH) in melanoma. The findings reveal distinct ITH modes influenced by immune dynamics and cell motility, impacting tumor evolution and treatment resistance.

Keywords:

Agent-based model Hallmarks of cancer Immune evasion Intratumor heterogeneity Melanoma

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Last Updated: May 13, 2026

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

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Comparative Lesions Analysis Through a Targeted Sequencing Approach

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Published on: November 5, 2019

Area of Science:

Computational Biology
Cancer Research
Evolutionary Biology

Background:

Intratumor heterogeneity (ITH) is a key factor in cancer progression and therapeutic resistance.
Understanding the evolutionary dynamics driving ITH is crucial for developing effective cancer treatments.

Purpose of the Study:

To develop a computational framework for studying ITH in melanoma.
To investigate the interplay of genetic, immune, and spatial factors in shaping ITH.
To model the emergence of distinct ITH modes and their impact on tumor behavior.

Main Methods:

Development of a hallmark-integrated branching evolution process agent-based model (BEP-HI).
Simulation of melanoma evolution under coupled selection pressures.
Analysis of ITH modes, tumor growth kinetics, immune interactions, and cell motility.

Main Results:

Identification of three distinct evolutionary ITH modes in melanoma.
Demonstration of a mechanistic decoupling between tumor growth and heterogeneity.
Immune recruitment identified as a primary driver of ITH via nonlinear immune-editing feedback.
Melanoma cell motility shapes tumor morphology consistent with clinical observations.

Conclusions:

The BEP-HI model provides a biologically grounded framework for studying ITH evolution.
Interactions between cancer hallmarks significantly influence ITH.
The model can generate virtual tumor cohorts linking genetic diversity to tumor behavior and treatment resistance.