Prostate Cancer Gleason Score
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Human Unigene3.1 cDNA Array 37.5K v1.0
SUBMITTER: 
Nicole Chui Pressinotti
PROVIDER: GSE15484 | GEO | 2010-03-31
SECONDARY ACCESSION(S): PRJNA115927
REPOSITORIES: GEO
Dataset's files
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Publications
Differential expression of apoptotic genes PDIA3 and MAP3K5 distinguishes between low- and high-risk prostate cancer.
Pressinotti Nicole Chui NC Klocker Helmut H Schäfer Georg G Luu Van-Duc VD Ruschhaupt Markus M Kuner Ruprecht R Steiner Eberhard E Poustka Annemarie A Bartsch Georg G Sültmann Holger H
Molecular cancer 20091227
<h4>Background</h4>Despite recent progress in the identification of genetic and molecular alterations in prostate cancer, markers associated with tumor progression are scarce. Therefore precise diagnosis of patients and prognosis of the disease remain difficult. This study investigated novel molecular markers discriminating between low and highly aggressive types of prostate cancer.<h4>Results</h4>Using 52 microdissected cell populations of low- and high-risk prostate tumors, we identified via g ...[more]
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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. Overall design: 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).
| GSE32571 | GEO
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 | ArrayExpress
Project description:Diagnosis of prostate cancer is based on histologic evaluation of tumor architecture using a system known as the "Gleason score." This diagnostic paradigm, while the standard of care, is time-consuming, shows intraobserver variability, and provides no information about the altered metabolic pathways, which result in altered tissue architecture. Characterization of the molecular composition of prostate cancer and how it changes with respect to the Gleason score (GS) could enable a more objective and faster diagnosis. It may also aid in our understanding of disease onset and progression. In this work, we present mass spectrometry imaging for identification and mapping of lipids and metabolites in prostate tissue from patients with known prostate cancer with GS from 6 to 9. A gradient of changes in the intensity of various lipids was observed, which correlated with increasing GS. Interestingly, these changes were identified in both regions of high tumor cell density, and in regions of tissue that appeared histologically benign, possibly suggestive of precancerous metabolomic changes. A total of 31 lipids, including several phosphatidylcholines, phosphatidic acids, phosphatidylserines, phosphatidylinositols, and cardiolipins were detected with higher intensity in GS (4+3) compared with GS (3+4), suggesting they may be markers of prostate cancer aggression. Results obtained through mass spectrometry imaging studies were subsequently correlated with a fast, ambient mass spectrometry method for potential use as a clinical tool to support image-guided prostate biopsy. IMPLICATIONS: In this study, we suggest that metabolomic differences between prostate cancers with different Gleason scores can be detected by mass spectrometry imaging.
2019-01-01 | S-EPMC6497547 | BioStudies
Project description:Prostate cancer incidence is sensitive to screening practices, however the impact of recent screening recommendations from the United States Preventative Services Task Force on prostate cancer incidence by age, stage, race, and Gleason score is unknown. This study described the timing and magnitude of changes in prostate cancer incidence trends in the United States by month of diagnosis, and evaluated trends by age, Gleason score, and stage at diagnosis. We analyzed prostate cancer incidence trends using Surveillance, Epidemiology, and End Results (SEER) program data for men diagnosed with invasive prostate cancer from 2007 through 2012. JoinPoint analysis was used to detect changes in the rate of annual percent change (APC) in prostate cancer incidence for all diagnoses and by age, Gleason score, race, and stage. Prostate cancer incidence declined at an estimated -19.6% APC beginning May 2011. This decline was observed in all age groups. Low-grade tumors (Gleason score ≤6) showed a steeper decline (-29.1% APC) than high-grade tumors (Gleason score 8-10: -10.8% APC). Only stage I/II and stage III tumors saw declines (-24.2% and -16.7% APC, respectively). A sharp decline in prostate cancer incidence began before release of the United States Preventative Services Task Force October 2011 draft and May 2012 final screening recommendation. The greatest change occurred with incidence of low-grade tumors, although there is concern that some high-grade tumors may now go undetected.
