Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA289378 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Accurate prediction of prostate cancer clinical courses remains elusive. In this study, we performed whole genome copy number analysis on leukocytes of 273 prostate cancer patients using Affymetrix SNP6.0 chip. Copy number variations (CNV) were found across all chromosomes of the human genome. An average of 152 CNV fragments per genome was identified in the leukocytes from prostate cancer patients. The size distributions of CNV in the genome of leukocytes were highly correlative with prostate cancer aggressiveness. A prostate cancer outcome prediction model was developed based on large size ratio of CNV from the leukocyte genomes. This prediction model generated an average prediction rate of 75.2%, with sensitivity of 77.3% and specificity of 69.0% for prostate cancer recurrence. When combined with Nomogram and the status of fusion transcripts, the average prediction rate was improved to 82.5% with sensitivity of 84.8% and specificity of 78.2%. In addition, the leukocyte prediction model was 62.6% accurate in predicting short prostate specific antigen doubling time. When combined with Gleason’s grade, Nomogram and the status of fusion transcripts, the prediction model generated a correct prediction rate of 77.5% with 73.7% sensitivity and 80.1% specificity. To our knowledge, this is the first study showing that CNVs in leukocyte genomes are predictive of clinical outcomes of a human malignancy.
2017-02-09 | GSE70650 | GEO
Project description:Copy Number Variations in Genomic Disorders
| PRJNA75521 | ENA
Project description:The level of copy number alteration (CNA), or CNA burden, in cancer genomes is associated with recurrence and metastasis in prostate cancer. As clinical genomic analysis of tumors and tumor biopsies becomes widespread, there is a growing need to understand the prognostic factors captured by genomic features, especially in prostate cancer where conservative treatment approaches are increasingly common. Here we analyze the CNA landscape of conservatively treated prostate cancer in a prostate cancer biopsy and transurethral resection cohort. We find that CNA burden is prognostic for metastasis and cancer-specific survival, independent of clinical prognostic factors such as Gleason and CAPRA score, in conservatively treated prostate cancer.
2018-08-18 | GSE103665 | GEO
Project description:The genomic and immune landscapes of prostate cancer differ by self-identified race. However, few studies have examined the genome-wide copy number landscape and immune content of matched cohorts with genetic ancestry data and clinical outcomes. Here, we assessed prostate cancer somatic copy number alterations (sCNA) and tumor immune content of a grade-matched, surgically-treated cohort of 145 self-identified Black (BL) and 145 self-identified white (WH) patients with genetic ancestry estimation. A generalized linear model adjusted with age, pre-operative PSA, and Grade Group and filtered for germline copy number variations (gCNV) identified 143 loci where copy number varied significantly by percent African ancestry, clustering on chromosomes 6p, 10q, 11p, 12p, and 17p. Multivariable Cox regression models adjusted for age, pre-operative PSA levels, and Grade Group revealed that chromosome 8q gains (including MYC) were significantly associated with biochemical recurrence and metastasis, independent of genetic ancestry. Finally, regulatory T-cell density in BL and WH patients was significantly correlated with percent genome altered, and these findings were validated in the TCGA cohort. Taken together, our findings identify specific sCNA linked to genetic ancestry and outcome in primary prostate cancer and demonstrate that regulatory T-cell infiltrate varies by global sCNA burden in primary disease.
2023-05-31 | GSE221219 | GEO
Project description:Somatic DNA copy number variations (CNVs) are prevalent in cancer and can drive cancer progression albeit with often uncharacterized roles in altering cell signaling states. We developed a computational approach to predict regulators of signaling from the integrative analysis of genomic and proteomic pan-cancer datasets. Among the predictions, we identified ARHGEF17 to be a regulator of hippo-signaling and performed (phospho)proteomics analysis to test these predictions.
2021-04-06 | PXD021031 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE4016: Gene expression variations in prostate cancer cell lines GSE4017: DNA copy number changes in prostate cancer cell lines Abstract: BACKGROUND: The aim of this study was to characterize gene expression and DNA copy number profiles in androgen sensitive (AS) and androgen insensitive (AI) prostate cancer cell lines on a genome-wide scale. METHODS: Gene expression profiles and DNA copy number changes were examined using DNA microarrays in eight commonly used prostate cancer cell lines. Chromosomal regions with DNA copy number changes were identified using cluster along chromosome (CLAC). RESULTS: There were discrete differences in gene expression patterns between AS and AI cells that were not limited to androgen-responsive genes. AI cells displayed more DNA copy number changes, especially amplifications, than AS cells. The gene expression profiles of cell lines showed limited similarities to prostate tumors harvested at surgery. CONCLUSIONS: AS and AI cell lines are different in their transcriptional programs and degree of DNA copy number alterations. This dataset provides a context for the use of prostate cancer cell lines as models for clinical cancers. Refer to individual Series
2006-03-07 | E-GEOD-4396 | biostudies-arrayexpress
Project description:Adenocarcinoma at the gastroesophageal junction (ACGEJ) has dismal clinical outcomes and there are currently few specific effective therapies because of limited knowledge on its genomic and transcriptomic alterations. The present study investigates genomic and transcriptomic changes in ACGEJ from Chinese patients and analyzes their drug vulnerabilities and associations with the survival time. Here we show that the major genomic changes of Chinese ACGEJ patients are chromosome instability promoted tumorigenic focal copy-number variations and COSMIC Signature 17-featured single nucleotide variations. We provide a comprehensive profile of genetic changes that are potentially vulnerable to existing therapeutic agents and identify Signature 17-correlated IFN-α response pathway as a prognostic marker that might have practical value for clinical prognosis of ACGEJ. These findings further our understanding on the molecular biology of ACGEJ and may help develop more effective therapeutic strategies.
2020-11-09 | GSE159721 | GEO
Project description:Meningiomas, as the most common primary tumor of the central nervous system, are known to harbor genomic aberrations that associate with clinical phenotypes. Here we performed genome-wide genotyping for cranial meningiomas in 383 Chinese patients and identified 9,821 copy number variations (CNVs).
2020-03-28 | GSE147673 | GEO
Project description:Copy number analyses of regionally separated intratumoral biopsies of prostate cancers. Intratumoral heterogeneity (ITH) leads to regional biases of the mutational landscape in a single tumor and may influence the single biopsy-based clinical diagnosis and treatment decision. To evaluate the extent of ITH in unifocal prostate cancers (PCAs) that had not been sought, we analyzed multiple regional biopsies from three PCAs using DNA copy number analyses. DNA copy number showed ITH including regional biases in the presentation of a well-known driver of TMPRSS2-ERG fusion. Our analyses identified a substantial level of genetic ITH in unifocal PCAs at the genomic levels, which should be taken into account for the curation of biomarkers in the clinical setting.
2014-01-18 | GSE54185 | GEO