Abstract
During replication, the primary function of the eukaryotic DNA mismatch repair (MMR) system is to recognize and correct mismatched base pairs within the DNA helix. Deficiencies in MMR have been reported previously in cases of hereditary nonpolyposis colorectal cancer and sporadic tumors occurring in a variety of tissues including gliomas. Furthermore, recent evidence indicates that the MMR system may be involved in mediating therapeutic sensitivity to alkylating agents. In this study, 22 neoplastic tissue samples from 22 patients who underwent surgical resection for medulloblastoma, a common cerebellar tumor of childhood, were assayed for the presence or absence of MMR polypeptides using Western blot and immunohistochemical techniques. Results from these experiments indicate that the MMR system is not commonly deficient in medulloblastoma.
MeSH terms
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Adaptor Proteins, Signal Transducing
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Adenosine Triphosphatases*
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Adolescent
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Carrier Proteins
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Cell Nucleus / metabolism
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Cerebellar Neoplasms / genetics
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Cerebellar Neoplasms / metabolism*
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Cerebellar Neoplasms / pathology
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Cerebellar Neoplasms / surgery
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Child
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DNA Repair Enzymes*
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DNA Repair*
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DNA-Binding Proteins*
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Humans
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Medulloblastoma / genetics
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Medulloblastoma / metabolism*
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Medulloblastoma / pathology
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Medulloblastoma / surgery
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Mismatch Repair Endonuclease PMS2
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MutL Protein Homolog 1
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MutS Homolog 2 Protein
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Neoplasm Proteins / analysis
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Neoplasm Recurrence, Local
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Nuclear Proteins
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Palatine Tonsil / metabolism
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Proteins / analysis
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Proto-Oncogene Proteins / analysis
Substances
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Adaptor Proteins, Signal Transducing
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Carrier Proteins
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DNA-Binding Proteins
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MLH1 protein, human
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Neoplasm Proteins
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Nuclear Proteins
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Proteins
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Proto-Oncogene Proteins
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Adenosine Triphosphatases
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PMS2 protein, human
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MSH2 protein, human
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Mismatch Repair Endonuclease PMS2
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MutL Protein Homolog 1
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MutS Homolog 2 Protein
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DNA Repair Enzymes