2016-01-01 | S-EPMC4708896 | BioStudies
Project description:Background. Protective factors against Gleason upgrading and its impact on outcomes after surgery warrant better definition. Patients and Methods. Consecutive 343 patients were categorized at biopsy (BGS) and prostatectomy (PGS) as Gleason score, ?6, 7, and ?8; 94 patients (27.4%) had PSA recurrence, mean followup 80.2 months (median 99). Independent predictors of Gleason upgrading (logistic regression) and disease-free survival (DFS) (Kaplan-Meier, log-rank) were determined. Results. Gleason discordance was 45.7% (37.32% upgrading and 8.45% downgrading). Upgrading risk decreased by 2.4% for each 1?g of prostate weight increment, while it increased by 10.2% for every 1?ng/mL of PSA, 72.0% for every 0.1 unity of PSA density and was 21 times higher for those with BGS 7. Gleason upgrading showed increased clinical stage (P = 0.019), higher tumor extent (P = 0.009), extraprostatic extension (P = 0.04), positive surgical margins (P < 0.001), seminal vesicle invasion (P = 0.003), less "insignificant" tumors (P < 0.001), and also worse DFS, ? (2) = 4.28, df = 1, P = 0.039. However, when setting the final Gleason score (BGS ?6 to PGS 7 versus BGS 7 to PGS 7), avoiding allocation bias, DFS impact is not confirmed, ? (2) = 0.40, df = 1, P = 0.530.Conclusions. Gleason upgrading is substantial and confers worse outcomes. Prostate weight is inversely related to upgrading and its protective effect warrants further evaluation.
2013-01-01 | S-EPMC3833008 | BioStudies
Project description:Purpose: The molecular features that account for the distinct histology and aggressive biological behavior of Gleason pattern 4 (Gp4) versus Gp3 prostate cancer, and whether Gp3 tumors progress directly to Gp4, remain to be established.Experimental Design: Whole-exome sequencing and transcriptome profiling of laser capture-microdissected adjacent Gp3 and cribiform Gp4 were used to determine the relationship between these entities.Results: Sequencing confirmed that adjacent Gp3 and Gp4 were clonal based on multiple shared genomic alterations. However, large numbers of unique mutations in the Gp3 and Gp4 tumors showed that the Gp4 were not derived directly from the Gp3. Remarkably, the Gp3 tumors retain their indolent-appearing morphology despite acquisition of multiple genomic alterations, including tumor suppressor losses. Although there were no consistent genomic alterations that distinguished Gp3 from Gp4, pairwise transcriptome analyses identified increased c-Myc and decreased p53 activity in Gp4 versus adjacent clonal Gp3 foci.Conclusions: These findings establish that at least a subset of Gp3 and aggressive Gp4 tumors have a common origin, and support a branched evolution model wherein the Gp3 and Gp4 tumors emerge early from a common precursor and subsequently undergo substantial divergence. Genomic alterations detectable in the Gp3 may distinguish these tumors from truly indolent Gp3. Screening for a panel of these genomic alterations in men who have prostate biopsies showing only Gp3 (Gleason score 6, Gs6) may allow for more precise selection of men who can be safely managed by active surveillance versus those who may benefit from further intervention. Clin Cancer Res; 23(14); 3823-33. ©2017 AACR.
2017-01-01 | S-EPMC5511561 | BioStudies
Project description:Systemic inflammation and immune responses are reported to be associated with progressive prostate cancer. In this study, we explored which among the fractions of white blood cell (WBC) and C-reactive protein (CRP) level were associated with high Gleason score prostate cancer. Prostate needle biopsy was performed in 966 men with suspicion of prostate cancer. We assessed age, serum prostate-specific antigen (PSA), prostate volume, WBC count, fractions of WBCs (neutrophils, lymphocytes, monocytes, basophils, and eosinophils), and CRP level before biopsy for associations with biopsy findings. Among all men, 553 (57.2%) were positive for prostate cancer including 421 with high Gleason score cancer (Gleason score ?7). Age, PSA, PSA density (PSAD), serum monocyte fraction of WBC, monocyte-to-lymphocyte ratio (MLR), and CRP were significantly associated with high Gleason score cancer (p<0.01). Multivariate analysis showed that age, PSA, PSAD, and serum monocyte fraction were significantly associated with high Gleason score prostate cancer (p <0.01). In 571 patients with PSA of <10 ng/ml, age, PSA, PSAD, serum WBC count, neutrophil fraction, monocyte fraction, and MLR were significantly associated with high Gleason score prostate cancer (p<0.05). Multivariate analysis showed that age, PSAD, and serum monocyte fraction were significantly associated with high Gleason score prostate cancer (p<0.01). The monocyte fraction of WBCs was increased in patients with high Gleason score prostate cancer, suggesting an interaction of monocytes with the progression of prostate cancer.
