Occurrence, intratumoral heterogeneity, prognostic and predictive potential of microsatellite instability following surgical resection of primary colorectal carcinomas and corresponding liver metastases

被引:2
作者
Agoston Emese Irma [1 ]
Baranyai Zsolt [1 ]
Dede Kristof [4 ]
Bodoky Gyorgy [3 ]
Kulka Janina [2 ]
Bursics Attila [4 ]
Harsanyi Laszlo [1 ]
Szasz, A. Marcell [2 ]
机构
[1] Semmelweis Egyet, Altalanos Orvostudomanyi Kar, Sebeszeti Klin 1, Budapest, Hungary
[2] Semmelweis Egyet, Altalanos Orvostudomanyi Kar, Patol Intezet 2, Budapest, Hungary
[3] Egyesitett Szt Istvan & Szt Laszlo Korhaz, Onkol Osztaly, Budapest, Hungary
[4] Fovarosi Onkormanyzat Uzsoki Utcai Korhaz, Sebeszeti Onkosebeszeti Osztaly, Budapest, Hungary
关键词
colorectal cancer; liver metastasis; microsatellite instability; SPORADIC-COLON-CANCER; DNA MISMATCH REPAIR; ADJUVANT CHEMOTHERAPY; STAGE-II; REPLICATION ERRORS; MANAGEMENT; MUTATIONS; GENETICS; EFFICACY; MARKER;
D O I
10.1556/650.2015.30218
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Introduction: Besides clinicopathological parameters, molecular markers can be very important, and further characterize colorectal carcinomas into chromosomally unstable, microsatellite instable and "CqG-island methylator phenotype" groups. Aim: To study the frequency of microsatellite instability using immunohistochemical evaluation of MLH1, MSH2, MSH6 and PMS2 proteins in colorectal carcinoma. Method: 122 colorectal carcinomas as well as in 69 paired liver metastases were evaluated. Additionally, prognostic and predictive potential of mismatch repair status was tested. Results: Microsatellite instable phenotype was identified in 11.5% (14/122) of the tumours. There were no differences regarding staining intensity of tumour regions. Mismatch repair status was discordant in primaries vs. metastases in 20.2%. There was no difference in progression free- and overall survival according to mismatch repair status. The mismatch repair status was not predictive for survival within systemic therapy regimen groups. Conclusions: The subgroups of colorectal carcinomas could be evaluated in a larger and homogenised patient cohort to predict prognosis and response to therapy.
引用
收藏
页码:1460 / 1471
页数:12
相关论文
共 50 条
  • [1] CLUES TO THE PATHOGENESIS OF FAMILIAL COLORECTAL-CANCER
    AALTONEN, LA
    PELTOMAKI, P
    LEACH, FS
    SISTONEN, P
    PYLKKANEN, L
    MECKLIN, JP
    JARVINEN, H
    POWELL, SM
    JEN, J
    HAMILTON, SR
    PETERSEN, GM
    KINZLER, KW
    VOGELSTEIN, B
    DELACHAPELLE, A
    [J]. SCIENCE, 1993, 260 (5109) : 812 - 816
  • [2] Role of BAX mutations in mismatch repair-deficient colorectal carcinogenesis
    Abdel-Rahman, WM
    Georgiades, IB
    Curtis, LJ
    Arends, MJ
    Wyllie, AH
    [J]. ONCOGENE, 1999, 18 (12) : 2139 - 2142
  • [3] Molecular pathways in colorectal cancer
    Al-Sohaily, Sam
    Biankin, Andrew
    Leong, Rupert
    Kohonen-Corish, Maija
    Warusavitarne, Janindra
    [J]. JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 2012, 27 (09) : 1423 - 1431
  • [4] Barnetson R, 2000, GENE CHROMOSOME CANC, V29, P130, DOI 10.1002/1098-2264(200010)29:2<130::AID-GCC1023>3.0.CO
  • [5] 2-Z
  • [6] There is no increase in frequency of somatic mutations in metastases compared with primary colorectal carcinomas with microsatellite instability
    Barnetson, R
    Eckstein, R
    Robinson, B
    Schnitzler, M
    [J]. GENES CHROMOSOMES & CANCER, 2003, 38 (02) : 149 - 156
  • [7] Bläker H, 1999, J PATHOL, V188, P258, DOI 10.1002/(SICI)1096-9896(199907)188:3<258::AID-PATH350>3.0.CO
  • [8] 2-9
  • [9] Boland CR, 2010, GASTROENTEROLOGY, V138, P2073, DOI [10.1053/j.gastro.2009.12.064, 10.1053/j.gastro.2010.04.024]
  • [10] Bubb VJ, 1996, ONCOGENE, V12, P2641