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Updated: Jan 25, 2026
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Flow-sorting and Exome Sequencing of the Reed-Sternberg Cells of Classical Hodgkin Lymphoma
Published on: June 10, 2017
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Somatic mutations render human exome and pathogen DNA more similar.
Ehsan Ebrahimzadeh1, Maggie Engler2, David Tse2
1Department of Electrical Engineering, UCLA, Los Angeles, California, United States of America.
Plos One
|May 3, 2019
Summary
Cancer mutations, particularly from UV light or smoking, can mimic pathogen DNA, potentially enhancing immunotherapy response. Higher mutation rates increase this similarity, suggesting a role for pathogen recognition in anti-tumor immunity.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Immunotherapy shows promise in cancer treatment.
- Tumor mutation load correlates with immunotherapy response.
- Pathogen-associated mutational signatures may improve response prediction.
Purpose of the Study:
- To investigate the in silico relationship between cancer mutations, pathogen similarity, and immunogenicity.
- To determine if mutagenic processes increase cancer exome similarity to pathogen DNA.
- To explore the impact of mutation rate and type on immune recognition.
Main Methods:
- In silico analysis of cancer exome data.
- Comparison of somatic mutations from UV and smoking with pathogen DNA.
- Assessment of mutation rate and distribution effects on sequence similarity.
- Evaluation of functional tolerance to mutagenic processes.
Main Results:
- Mutagenic processes (UV, smoking) increase cancer exome similarity to pathogen DNA (4-5 amino acid peptides).
- Increased similarity can occur with specific mutation distributions or random mutations.
- Higher mutation rates generally enhance cancer exome-pathogen DNA similarity.
- Functional tolerance varies between natural and artificial mutagenic processes.
Conclusions:
- Somatic mutations can create pathogen-like sequences in cancer exomes.
- Mutation rate and type influence the degree of similarity to pathogen DNA.
- These findings support the role of pathogen sequence recognition and differential tolerance in anti-tumor immune responses.
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