Abstract
Little is known about the biology of post-transplant lymphoproliferative disorders (PTLDs). The objective of this study was to determine the molecular alterations that occur at the protein level in patients with PTLDs. Six tumor samples from adult patients with PTLD and four benign lymph nodes were studied using protein microarray technique. Proteins that were dysregulated included proteins in the PI3K/mTOR, NFkB and HSP90 pathways. Inhibitors of these proteins induced cytotoxicity and apoptosis in EBV+ve and -ve cell lines. These results provide insight into pathways that are dysregulated in PTLD and can be targeted in future clinical trials.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Epstein-Barr Virus Infections / metabolism*
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Epstein-Barr Virus Infections / virology
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Female
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Gene Expression Profiling / methods
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Gene Expression Regulation*
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HSP90 Heat-Shock Proteins / biosynthesis
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Herpesvirus 4, Human*
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Humans
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Lymphoproliferative Disorders / metabolism*
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Lymphoproliferative Disorders / virology
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Male
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NF-kappa B / biosynthesis
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Oligonucleotide Array Sequence Analysis / methods
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Organ Transplantation*
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Phosphatidylinositol 3-Kinases / biosynthesis
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Protein Kinases / biosynthesis
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Proteomics / methods
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Stem Cell Transplantation*
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TOR Serine-Threonine Kinases
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Transplantation, Homologous
Substances
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HSP90 Heat-Shock Proteins
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NF-kappa B
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Protein Kinases
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MTOR protein, human
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TOR Serine-Threonine Kinases