scholarly journals The Cancer Genome Anatomy Project: EST Sequencing and the Genetics of Cancer Progression

Neoplasia ◽  
1999 ◽  
Vol 1 (2) ◽  
pp. 101-106 ◽  
Author(s):  
David B. Krizman ◽  
Lukas Wagner ◽  
Alex Lash ◽  
Robert L. Strausberg ◽  
Michael R. Emmert-Buck
2002 ◽  
Vol 20 (7-8) ◽  
pp. 1038-1050 ◽  
Author(s):  
Robert L. Strausberg ◽  
Kenneth H. Buetow ◽  
Susan F. Greenhut ◽  
Lynette H. Grouse ◽  
Carl F. Schaefer

2001 ◽  
Vol 11 (11) ◽  
pp. S66-S71 ◽  
Author(s):  
Robert L Strausberg ◽  
Susan F Greenhut ◽  
Lynette H Grouse ◽  
Carl F Schaefer ◽  
Kenneth H Buetow

2019 ◽  
Author(s):  
Reka Toth ◽  
Heiko Schiffmann ◽  
Claudia Hube-Magg ◽  
Franziska Büscheck ◽  
Doris Höflmayer ◽  
...  

AbstractThe clinical course of prostate cancer (PCa) is highly variable, demanding an individualized approach to therapy and robust prognostic markers for treatment decisions. We present a random forest-based classification model to predict aggressive behaviour of PCa. DNA methylation changes between PCa cases with good or poor prognosis (discovery cohort with n=70) were used as input. The model was validated with data from two large independent PCa cohorts from the “International Cancer Genome Consortium” (ICGC) and “The Cancer Genome Atlas” (TCGA). Ranking of cancer progression-related DNA methylation changes allowed selection of candidate genes for additional validation by immunohistochemistry. We identified loss of ZIC2 protein expression, mediated by alterations in DNA methylation, as a promising novel prognostic biomarker for PCa in >12,000 tissue micro-array tumors. The prognostic value of ZIC2 proved to be independent from established clinico-pathological variables including Gleason grade, tumor stage, nodal stage and PSA. In summary, we have developed a PCa classification model, which either directly orviaexpression analyses of the identified top ranked candidate genes might help in decision making related to the treatment of prostate cancer patients.


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6301 ◽  
Author(s):  
Ping Wang ◽  
Zengli Zhang ◽  
Yujie Ma ◽  
Jun Lu ◽  
Hu Zhao ◽  
...  

Early detection and prediction of prognosis and treatment responses are all the keys in improving survival of ovarian cancer patients. This study profiled an ovarian cancer progression model to identify prognostic biomarkers for ovarian cancer patients. Mouse ovarian surface epithelial cells (MOSECs) can undergo spontaneous malignant transformation in vitro cell culture. These were used as a model of ovarian cancer progression for alterations in gene expression and signaling detected using the Illumina HiSeq2000 Next-Generation Sequencing platform and bioinformatical analyses. The differential expression of four selected genes was identified using the gene expression profiling interaction analysis (http://gepia.cancer-pku.cn/) and then associated with survival in ovarian cancer patients using the Cancer Genome Atlas dataset and the online Kaplan–Meier Plotter (http://www.kmplot.com) data. The data showed 263 aberrantly expressed genes, including 182 up-regulated and 81 down-regulated genes between the early and late stages of tumor progression in MOSECs. The bioinformatic data revealed four genes (i.e., guanosine 5′-monophosphate synthase (GMPS), progesterone receptor (PR), CD40, and p21 (cyclin-dependent kinase inhibitor 1A)) to play an important role in ovarian cancer progression. Furthermore, the Cancer Genome Atlas dataset validated the differential expression of these four genes, which were associated with prognosis in ovarian cancer patients. In conclusion, this study profiled differentially expressed genes using the ovarian cancer progression model and identified four (i.e., GMPS, PR, CD40, and p21) as prognostic markers for ovarian cancer patients. Future studies of prospective patients could further verify the clinical usefulness of this four-gene signature.


2001 ◽  
Vol 11 ◽  
pp. S66-S71 ◽  
Author(s):  
Robert L. Strausberg ◽  
Susan F. Greenhut ◽  
Lynette H. Grouse ◽  
Carl F. Schaefer ◽  
Kenneth H. Buetow

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