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Why are Some Tissues More Vulnerable? Revisiting Tissue Specificity in Hereditary Cancer Syndromes
Vanessa N Kozak1, Jaqueline C Oliveira1, Daniela F Gradia1
1Department of Genetics, Postgraduate Program in Genetics, Federal University of Parana (UFPR), Centro Politecnico, Laboratory of Human Cytogenetics and Oncogenetics (LabCHO), Jardim das Americas, Curitiba, Parana, 81531-990, Brazil.
Molecular Diagnosis & Therapy
|May 14, 2026
Summary
Understanding hereditary cancer predisposition syndromes (HCPSs) is advancing, but why cancers develop in specific tissues remains unclear. Research suggests a complex interplay of genetics, epigenetics, and environmental factors determines tissue specificity in these inherited cancer risks.
Area of Science:
- Genetics and Epigenetics
- Oncology
- Molecular Biology
Background:
- Hereditary cancer predisposition syndromes (HCPSs) are linked to specific gene mutations, yet the tissue tropism of cancer development is poorly understood.
- Ubiquitous expression of cancer predisposition genes and their DNA repair functions challenge explanations for organ-specific cancer incidence.
Purpose of the Study:
- To provide a comprehensive literature review on the tissue specificity of HCPSs.
- To integrate insights from molecular biology, epigenetics, and multi-omics to explain organ tropism in hereditary cancers.
Main Methods:
- Structured literature search of PubMed (March 2023-September 2025) using keywords related to tissue specificity and hereditary cancer.
- Screening of reference lists to identify relevant studies.
- Synthesis of findings from molecular biology, epigenetics, and multi-omics research.
Main Results:
- No single mechanism fully explains tissue specificity; proposed factors include proliferation rates and mutation acquisition patterns.
- Germline defects interact with tissue-specific epigenetic landscapes, gene interactions, and compensatory pathways.
- Tissue vulnerability is shaped by inherited DNA repair defects, genotoxic exposures, and differential thresholds for apoptosis versus malignant transformation.
Conclusions:
- Tissue specificity in HCPSs is multifactorial, resulting from the convergence of germline defects with tissue-specific epigenetics, regulatory networks, and environmental exposures.
- Understanding these complex interactions is crucial for developing tailored surveillance strategies and guiding future research in hereditary cancer.
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