ISSN: 1300-0292
İndekslendiği Dizinler: SCIENCE CITATION INDEX EXPANDED
CINAHL, Index Copernicus,
Chemical Abstracts (CA),
Excerpta Medica / EMBASE
Dil: Türkçe, İngilizce
İçerik: Orijinal Araştırma, Derleme, Editöre Mektup, Olgu Sunumu, Tıp Eğitimi, Tıbbi Kitap İncelemeleri
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Role Of The P53 Tumor Suppressor Gene In Gastric Cancer
Ali KARAMAN*
* Uz.Dr., Erzurum Numune Hastanesi Genetik Bölümü, ERZURUM
Although gastric cancer is still one of the most common malignancies in the world, the molecular basis of gastric carcinogensis is currently being explored. The conversion of normal cells to cancer cells in gastric cancer is also needed for a multistage process, that is intimately associated with an accumulation of multiple gene changes including oncogenes and tumor suppressor genes. Among them, p53 gene was widely examined in gastric cancers. Loss of heterozygosity (LOH) on chromosome 17p (p53 locus) and mutation of the p53 gene are frequently observed in gastric cancer cell lines and advanced gastric cancer as well as in early gastric cancer. Now it is well known that this p53 change occurs from the early stage of gastric carcinogenesis. The p53 tumor suppressor gene has come to the forefront of cancer research because it is commonly mutated in human cancer and the spectrum of p53 mutations in these cancers is providing clues to the etiology and molecular pathogenesis of neoplasia. Detection of p53 abnormalities may have diagnostic, prognostic, and therapeutic implications. Recent studies investigating the mechanisms underlying the biological activity of p53 indicate that the protein is involved in gene transcription, DNA synthesis and repair, genomic plasticity, and programmed cell death.A lot of studies indicate that LOH on chromosome 17p is a common event of gastric carcinoma and takes place from an earlier stage (60%). Additionally, recent evidence indicates that most tumors with allele loss at the p53 gene contain point mutation in the remaining (nondeleted allel) p53 gene.Keywords: Stomach Neoplasms, Genes, p53, Cell Cycle, Loss of HeterozygosityTurkiye Klinikleri J Med Sci 2003, 23:67-73
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