Literature DB >> 9754644

Loss of heterozygosity on chromosome 14 in nasopharyngeal carcinoma.

A Mutirangura1, W Pornthanakasem, V Sriuranpong, P Supiyaphun, N Voravud.   

Abstract

The main objective of this study was to determine the precise frequency of chromosome 14q loss of heterozygosity in nasopharyngeal carcinomas and to define its minimal deletion regions. Thirty-nine tumors were selected for PCR-based deletion mapping using 19 microsatellite polymorphic markers spanning the long arm of this chromosome. Loss of heterozygosity for at least one marker was observed in 29 (74.4%) tumors, while 24 of these tumors displayed partial loss and provided an informative basis for detailed deletion mapping. Three minimal regions of loss were delineated, the first defined by markers D14S278 and D14S288, the second being between D14S51 and the telomere. These data confirmed 2 potential tumor-suppressor-gene loci at 14q12-13 and 14q32. Interestingly, the third region of loss was located at the T-cell-receptor delta-chain locus. This may reflect another tumor-suppressor-gene locus at 14q11.2, or may be the consequence of a specific genomic rearrangement of this region. In addition, these allelic losses occurred with high frequency in all tumor grades and stages and in all histological sub-types. These findings suggest that the genetic alteration of chromosome 14 is common and crucial during nasopharyngeal-carcinoma development.

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Year:  1998        PMID: 9754644     DOI: 10.1002/(sici)1097-0215(19981005)78:2<153::aid-ijc5>3.0.co;2-y

Source DB:  PubMed          Journal:  Int J Cancer        ISSN: 0020-7136            Impact factor:   7.396


  14 in total

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Review 8.  Locally advanced nasopharyngeal cancer.

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9.  N-myc downstream-regulated gene 2 (NDRG2) promoter methylation and expression in pituitary adenoma.

Authors:  Paulina Vaitkiene; Indre Valiulyte; Brigita Glebauskiene; Rasa Liutkeviciene
Journal:  Diagn Pathol       Date:  2017-04-08       Impact factor: 2.644

10.  BRD7 suppresses the growth of Nasopharyngeal Carcinoma cells (HNE1) through negatively regulating beta-catenin and ERK pathways.

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