Table 1.
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.