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The human genome is over 99.9% identical between individuals, yet genetic differences exist at millions of bases. The human genome contains approximately 3 million variant positions per individual, many of which are heterozygous, contributing to genetic diversity and individual traits. Genetic variations include single-nucleotide polymorphisms (SNPs), insertions, deletions, and copy number variations (CNVs).SNPs, the most common variation, involve single-base changes in DNA. These can be...
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Related Experiment Video

Updated: May 2, 2026

Induction and Scoring of Graft-Versus-Host Disease in a Xenogeneic Murine Model and Quantification of Human T Cells in Mouse Tissues using Digital PCR
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Risk stratification of organ-specific GVHD can be improved by single-nucleotide polymorphism-based risk models.

D Kim1, H-H Won2, S Su3

  • 1Allogeneic blood and marrow transplantation program, Department of Medical Oncology and Hematology, Princess Margaret Hospital, Toronto, ON, Canada.

Bone Marrow Transplantation
|March 4, 2014
PubMed
Summary

Developing a risk model using single-nucleotide polymorphism (SNP) markers can improve the prediction of organ-specific graft-versus-host disease (GVHD). This genetic approach enhances risk stratification for transplant patients, identifying specific SNP markers linked to GVHD risk.

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Area of Science:

  • Immunogenetics
  • Transplantation Medicine
  • Genomic Risk Prediction

Background:

  • Graft-versus-host disease (GVHD) remains a significant complication following hematopoietic stem cell transplantation.
  • Accurate prediction of organ-specific GVHD is crucial for patient management and outcomes.

Purpose of the Study:

  • To develop and validate a risk model incorporating single-nucleotide polymorphism (SNP) markers for predicting organ-specific GVHD.
  • To identify specific genetic markers associated with increased risk of acute and chronic GVHD.
  • To evaluate the improvement in risk stratification by integrating genetic factors with clinical data.

Main Methods:

  • Genotyping of 259 SNPs across 53 genes in 394 transplant pairs.
  • Development of risk models using both clinical factors and identified SNP markers.
  • Stratification of patients into low, intermediate, and high-risk groups based on composite risk scores.

Main Results:

  • Several SNP markers in cytokine-, apoptosis-, TGF-β-, and PDGF-mediated pathways were correlated with acute and chronic GVHD.
  • Common biologic pathways were implicated across different organ-specific GVHDs.
  • Specific SNPs (e.g., FCGR2A for oral, FAS and TGFB1 for lung GVHD) were identified for organ-specific risks.
  • Integration of genetic risk factors improved the stratification power for organ-specific GVHD compared to clinical factors alone.

Conclusions:

  • A risk model incorporating SNP markers significantly enhances the stratification of organ-specific GVHD risk.
  • The identified SNP markers provide insights into the genetic underpinnings of GVHD pathogenesis.
  • SNP-based risk stratification offers a promising approach to personalize GVHD management in transplant recipients.