Table 1.
Signature No | Phenotype | Samples used to generate signature | Author | Available genes | In Network* |
1 | Aggressive disease | Divided 66 microdissected prostate cancer specimens into two groups based on clinical aggressiveness defined as prostate-specific antigen (PSA) relapse following radical retropubic prostatectomy (RRP), distant metastasis, or cancer invasion into adjacent organs | Yu et al28 | 26 | Yes |
2 | Benign versus cancerous prostate tissue | Proteomic screen of microdissected prostate tissue embedded in tissue microarray for genes that best discriminated between benign, localized prostate cancer and metastatic disease | Bismar et al18 | 12 | Yes |
3 | High-grade tumor | Examined 12 microdissected RRP Gleason pattern 3 specimens compared with that of 12 Gleason pattern 4 and eight Gleason pattern 5 | True et al27 | 85 | Yes |
4 | PTEN pathway/poor prognosis | Comparison of 35 phosphatase and tensin homolog (PTEN) negative and 70 PTEN positive based on immunohistochemistry from stage II estrogen receptor status-matched breast cancer specimens. Signature subsequently validated in a historic dataset of 79 prostate cancer specimens19 described above in the Sun et al signature | Saal et al24 | 184 | Yes |
5 | Recurrence signature in solid tumors | Comparison of gene expression signature from 12 metastatic adenocarcinoma nodules from prostate and five other tissue types compared to 64 primary adenocarcinomas from primary tumors | Ramaswamy et al23 | 17 | Yes |
6 | Recurrent/aggressive disease | Evaluated 62 primary prostate tumors, 41 normal prostate specimens and nine lymph node metastases to develop a two-gene model of recurrence | Lapointe et al21 | 2 | No |
7 | Recurrent disease | 79 patient RRP specimens from patients with clinically localized prostate cancer. 39 cases with recurrence defined as three consecutive elevations in PSA for at least 5 years | Sun and Goodison26 | 11 | No |
8 | Recurrent disease | Using 21 prostate cancer samples, five genes using k-nn clustering were identified. | Singh et al25 | 5 | No |
9 | Recurrent disease /High-Gleason score | 512 candidate genes were analyzed for correlation with Gleason score from 71 patient RRP specimens (16 patients with relapsed disease defined as two consecutive PSA elevations over 84 months) | Bibikova et al16 | 16 | Yes |
10 | Relapse-free survival | Using 21 prostate cancer samples from Singh et al, the authors identified three signatures of recurrence and subsequently validated these signatures on a set of 79 tumors | Glinsky et al19 | 4/4/5 | No |
11 | Stem cell nature | Comparison of CD133+/α2β1hi cell culture specimens from 12 human prostate cancers compared with eight CD133–/α2β1low specimens. | Birnie et al17 | 22 | Yes |
12 | Systemic disease after relapse, Sig 1 | 213 patients with prostate cancer PSA relapse and no evidence of systemic disease (defined as a positive bone scan or CT scan) were compared with 213 patients with prostate cancer with PSA relapse | Nakagawa et al22 | 17 | No |
13 | Systemic disease after relapse, Sig 2 | Reanalysis of the above Nagakawa et al (Mayo Clinic dataset) as described in the Methods section | 133 | Yes |
In Network indicates that the listed gene signature connects to the Sanger cancer genes via SPAN and composes part of the interactor signature.