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Oncology Reports
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Print ISSN: 1021-335X Online ISSN: 1791-2431
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January-February 2003 Volume 10 Issue 1

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International Journal of Molecular Medicine

International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

International Journal of Oncology

International Journal of Oncology

International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

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Molecular Medicine Reports

Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

Oncology Reports

Oncology Reports

Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

Experimental and Therapeutic Medicine

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Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

Oncology Letters

Oncology Letters

Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

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Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.

Molecular and Clinical Oncology

Molecular and Clinical Oncology

International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.

World Academy of Sciences Journal

World Academy of Sciences Journal

Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.

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International Journal of Functional Nutrition

Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.

International Journal of Epigenetics

International Journal of Epigenetics

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Article

P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer

  • Authors:
    • Corrado Ficorella
    • Katia Cannita
    • Enrico Ricevuto
    • Elena Toniato
    • Carlo Fusco
    • Nuntia Teresa Sinopoli
    • Federica De Galitiis
    • Zorika Christiana Di Rocco
    • G. Porzio
    • Luigi Frati
    • Alberto Gulino
    • Stefano Martinotti
    • Paolo Marchetti
  • View Affiliations / Copyright

    Affiliations: Universita degli Studi L'Aquila, Dipartimento di Medicina Sperimentale, Coppito II, I-67100 L'Aquila, Italy. ricevuto@fismedw2.univaq.it
  • Pages: 169-173
    |
    Published online on: January 1, 2003
       https://doi.org/10.3892/or.10.1.169
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Abstract

The objective of this study was to investigate the contribution of p16 inactivation in gastric cancer and to compare it with p53. A cohort of 34 primary GCs were analyzed for p16 mutations and transcriptional silencing of the gene due to hypermethylation of the promoter. SSCP analysis and direct sequencing of exons 1 and 2 of the p16 gene were performed to detect any structural alterations. The methylation specific PCR (MSP) assay was applied to reveal hypermethylation of the ‘CpG’ island in the regulatory region using specific primer pairs for methylated and unmethylated nucleotides after a chemical reaction converting cytosines into uracile when unmethylated. SSCP and direct sequencing analysis did not detect any p16 mutations. The MSP assay showed 4 MSP+ variants (11.8%). Three MSP+ were stage III-IV disease and 1 MSP+ was detected in an early stage disease (IB). All MSP+ were diffuse type adenocarcinomas. The MSP+ samples were different from previously reported samples harboring p53 mutations in the same cohort. These data increase the number of gastric cancers showing alterations of either p53 or p16 to 29.4% (10/34). Functional inactivation by hypermethylation of the p16 locus and p53 mutations could play a significant, complementary role in the pathogenesis of sporadic gastric cancer.

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Copy and paste a formatted citation
Spandidos Publications style
Ficorella C, Cannita K, Ricevuto E, Toniato E, Fusco C, Sinopoli NT, De Galitiis F, Di Rocco ZC, Porzio G, Frati L, Frati L, et al: P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer. Oncol Rep 10: 169-173, 2003.
APA
Ficorella, C., Cannita, K., Ricevuto, E., Toniato, E., Fusco, C., Sinopoli, N.T. ... Marchetti, P. (2003). P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer. Oncology Reports, 10, 169-173. https://doi.org/10.3892/or.10.1.169
MLA
Ficorella, C., Cannita, K., Ricevuto, E., Toniato, E., Fusco, C., Sinopoli, N. T., De Galitiis, F., Di Rocco, Z. C., Porzio, G., Frati, L., Gulino, A., Martinotti, S., Marchetti, P."P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer". Oncology Reports 10.1 (2003): 169-173.
Chicago
Ficorella, C., Cannita, K., Ricevuto, E., Toniato, E., Fusco, C., Sinopoli, N. T., De Galitiis, F., Di Rocco, Z. C., Porzio, G., Frati, L., Gulino, A., Martinotti, S., Marchetti, P."P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer". Oncology Reports 10, no. 1 (2003): 169-173. https://doi.org/10.3892/or.10.1.169
Copy and paste a formatted citation
x
Spandidos Publications style
Ficorella C, Cannita K, Ricevuto E, Toniato E, Fusco C, Sinopoli NT, De Galitiis F, Di Rocco ZC, Porzio G, Frati L, Frati L, et al: P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer. Oncol Rep 10: 169-173, 2003.
APA
Ficorella, C., Cannita, K., Ricevuto, E., Toniato, E., Fusco, C., Sinopoli, N.T. ... Marchetti, P. (2003). P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer. Oncology Reports, 10, 169-173. https://doi.org/10.3892/or.10.1.169
MLA
Ficorella, C., Cannita, K., Ricevuto, E., Toniato, E., Fusco, C., Sinopoli, N. T., De Galitiis, F., Di Rocco, Z. C., Porzio, G., Frati, L., Gulino, A., Martinotti, S., Marchetti, P."P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer". Oncology Reports 10.1 (2003): 169-173.
Chicago
Ficorella, C., Cannita, K., Ricevuto, E., Toniato, E., Fusco, C., Sinopoli, N. T., De Galitiis, F., Di Rocco, Z. C., Porzio, G., Frati, L., Gulino, A., Martinotti, S., Marchetti, P."P16 hypermethylation contributes to the characterization of gene inactivation profiles in primary gastric cancer". Oncology Reports 10, no. 1 (2003): 169-173. https://doi.org/10.3892/or.10.1.169
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