1000-01-01 | S-EPMC5471051 | BioStudies
Project description:Purpose: Use of quantitative imaging features and encoding the intra-tumoral heterogeneity from multi-parametric magnetic resonance imaging (mpMRI) for the prediction of Gleason score is gaining attention as a non-invasive biomarker for prostate cancer (PCa). This study tested the hypothesis that radiomic features, extracted from mpMRI, could predict the Gleason score pattern of patients with PCa. Methods: This analysis included T2-weighted (T2-WI) and apparent diffusion coefficient (ADC, computed from diffusion-weighted imaging) scans of 99 PCa patients from The Cancer Imaging Archive (TCIA). A total of 41 radiomic features were calculated from a local tumor sub-volume (i.e., regions of interest) that is determined by a centroid coordinate of PCa volume, grouped based on their Gleason score patterns. Kruskal-Wallis and Spearman's rank correlation tests were used to identify features related to Gleason score groups. Random forest (RF) classifier model was used to predict Gleason score groups and identify the most important signature among the 41 radiomic features. Results: Gleason score groups could be discriminated based on zone size percentage, large zone size emphasis and zone size non-uniformity values (p < 0.05). These features also showed a significant correlation between radiomic features and Gleason score groups with a correlation value of -0.35, 0.32, 0.42 for the large zone size emphasis, zone size non-uniformity and zone size percentage, respectively (corrected p < 0.05). RF classifier model achieved an average of the area under the curves of the receiver operating characteristic (ROC) of 83.40, 72.71, and 77.35% to predict Gleason score groups (G1) = 6; 6 < (G2) < (3 + 4) and (G3) ? 4 + 3, respectively. Conclusion: Our results suggest that the radiomic features can be used as a non-invasive biomarker to predict the Gleason score of the PCa patients.
2018-01-01 | S-EPMC6305278 | BioStudies
Project description:Heat shock protein 27 (Hsp-27) encoded by gene HSPB1 is a critical regulator of the behavioral phenotype of human prostate cancer (PCa) cells, enhanced expression being associated with highly aggressive disease and poor clinical outcome. In contrast, the protein is not expressed in PCas of low malignant potential. To gain insight into the mechanism regulating its expression, we tested the hypothesis that differential methylation of CpG islands within HSPB1 controls transcription and subsequent translation of the gene.We studied prostate epithelial cell lines and tissue biopsies, including 59 BPH and 415 PCas, of which 367 were a cohort of men with up to 20 years of follow-up. Methylation across the gene (DNA methylation (DNAme)) was assayed by pyrosequencing. Hsp-27 expression was assessed by western blot and immunohistochemistry.In cancer tissues, methylation increased in a 3' direction (P < 0.0001) whereas in benign hyperplasia methylation was constantly below 5%, a cutoff giving a specificity of 100% and sensitivity of 50%. Although methylation of the promoter region was significantly discriminating between benign and malignant prostatic epithelia, it compared poorly with methylation of the first intron. The prognostic value of HSPB1 DNAme was confirmed by both univariate (hazard ratio 1.77 per 50% increment, P = 0.02) and multivariate models. Interaction between HSPB1 methylation and Gleason score revealed high DNAme to be a reliable prognostic marker of poor outcome in men with low Gleason score (P = 0.014).Our data indicate CpG methylation of the first HSPB1 intron to be an important biomarker that identifies aggressive PCas otherwise regarded as low risk by current clinical criteria but that, biologically, require immediate active management.
2013-01-01 | S-EPMC3572391 | BioStudies
Project description:Prostate carcinoma (PRAD) is one of the most frequently diagnosed malignancies amongst men worldwide. It is well-known that androgen receptor (AR) plays a pivotal role in a vast majority of prostate tumors. However, recent evidence emerged stating that estrogen receptors (ERs) may also contribute to prostate tumor development. Moreover, progression and aggressiveness of prostate cancer may be associated with differential expression genes of epithelial-to-mesenchymal transition (EMT). Therefore we aimed to assess the significance of receptors status as well as EMT marker genes expression among PRAD patients in accordance to their age and Gleason score.We analyzed TCGA gene expression profiles of 497 prostate tumor samples according to 43 genes involved in EMT and 3 hormone receptor genes (AR, ESR1, ESR2) as well as clinical characteristic of cancer patients. Then patients were divided into four groups according to their age and 5 groups according to Gleason score. Next, we evaluated PRAD samples according to relationship between the set of variables in different combinations and compared differential expression in subsequent groups of patients. The analysis was applied using R packages: FactoMineR, gplots, RColorBrewer and NMF.MFA analysis resulted in distinct grouping of PRAD patients into four age categories according to expression level of AR, ESR1 and ESR2 with the most distinct group of age less than 50 years old. Further investigations indicated opposite expression profiles of EMT markers between different age groups as well as strong association of EMT gene expression with Gleason score. We found that depending on age of prostate cancer patients and Gleason score EMT genes with distinctly altered expression are: KRT18, KRT19, MUC1 and COL4A1, CTNNB1, SNAI2, ZEB1 and MMP3.Our major observation is that prostate cancer from patients under 50 years old compared to older ones has entirely different EMT gene expression profiles showing potentially more aggressive invasive phenotype, despite Gleason score classification.
2017-01-01 | S-EPMC5714348 | BioStudies