| 1 |
Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016 [J]. CA Cancer J Clin, 2016, 66(1):7-30.
|
| 2 |
Chen W, Zheng R, Baade PD, et al. Cancer statistics in China, 2015 [J]. CA Cancer J Clin, 2016, 66(2):115-132.
|
| 3 |
Humphrey PA. Gleason grading and prognostic factors in carcinoma of the prostate [J]. Mod Pathol, 2004, 17(3):292-306.
|
| 4 |
Tosoian JJ, Trock BJ, Landis P, et al. Active surveillance program for prostate cancer: an update of the Johns Hopkins experience [J]. J Clin Oncol, 2011, 29(16):2185-2190.
|
| 5 |
Robinson D, Van Allen EM, Wu YM, et al. Integrative clinical genomics of advanced prostate cancer [J]. Cell, 2015, 162(2):454.
|
| 6 |
Watson PA, Arora VK, Sawyers CL. Emerging mechanisms of resistance to androgen receptor inhibitors in prostate cancer [J]. Nat Rev Cancer, 2015, 15(12):701-711.
|
| 7 |
丁奕星，齐隽. TMPRSS2-ETS融合基因在前列腺癌中的研究进展及临床应用前景 [J]. 上海交通大学学报(医学版), 2011, 31(6):852-857.
|
| 8 |
Perner S, Demichelis F, Beroukhim R, et al. TMPRSS2: ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer [J]. Cancer Res, 2006, 66(17):8337-8341.
|
| 9 |
Tomlins SA, Bjartell A, Chinnaiyan AM, et al. ETS gene fusions in prostate cancer: from discovery to daily clinical practice [J]. Eur Urol, 2009, 56(2):275-286.
|
| 10 |
Pettersson A, Graff RE, Bauer SR, et al. The TMPRSS2: ERG rearrangement, ERG expression, and prostate cancer outcomes: a cohort study and meta-analysis [J]. Cancer Epidemiol Biomarkers Prev, 2012, 21(9):1497-509.
|
| 11 |
Giannico GA, Arnold SA, Gellert LL, et al. New and emerging diagnostic and prognostic immunohistochemical biomarkers in prostate pathology [J]. Adv Anat Pathol, 2017, 24(1):35-44.
|
| 12 |
Tomlins SA, Laxman B, Dhanasekaran SM, et al. Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer [J]. Nature, 2007, 448(7153):595-599.
|
| 13 |
Lin DW, Newcomb LF, Brown EC, et al. Urinary TMPRSS2: ERG and PCA3 in an active surveillance cohort: results from a baseline analysis in the Canary Prostate Active Surveillance Study [J]. Clin Cancer Res, 2013, 19(9):2442-2450.
|
| 14 |
Paju A, Hotakainen K, Cao Y, et al. Increased expression of tumor-associated trypsin inhibitor, TATI, in prostate cancer and in androgen-independent 22Rv1 cells [J]. Eur Urol, 2007, 52(6):1670-1679.
|
| 15 |
Tomlins SA, Rhodes DR, Yu J, et al. The role of SPINK1 in ETS rearrangement-negative prostate cancers [J]. Cancer Cell, 2008, 13(6):519-528.
|
| 16 |
滕梁红，高巍，卢德宏, 等. ERG和SPINK1蛋白在前列腺癌中表达的相互排斥性及其与预后的相关性 [J]. 中华病理学杂志, 2014, 43(3):149-153.
|
| 17 |
Leinonen KA, Tolonen TT, Bracken H, et al. Association of SPINK1 expression and TMPRSS2:ERG fusion with prognosis in endocrine-treated prostate cancer [J]. Clin Cancer Res, 2010, 16(10):2845-2851.
|
| 18 |
Zhang X, Yin X, Shen P, et al. The association between SPINK1 and clinical outcomes in patients with prostate cancer: a systematic review and meta-analysis [J]. Onco Targets Ther, 2017, 10:3123-3130.
|
| 19 |
郭鹏. Molecular Cell: SPOP通过促进ERG蛋白泛素化和降解抑制前列腺癌进展 [J]. 现代泌尿外科杂志, 2015, 20(10):749.
|
| 20 |
Abeshouse A, Ahn J, Akbani R, et al. The molecular taxonomy of primary prostate cancer [J]. Cell, 2015, 163(4):1011-1025.
