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首页> 外文期刊>Journal of Cellular Physiology >TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.
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TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.

机译：TP53 p16INK4A分子,但不是H-KI-Ras,在肿瘤发生和发展的多形性腺瘤。

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The putative role of TP53 and p16(INK4A) tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case of carcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/Single Strand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53 were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in 4% (1/28) and 7% (2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutations in K-Ras. p16(INK4A) promoter hypermethylation was found in 14% (4/28) of PAs and 100% (5/5) carcinomas. All genetic and epigenetic alterations were detected exclusively in the epithelial and transitional tumor components, and were absent in the mesenchymal parts. Our analysis suggests that TP53 mutations and p16(INK4A) promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in the malignant progression of PA into carcinoma.
机译：TP53的假定的角色和p16 (INK4A)肿瘤Ras抑制基因和致癌基因唾腺的开发和发展在28例多形性瘤进行了研究腺瘤(PA), 4例胆囊腺癌,和ex-PA癌1例。在上面的表观遗传学改变的基因分析了聚合酶链反应/单身链构象多态性(PCR SSCP)和甲基化特异pcr测序(MS-PCR)。不是(4/28)和60%(3/5)癌。k - ras基因突变在h和被确定4%(1/28)和7%(2/28),分别。只有20%(1/5)的癌筛选显示k - ras基因突变。甲基化在14%(4/28)的不被发现和100%(5/5)癌。表观遗传变化检测肿瘤上皮和过渡组件和间质中缺席部分。和p16 (INK4A)启动子甲基化,但不是改变在h - k - ras基因和基因,可能参与考评的恶性发展成癌。

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