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首页> 外文期刊>Japanese Journal of Cancer Research >Mutations of p53, c-kit, K-ras, and beta-Catenin Gene in Non-Hodgkin's Lymphoma of Adrenal Gland.
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Mutations of p53, c-kit, K-ras, and beta-Catenin Gene in Non-Hodgkin's Lymphoma of Adrenal Gland.

机译:肾上腺非霍奇金淋巴瘤中p53,c-kit,K-ras和β-Catenin基因的突变。

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Malignant lymphoma of the adrenal gland is a rare disease, usually with diffuse large cell morphology and B-cell immunophenotype, and often associated with Epstein-Barr virus infection. In this study, mutations of p53, c-kit, K-ras, and beta-catenin gene were analyzed in 17 cases (13 males and four females with ages ranging from 25 to 84 years) of such lymphomas by polymerase chain reaction-single strand conformation polymorphism followed by direct sequencing. Selected exons in each gene, representing hot spots, were analyzed. All 44 mutations detected were single-nucleotide substitutions and 33 were missense mutations. Nineteen mutations were detected in exon 5 and / or 7 of the p53 gene in nine of 17 cases (52.9%) and 21 in exon 11 and / or 17 of the c-kit gene in 10 of 14 cases (71.4%). Bilateral adrenal lesions in one case who had not received any adjuvant therapy showed different mutational patterns of the p53 and c-kit genes, suggesting different clonal evolution of lymphoma between the left and right sides. Mutation at codon 13 of the K-ras gene was detected in one of 14 cases (7.1%), and in exon 3 of the beta-catenin gene in three of 12 cases (25%). All but one mutation were transition mutations, indicating that some endogenous mutagens act in lymphomagenesis in the adrenal gland. Our results suggest that p53 and c-kit gene mutations might play a role in adrenal lymphomagenesis.
机译:肾上腺的恶性淋巴瘤是一种罕见的疾病,通常具有弥散的大细胞形态和B细胞免疫表型,并经常与爱泼斯坦-巴尔病毒感染相关。在这项研究中,通过单次聚合酶链反应分析了17例此类淋巴瘤(13例男性和4例女性,年龄在25至84岁之间)中的p53,c-kit,K-ras和β-catenin基因突变。链构象多态性,然后直接测序。分析了每个基因中代表热点的选定外显子。检测到的所有44个突变均为单核苷酸取代,而33个为错义突变。 17例中的9例(52.9%)在p53基因的5号和/或7号外显子中检测到19个突变,14例10例(71.4%)在c-kit基因的11号和/或17号外显子中检测到21个突变。在没有接受任何辅助治疗的一例中,双侧肾上腺病变显示出p53和c-kit基因的突变模式不同,表明左侧和右侧之间淋巴瘤的克隆进化不同。 14例中的1例(7.1%)检测到K-ras基因第13位密码子突变,而12例中的3例(25%)检测到β-catenin基因第3外显子突变。除一个突变外,所有突变均为过渡突变,表明某些内源性诱变在肾上腺的淋巴瘤发生中起作用。我们的结果表明,p53和c-kit基因突变可能在肾上腺淋巴瘤的发生中起作用。

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