Molecular Correlate to Gleason Grade in Prostate Adenocarcinoma
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE5132 | GEO | 2006/07/14
SECONDARY ACCESSION(S): PRJNA96639
REPOSITORIES: GEO
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Project description:In this dataset, we report the gene expression of adjacent Gleason 3 and Gleason 4 foci microdissected from the same prostate cancer sample. We found a striking similarity between adjacent G3 and G4 tumors, consistent with their clonal origin, but very few recurrently up- or down- regulated genes across patients.
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Project description:The identification of novel oncogenic and druggable targets in patient subgroups with poor prognosis may help to develop corresponding targeted therapy approaches. Microarray data analyses of 59 prostate cancer and 39 benign tissue samples revealed major transcriptional differences. More than 5.000 genes were identified to be differentially expressed between matched tumor and benign samples. In the prostate cancer samples we identified 144 differentially expressed associated with Gleason pattern. Illumina microarray experiments were done from of 59 prostate cancer and 39 matched benign tissue samples. We analyzed for differentially expressed genes between tumor and benign tissues, and between tumors with higher Gleason patter (4+3 and higher) against lower Gleason patter (3+4 and lower).
2012-10-19 | E-GEOD-32571 | biostudies-arrayexpress
Project description:The identification of novel oncogenic and druggable targets in patient subgroups with poor prognosis may help to develop corresponding targeted therapy approaches. Microarray data analyses of 59 prostate cancer and 39 benign tissue samples revealed major transcriptional differences. More than 5.000 genes were identified to be differentially expressed between matched tumor and benign samples. In the prostate cancer samples we identified 144 differentially expressed associated with Gleason pattern.
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Project description:PSA screening has led to enormous overtreatment of prostate cancer, due to the inability to distinguish potentially lethal disease at diagnosis. We reasoned that by identifying an mRNA signature of Gleason grade, the best predictor of prognosis, we could improve prediction of lethal disease among men with moderate Gleason 7 tumors, the most common grade, and most indeterminate in terms of prognosis. Using the complementary DNA (cDNA)–mediated annealing, selection, extension, and ligation assay, we measured the mRNA expression of 6,100 genes in prostate tumor tissue in the Swedish Watchful Waiting cohort (N=358) and Physicians’ Health Study (PHS; N=109). We developed an mRNA signature of Gleason comparing individuals with Gleason ≤6 to those with Gleason ≥8 tumors, and applied the model among Gleason 7 cases to discriminate lethal cases. We built a157-gene signature using the Swedish data that predicted Gleason with low misclassification (AUC=0.91); when this signature was tested in the PHS validation set, the discriminatory ability remained high (AUC=0.94). In men with Gleason 7 tumors, who were excluded from the model building, the signature significantly improved the prediction of lethal disease beyond knowing whether the Gleason score was 4+3 or 3+4 (p=0.006). Our expression signature and the genes identified may improve our understanding of the de-differentiation process of prostate tumors. Additionally, the signature may have clinical applications among men with Gleason 7, by further estimating their risk of lethal prostate cancer and thereby guiding therapy decisions to improve outcomes and reduce overtreatment.
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Project description:PSA screening has led to enormous overtreatment of prostate cancer, due to the inability to distinguish potentially lethal disease at diagnosis. We reasoned that by identifying an mRNA signature of Gleason grade, the best predictor of prognosis, we could improve prediction of lethal disease among men with moderate Gleason 7 tumors, the most common grade, and most indeterminate in terms of prognosis. Using the complementary DNA (cDNA)M-bM-^@M-^Smediated annealing, selection, extension, and ligation assay, we measured the mRNA expression of 6,100 genes in prostate tumor tissue in the Swedish Watchful Waiting cohort (N=358) and PhysiciansM-bM-^@M-^Y Health Study (PHS; N=109). We developed an mRNA signature of Gleason comparing individuals with Gleason M-bM-^IM-$6 to those with Gleason M-bM-^IM-%8 tumors, and applied the model among Gleason 7 cases to discriminate lethal cases. We built a157-gene signature using the Swedish data that predicted Gleason with low misclassification (AUC=0.91); when this signature was tested in the PHS validation set, the discriminatory ability remained high (AUC=0.94). In men with Gleason 7 tumors, who were excluded from the model building, the signature significantly improved the prediction of lethal disease beyond knowing whether the Gleason score was 4+3 or 3+4 (p=0.006). Our expression signature and the genes identified may improve our understanding of the de-differentiation process of prostate tumors. Additionally, the signature may have clinical applications among men with Gleason 7, by further estimating their risk of lethal prostate cancer and thereby guiding therapy decisions to improve outcomes and reduce overtreatment. 198 cases from the population-based Swedish-Watchful Waiting cohort. The cohort consists of men with localized prostate cancer (clinical stage T1-T2, Mx, N0); expression profiles from tumors with Gleason M-bM-^IM-%8 (N=89) were compared to those from tumors with Gleason M-bM-^IM-$6 (N=109)
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