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Published on: February 2, 2024
Developmental reprogramming of cancer susceptibility
Cheryl Lyn Walker1, Shuk-mei Ho
1Institute of Biosciences and Technology, Texas A&M Health Science Center, 2121 W. Holcombe Boulevard, Houston, TX 77030, USA. cwalker@ibt.tamhsc.edu
Environmental exposures during development can reprogram the epigenome, increasing cancer susceptibility without causing genetic mutations. This epigenetic reprogramming represents a novel gene-environment interaction mechanism.
Area of Science:
- Epigenetics
- Cancer Biology
- Developmental Origins of Health and Disease (DOHAD)
Background:
- Traditional gene-environment interactions in carcinogenesis involve acquiring mutations.
- Inherited defects in tumor suppressor genes necessitate additional mutations for cancer development.
- The DOHAD hypothesis proposes developmental environmental exposures increase adult cancer susceptibility via epigenetic reprogramming, not genetic mutation.
Purpose of the Study:
- To propose epigenetic reprogramming as a novel mechanism of gene-environment interaction in cancer susceptibility.
- To challenge the traditional view of carcinogenesis solely driven by genetic mutations.
- To highlight the role of environmental exposures during development in altering the epigenome.
Main Methods:
- This study is primarily theoretical, proposing a hypothesis based on existing literature.
- It integrates concepts from carcinogenesis, epigenetics, and the DOHAD hypothesis.
- No new experimental data was generated; the focus is on conceptual synthesis.
Main Results:
- Environmental exposures during development can lead to epigenetic reprogramming.
- This reprogramming increases susceptibility to cancer in adulthood.
- Epigenetic reprogramming acts as a novel form of gene-environment interaction.
Conclusions:
- Epigenetic reprogramming by developmental environmental exposures is a plausible mechanism for increased cancer susceptibility.
- This mechanism offers an alternative to mutation-driven carcinogenesis models.
- Further research is warranted to investigate the specific epigenetic modifications and their role in cancer development.
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