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. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: Curr Oncol Rep. 2010 May;12(3):193–201. doi: 10.1007/s11912-010-0093-4

Table 1.

Gene expression studies in RCC

Study Year Samples Analytical focus Results
Clinically driven analyses
    Takahashi et al. [24] 2001 29 cc
29 normal
5-year survival 51 probes associate with survival, 96% accuracy
    Vasselli et al. [25] 2003 51 cc
6 papillary
1 unknown
Survival 45 genes most associated with survival; VCAM-1 alone can stratify patients by survival
    Jones et al. [28] 2005 22 cc
10 metastases
37 other
24 normal
Progression and metastases 31 genes that are continuously deregulated in disease progression; 155 genes that associate with metastases, 88.9% accuracy
    Kosari et al. [29] 2005 10 aggressive cc
9 non-aggressive cc
9 metastatic cc
12 normal
Tumor aggressiveness 35 genes distinguish between non-aggressive and aggressive tumors; survivin expression associated with survival by multivariate analysis in 183 patients
    Zhao et al. [32•] 2006 177 cc Unsupervised 2 primary clusters composed of 5 subclusters with survival difference
    Yao et al. [27] 2008 25 cc
(14 metastatic)
2 metastases
Metastatic vs nonmetastatic 3 genes (VCAM-1, EDNRB, RGS5) that by qRT-PCR associate with survival
Biology-driven analyses
    Vasselli et al. [25] 2003 51 cc
6 papillary
1 unknown
Unsupervised 2 clusters of metastatic tumors with survival difference
    Skubitz et al. [35] 2006 16 cc
21 normal
Unsupervised 2 subtypes distinguishable by 546 genes, with possible pathway differences
    Zhao et al. [32•] 2006 177 cc Survival 259 genes associated with survival by univariate and multivariate analysis
    Gordan et al. [16••] 2008 21 cc Wild-type VHL vs H1H2 vs H2 tumors 3 groups have distinct biological pathways; H2 tumors overexpress c-Myc, leading to increased proliferation
    Zhao et al. [33] 2009 177 cc Biology of survival gene set Good prognosis tumors resemble normal renal cortex or glomerulus; poor prognosis tumors associated with wound healing and loss of differentiation gene sets
    Brannon et al. [36] 2010 48 cc
18 normal
Unsupervised consensus clustering 2 subtypes of cc (ccA and ccB) with pathway and survival differences, differentiable by < 120 probes
Gene expression and cytogenetics/sequencing analyses
    Furge et al. [18] 2004 60 cc
5 papillary
16 chromophobe
Histological classification by virtual cytogenetics 1018 gene classifier and cytogenetic classifier to distinguish between 3 subtypes, 99% and 81% accuracy, respectively
    Sultmann et al. [19] 2005 65 cc
13 papillary
9 chromophobe
25 normal
Cytogenetics; metastases and survival 136 genes significantly associated with cytogenetic abnormalities; 45 genes associated with survival; 85 genes associated with metastasis formation
    Beroukhim et al. [21•] 2009 49 sporadic cc
5 metastases
36 VHL tumors
VHL disease vs sporadic clear cell VHL disease and sporadic clear cell tumors have similar gene expression and cytogenetic profiles, but sporadic cases have more frequent alterations
    Dalgliesh et al. [17••] 2010 96 cc Genetics by sequencing Mutations in histone modification and DNA damage repair genes may be important in RCC development or progression

cc—clear cell; H1H2—HIF-1 and HIF-2 overexpressing; H2—HIF-2 only overexpressing; PCR—polymerase chain reaction; RCC—renal cell carcinoma; VCAM—vascular cell adhesion molecule; VHL—von Hippel Lindau.