|
| 21 |
Kwon JE, La M, Oh KH, et al. BTB domain-containing speckle-type POZ protein (SPOP) serves as an adaptor of Daxx for ubiquitination by Cul3-based ubiquitin ligase [J]. J Biol Chem, 2006, 281(18):12664-12672.
|
| 22 |
Zhang Q, Shi Q, Chen Y, et al. Multiple Ser/Thr-rich degrons mediate the degradation of Ci/Gli by the Cul3-HIB/SPOP E3 ubiquitin ligase [J]. Proc Natl Acad Sci U S A, 2009, 106(50):21191-21196.
|
| 23 |
Wu F, Dai X, Gan W, et al. Prostate cancer-associated mutation in SPOP impairs its ability to target Cdc20 for poly-ubiquitination and degradation [J]. Cancer Lett, 2017, 385:207-214.
|
| 24 |
Geng C, He B, Xu L, et al. Prostate cancer-associated mutations in speckle-type POZ protein (SPOP) regulate steroid receptor coactivator 3 protein turnover [J]. Proc Natl Acad Sci U S A, 2013, 110(17):6997-7002.
|
| 25 |
An J, Wang C, Deng Y, et al. Destruction of full-length androgen receptor by wild-type SPOP, but not prostate-cancer-associated mutants [J]. Cell Rep, 2014, 6(4):657-669.
|
| 26 |
An J, Ren S, Murphy SJ, et al. Truncated ERG Oncoproteins from TMPRSS2-ERG fusions are resistant to SPOP-mediated proteasome degradation [J]. Mol Cell, 2015, 59(6):904-916.
|
| 27 |
Blattner M, Lee DJ, O′reilly C, et al. SPOP mutations in prostate cancer across demographically diverse patient cohorts [J]. Neoplasia, 2014, 16(1):14-20.
|
| 28 |
Liu W, Lindberg J, Sui G, et al. Identification of novel CHD1-associated collaborative alterations of genomic structure and functional assessment of CHD1 in prostate cancer [J]. Oncogene, 2012, 31(35):3939-3948.
|
| 29 |
Huang S, Gulzar ZG, Salari K, et al. Recurrent deletion of CHD1 in prostate cancer with relevance to cell invasiveness [J]. Oncogene, 2012, 31(37):4164-4170.
|
| 30 |
Garcia-Flores M, Casanova-Salas I, Rubio-Briones J, et al. Clinico-pathological significance of the molecular alterations of the SPOP gene in prostate cancer [J]. Eur J Cancer, 2014, 50(17):2994-3002.
|
| 31 |
Vinceneux A, Bruyere F, Haillot O, et al. Ductal adenocarcinoma of the prostate: clinical and biological profiles [J]. Prostate, 2017, 77(12):1242-1250.
|
| 32 |
Mulholland DJ, Kobayashi N, Ruscetti M, et al. Pten loss and RAS/MAPK activation cooperate to promote EMT and metastasis initiated from prostate cancer stem/progenitor cells [J]. Cancer Res, 2012, 72(7):1878-1889.
|
| 33 |
Jin G, Kim MJ, Jeon HS, et al. PTEN mutations and relationship to EGFR, ERBB2, KRAS, and TP53 mutations in non-small cell lung cancers [J]. Lung Cancer, 2010, 69(3):279-283.
|
| 34 |
Barnett CM, Heinrich MC, Lim J, et al. Genetic profiling to determine risk of relapse-free survival in high-risk localized prostate cancer [J]. Clin Cancer Res, 2014, 20(5):1306-1312.
|
| 35 |
Ronen A, Glickman BW. Human DNA repair genes [J]. Environ Mol Mutagen, 2001, 37(3):241-283.
|
| 36 |
Amin Al Olama A, Kote-Jarai Z, Schumacher FR, et al. A meta-analysis of genome-wide association studies to identify prostate cancer susceptibility loci associated with aggressive and non-aggressive disease [J]. Hum Mol Genet, 2013, 22(2):408-415.
|
| 37 |
Helfand BT, Roehl KA, Cooper PR, et al. Associations of prostate cancer risk variants with disease aggressiveness: results of the NCI-SPORE Genetics Working Group analysis of 18,343 cases [J]. Hum Genet, 2015, 134(4):439-450.
|
| 38 |
Ciccarese C, Massari F, Iacovelli R, et al. Prostate cancer heterogeneity: discovering novel molecular targets for therapy [J]. Cancer Treat Rev, 2017, 54:68-73.
|