Molecular biomarkers in urothelial bladder cancer

被引:99
作者
Kim, Wun-Jae [1 ,3 ]
Bae, Suk-Chul [2 ,3 ]
机构
[1] Chungbuk Natl Univ, Coll Med, Dept Urol, Cheonju, South Korea
[2] Chungbuk Natl Univ, Coll Med, Dept Biochem, Cheonju, South Korea
[3] Inst Tumor Res, Cheonju 361763, South Korea
来源
CANCER SCIENCE | 2008年 / 99卷 / 04期
关键词
D O I
10.1111/j.1349-7006.2008.00735.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Bladder cancers are a mixture of heterogeneous cell populations, and numerous factors are likely to be involved in dictating their recurrence, progression, and the patient's survival. For any candidate prognostic marker to have considerable clinical relevance, it must add some predictive capacity beyond that offered by the conventional clinical and pathological parameters. None of the biomarkers reported to date have shown sufficient sensitivity and specificity for detecting the whole spectrum of bladder cancer diseases in routine clinical practice. The limitations of established prognostic markers requires us to identify better molecular parameters that could be of interest in predicting the prognosis of bladder cancer patients, in particular, the high-risk patient groups that are at risk of progression and recurrence. Recent progress in epigenetic modification and gene silencing opened a new avenue for the identification of epigenetic markers, which appears to be more useful for cancer diagnosis and prognosis. Although epigenetic markers also have limitations, the combined epigenetic marker approach may increase sensitivity and reliability. The epigenetic silencing of tumor-suppressor genes is interesting from a clinical standpoint because of the possibility of reversing epigenetic changes and restoring gene function in a cell. In addition, microarray technology provides us with additional tools for the analysis of global gene-expression analysis of tumor samples. Future microarray analyses are likely to reveal particular gene-expression signatures that predict the likelihood of bladder cancer progression and recurrence, as well as a patient's survival and responsiveness to different anticancer therapies, with great specificity and sensitivity.
引用
收藏
页码:646 / 652
页数:7
相关论文
共 81 条
  • [1] Tumor suppressor activity of RUNX3
    Bae, SC
    Choi, JK
    [J]. ONCOGENE, 2004, 23 (24) : 4336 - 4340
  • [2] Cancer - New-age tumour suppressors
    Balmain, A
    [J]. NATURE, 2002, 417 (6886) : 235 - 237
  • [3] Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancer
    Baylin, SB
    Esteller, M
    Rountree, MR
    Bachman, KE
    Schuebel, K
    Herman, JG
    [J]. HUMAN MOLECULAR GENETICS, 2001, 10 (07) : 687 - 692
  • [4] DNA hypermethylation in tumorigenesis - epigenetics joins genetics
    Baylin, SB
    Herman, JG
    [J]. TRENDS IN GENETICS, 2000, 16 (04) : 168 - 174
  • [5] Baylin SB, 1998, ADV CANCER RES, V72, P141
  • [6] Bladder cancer outcome and subtype classification by gene expression
    Blaveri, E
    Simko, JP
    Korkola, JE
    Brewer, JL
    Baehner, F
    Mehta, K
    DeVries, S
    Koppie, T
    Pejavar, S
    Carroll, P
    Waldman, FM
    [J]. CLINICAL CANCER RESEARCH, 2005, 11 (11) : 4044 - 4055
  • [7] BRINGUIER PP, 1993, CANCER RES, V53, P3241
  • [8] Brockmoller J, 1996, CANCER RES, V56, P3915
  • [9] High-throughput microarray technologies: From genomics to clinics
    Bubendorf, L
    [J]. EUROPEAN UROLOGY, 2001, 40 (02) : 231 - 238
  • [10] Promoter hypermethylation is associated with tumor location, stage, and subsequent progression in transitional cell carcinoma
    Catto, JWF
    Azzouzi, AR
    Rehman, I
    Feeley, KM
    Cross, SS
    Amira, N
    Fromont, G
    Sibony, M
    Cussenot, O
    Meuth, M
    Hamdy, FC
    [J]. JOURNAL OF CLINICAL ONCOLOGY, 2005, 23 (13) : 2903 - 2910