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07:54
Heterogeneity Mapping of Protein Expression in Tumors using Quantitative Immunofluorescence
Published on: October 25, 2011
Tissue, cell and stage specificity of (epi)mutations in cancers
Oliver M Sieber1, Simon R Tomlinson, Ian P M Tomlinson
1Molecular and Population Genetics Laboratory, Cancer Research UK, London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. oliver.sieber@cancer.org.uk
Nature Reviews. Cancer
|August 2, 2005
Summary
Most cancer-causing mutations are specific to tumor type or stage. The cellular environment likely selects these specific genetic changes, which must be within a permissive range for tumor growth.
Area of Science:
- Cancer Biology
- Genetics
- Epigenetics
Background:
- Most (epi)mutations in cancers exhibit specificity to particular tumors or developmental stages.
- Simple molecular mechanisms like tissue-restricted gene expression rarely explain this specificity.
Approach:
- Investigating the role of the cellular environment in selecting specific (epi)mutations.
- Analyzing the functional constraints on genetic changes during tumorigenesis.
Key Points:
- The specificity of cancer (epi)mutations is likely driven by selection within the cellular environment.
- Functional defects arising from these mutations must fall within a specific range, neither too strong nor too weak, to permit tumor growth.
- This 'permissive window' highlights a critical regulatory principle in tumorigenesis.
Conclusions:
- The cellular environment plays a crucial role in shaping the landscape of cancer (epi)mutations.
- Understanding these selection pressures and functional constraints is key to deciphering cancer development and identifying therapeutic targets.
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