Chromosomal Instability in Gastric Cancer Biology

被引:44
作者
Maleki, Saffiyeh Saboor [1 ]
Rocken, Christoph [1 ]
机构
[1] Univ Kiel, Dept Pathol, Arnold Heller Str 3,Haus 14, D-24105 Kiel, Germany
来源
NEOPLASIA | 2017年 / 19卷 / 05期
关键词
MITOTIC CHECKPOINT GENES; CENTROSOME AMPLIFICATION; GENOMIC INSTABILITY; CELL-CYCLE; MICROSATELLITE INSTABILITY; SPINDLE ABNORMALITIES; COLORECTAL CANCERS; AURORA KINASE; ANEUPLOIDY; EXPRESSION;
D O I
10.1016/j.neo.2017.02.012
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Gastric cancer (GC) is the fifth most common cancer in the world and accounts for 7% of the total cancer incidence. The prognosis of GC is dismal in Western countries due to late diagnosis: approximately 70% of the patients die within 5 years following initial diagnosis. Recently, integrative genomic analyses led to the proposal of a molecular classification of GC into four subtypes, i.e., microsatellite-instable, Epstein-Barr virus-positive, chromosomal-instable (CIN), and genomically stable GCs. Molecular classification of GC advances our knowledge of the biology of GC and may have implications for diagnostics and patient treatment. Diagnosis of microsatellite-instable GC and Epstein-Barr virus-positive GC is more or less straightforward. Microsatellite instability can be tested by immunohistochemistry (MLH1, PMS2, MSH2, and MSH6) and/or molecular-biological analysis. Epstein-Barr virus-positive GC can be tested by in situ hybridization (Epstein-Barr virus encoded small RNA). However, with regard to CIN, testing may be more complicated and may require a more in-depth knowledge of the underlying mechanism leading to CIN. In addition, CIN GC may not constitute a distinct subgroup but may rather be a compilation of a more heterogeneous group of tumors. In this review, we aim to clarify the definition of CIN and to point out the molecular mechanisms leading to this molecular phenotype and the challenges faced in characterizing this type of cancer.
引用
收藏
页码:412 / 420
页数:9
相关论文
共 88 条
[81]   Expression of a p53 mutant in the epidermis of transgenic mice accelerates chemical carcinogenesis [J].
Wang, XJ ;
Greenhalgh, DA ;
Jiang, AB ;
He, DC ;
Zhong, L ;
Medina, D ;
Brinkley, BR ;
Roop, DR .
ONCOGENE, 1998, 17 (01) :35-45
[82]   Three classes of genes mutated in colorectal cancers with chromosomal instability [J].
Wang, ZH ;
Cummins, JM ;
Shen, D ;
Cahill, DP ;
Jallepalli, PV ;
Wang, TL ;
Parsons, DW ;
Traverso, G ;
Awad, M ;
Silliman, N ;
Ptak, J ;
Szabo, S ;
Willson, JKV ;
Markowitz, SD ;
Goldberg, ML ;
Karess, R ;
Kinzler, KW ;
Vogelstein, B ;
Velculescu, VE ;
Lengauer, C .
CANCER RESEARCH, 2004, 64 (09) :2998-3001
[83]  
Watanabe T, 2012, J CLIN ONCOL, V2011, P2038
[84]   Genomic landscape and genetic heterogeneity in gastric adenocarcinoma revealed by whole-genome sequencing [J].
Wong, Swee Seong ;
Kim, Kyoung-Mee ;
Ting, Jason C. ;
Yu, Kun ;
Fu, Jake ;
Liu, Shawn ;
Cristescu, Razvan ;
Nebozhyn, Michael ;
Gong, Lara ;
Yue, Yong Gang ;
Wang, Jian ;
Chen Ronghua ;
Loboda, Andrey ;
Hardwick, James ;
Liu, Xiaoqiao ;
Dai, Hongyue ;
Jin, Jason Gang ;
Ye, Xiang S. ;
Kang, So Young ;
Do, In Gu ;
Park, Joon Oh ;
Sohn, Tae Sung ;
Reinhard, Christoph ;
Lee, Jeeyun ;
Kim, Sung ;
Aggarwal, Amit .
NATURE COMMUNICATIONS, 2014, 5
[85]   Increased expression of mitotic checkpoint genes in breast cancer cells with chromosomal instability [J].
Yuan, BB ;
Xu, Y ;
Woo, JH ;
Wang, YY ;
Bae, YK ;
Yoon, DS ;
Wersto, RP ;
Tully, E ;
Wilsbach, K ;
Gabrielson, E .
CLINICAL CANCER RESEARCH, 2006, 12 (02) :405-410
[86]   BRCA1, BRCA2, and DNA damage response: Collision or collusion? [J].
Zhang, HB ;
Tombline, G ;
Weber, BL .
CELL, 1998, 92 (04) :433-436
[87]   Overexpression of Separase induces aneuploidy and mammary tumorigenesis [J].
Zhang, Nenggang ;
Ge, Gouquing ;
Meyer, Rene ;
Sethi, Sumita ;
Basu, Dipanjan ;
Pradhan, Subhashree ;
Zhao, Yi-Jue ;
Li, Xiao-Nan ;
Cai, Wei-Wen ;
El-Naggar, Adel K. ;
Baladandayuthapani, Veerabhadran ;
Kittrell, Frances S. ;
Rao, Pulivarthi H. ;
Medina, Daniel ;
Pati, Debananda .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (35) :13033-13038
[88]   Tumour amplified kinase STK15/BTAK induces centrosome amplification, aneuploidy and transformation [J].
Zhou, HY ;
Kuang, J ;
Zhong, L ;
Kuo, WL ;
Gray, JW ;
Sahin, A ;
Brinkley, BR ;
Sen, S .
NATURE GENETICS, 1998, 20 (02) :189-193