We are analyzing https://link.springer.com/article/10.1007/s00432-008-0534-8.

Title:
Methylation status of p16 INK4A tumor suppressor gene in Iranian patients with sporadic breast cancer | Journal of Cancer Research and Clinical Oncology
Description:
Introduction p16 INK4A is a tumor suppressor encoding the Cdk inhibitor protein, which acts to repress Cdk4/6 and pRb phosphorylation. p16 INK4A gene can be inactivated by a variety of events, including promoter hypermethylation. Materials and methods To investigate the methylation status of the p16 INK4A gene in Iranian patients with breast carcinoma, promoter methylation was studied by methylation-specific PCR (MSP) and restriction enzyme-related PCR (REP). In addition, p16 INK4A promoter was analyzed by PCR-SSCP in order to detection of mutation and single nucleotide polymorphisms. Results Analysis of 70 patients by MPS and REP showed hypermethylation of p16 INK4A promoter in 35.7% (25/70) and 40% (28/70) of samples, respectively. Comparison of the molecular data and pathological information of the samples suggested that p16 INK4A gene might be inactivated at the early stages in breast cancer. Conclusion Therefore, it could be suggested that hypermethylation of p16 INK4A promoter is one of the epigenetic factors affecting the progress of sporadic breast carcinogenesis in Iranian patients.
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Keywords {🔍}

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Topics {✒️}

month download article/chapter encoded p16-ink4a protein rep showed hypermethylation restriction enzyme-related pcr tumor suppressor encoding sadeq vallian tumor suppressor genes cdkn2/p16/mts1 gene silent p14/p16 locus p16 ink4a gene article vallian sporadic breast cancer p16 gene deletion tumor-suppressive functions metastatic breast carcinoma human cancer cells full article pdf human ink4a locus human breast cancer human primary tumors sporadic breast carcinogenesis sporadic breast tumors related subjects p16 ink4a promoter normal breast tissue p16 ink4a genes cancer-related genes privacy choices/manage cookies including promoter hypermethylation cpg island methylation clinical oncology aims msp author correspondence aberrant dna methylation mts-1/cdkn2/ink4a mdr1 promoter hypermethylation methylation-specific pcr methylation specific pcr epigenetics joins genetics dna demethylating agent single nucleotide polymorphisms check access instant access t-cell lymphomas increased gene expression cdk inhibitor protein common human cancers aberrant promoter methylation dna hypermethylation p16 gene

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         headline:Methylation status of p16 INK4A tumor suppressor gene in Iranian patients with sporadic breast cancer
         description: p16 INK4A is a tumor suppressor encoding the Cdk inhibitor protein, which acts to repress Cdk4/6 and pRb phosphorylation. p16 INK4A gene can be inactivated by a variety of events, including promoter hypermethylation. To investigate the methylation status of the p16 INK4A gene in Iranian patients with breast carcinoma, promoter methylation was studied by methylation-specific PCR (MSP) and restriction enzyme-related PCR (REP). In addition, p16 INK4A promoter was analyzed by PCR-SSCP in order to detection of mutation and single nucleotide polymorphisms. Analysis of 70 patients by MPS and REP showed hypermethylation of p16 INK4A promoter in 35.7% (25/70) and 40% (28/70) of samples, respectively. Comparison of the molecular data and pathological information of the samples suggested that p16 INK4A gene might be inactivated at the early stages in breast cancer. Therefore, it could be suggested that hypermethylation of p16 INK4A promoter is one of the epigenetic factors affecting the progress of sporadic breast carcinogenesis in Iranian patients.
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            Hypermethylation
            Iranian population
            MSP
             p16 INK4A tumor suppressor gene
            REP
            Oncology
            Cancer Research
            Internal Medicine
            Hematology
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      headline:Methylation status of p16 INK4A tumor suppressor gene in Iranian patients with sporadic breast cancer
      description: p16 INK4A is a tumor suppressor encoding the Cdk inhibitor protein, which acts to repress Cdk4/6 and pRb phosphorylation. p16 INK4A gene can be inactivated by a variety of events, including promoter hypermethylation. To investigate the methylation status of the p16 INK4A gene in Iranian patients with breast carcinoma, promoter methylation was studied by methylation-specific PCR (MSP) and restriction enzyme-related PCR (REP). In addition, p16 INK4A promoter was analyzed by PCR-SSCP in order to detection of mutation and single nucleotide polymorphisms. Analysis of 70 patients by MPS and REP showed hypermethylation of p16 INK4A promoter in 35.7% (25/70) and 40% (28/70) of samples, respectively. Comparison of the molecular data and pathological information of the samples suggested that p16 INK4A gene might be inactivated at the early stages in breast cancer. Therefore, it could be suggested that hypermethylation of p16 INK4A promoter is one of the epigenetic factors affecting the progress of sporadic breast carcinogenesis in Iranian patients.
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      dateModified:2009-01-06T00:00:00Z
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         Breast cancer
         Hypermethylation
         Iranian population
         MSP
          p16 INK4A tumor suppressor gene
         REP
         Oncology
         Cancer Research
         Internal Medicine
         Hematology
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