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TwitterGEO SuperSeries of expression profiling of prostatic neoplasms.
This SuperSeries is composed of the SubSeries GSE21034, GSE21035, and GSM525577. Each one concerns measuring prostate cancer genomes and different arrays of expression data, including DNA copy number, mRNA and microRNA. The prostate tumor samples originated from 218 patients.
Each dataset in the SubSeries share the same description: "Current knowledge of prostate cancer genomes is largely based on relatively small patient cohorts using single modality analysis platforms. Here we report concordant assessment of DNA copy number, mRNA and microRNA expression and focused exon resequencing in prostate tumors from 218 patients with primary or metastatic prostate cancer with a median of 5 years clinical follow-up, now made available as a public resource. Mutations in known, commonly mutated oncogenes and tumor suppressor genes such as PIK3CA, KRAS, BRAF and TP53 are present but generally rare. However, integrative analysis of mutations with copy number alterations (CNAs) and expression changes reveal alterations in the PI3K, RAS/RAF and androgen receptor (AR) pathways in nearly all metastatic samples and in a higher frequency of primary samples than previously suspected based on single-gene studies. Other new findings include evidence that the nuclear receptor coactivator NCOA2 functions as a driver oncogene in ~20 percent of primaries. Tumors with the androgen-driven TMPRSS2-ERG fusion were significantly associated with a small, previously unrecognized, prostate-specific 3p14 deletion that, through mRNA expression and resequencing analysis, implicates FOXP1, RYBP and SHQ1 as candidate cooperative tumor suppressors. Comparison of transcriptome and DNA copy number data from primary tumors for prognostic impact revealed that CNAs robustly define clusters of low- and high-risk disease beyond that achieved by Gleason score. In sum, this integrative genomic analysis of a substantial cohort of tumors clarifies the role of several known cancer pathways in prostate cancer, implicates several new ones, reveals a previously unappreciated role for CNAs in prognosis and provides a blueprint for clinical development of pathway inhibitors."
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The analysis of cell-free DNA (cfDNA) is rapidly emerging as a powerful approach to guide the clinical care of cancer patients. Several comprehensive cfDNA assays designed to detect mutations across several genes are now available. Here, we analyzed the use of a cfDNA panel in colorectal cancer (CRC) patients. Twenty-eight CRC patients with relapse or metastatic disease and 31 patients with no evidence of disease (NED) were enrolled. Genomic alterations in cfDNA were analyzed by the Oncomine™ Pan-Cancer Cell-Free Assay that detects hotspot mutations, small indels, copy number changes, and gene fusions across 52 genes. In the NED group, genomic alterations in cfDNA were detected in 12/31 patients (38.7%). The detection of alterations was more common in patients who were ≥60 years old, and the most common genomic alteration was a TP53 mutation. Fifty percent of the TP53 mutations were frequently or very frequently found in human cancers. Among 28 patients with relapse or metastatic disease, 22 (78.6%) had genomic alterations in cfDNA. The alterations were detected most frequently in TP53 (n = 10), followed by KRAS (n = 9). Actionable targets for CRC, including ERBB2 amplification and BRAF mutations, could be identified by this cfDNA assay. Compared with mutational profiling routinely analyzed using tumor samples, several additional targets with currently available therapies, including IDH1, IDH2, and PDGFRA mutations, were discovered. The cfDNA assay could identify potentially actionable targets for CRC. Identifying how to filter out cancer-like genomic alterations not derived from tumors remains a challenge.
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The Behavioral Risk Factor Surveillance System (BRFSS) is the Unites States’s premier system of health-related telephone surveys that collect state data about U.S. residents regarding their health-related risk behaviors, chronic health conditions, and use of preventive services. Established in 1984 with 15 states, BRFSS now collects data in all 50 states as well as the District of Columbia and three U.S. territories. BRFSS completes more than 400,000 adult interviews each year, making it the largest continuously conducted health survey system in the world.
By collecting behavioral health risk data at the state and local level, BRFSS has become a powerful tool for targeting and building health promotion activities.
2011 to present. BRFSS combined land line and cell phone prevalence data. BRFSS is a continuous, state-based surveillance system that collects information about modifiable risk factors for chronic diseases and other leading causes of death. Data will be updated annually as it becomes available. Detailed information on sampling methodology and quality assurance can be found on the BRFSS website (http://www.cdc.gov/brfss).
2,289,902 rows by 27 columns
Each entry contains the number and percent of responses to a survey question for a given year and demographic category sub-group.
Methodology Glossary Original data source Date Created: June 4, 2015 Last Updated: October 21, 2022
This data comes under public domain licensing. Please use it responsibly and ethically. Thank you :)
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TwitterRank, number of deaths, percentage of deaths, and age-specific mortality rates for the leading causes of death, by age group and sex, 2000 to most recent year.
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TwitterGEO SuperSeries of expression profiling of prostatic neoplasms.
This SuperSeries is composed of the SubSeries GSE21034, GSE21035, and GSM525577. Each one concerns measuring prostate cancer genomes and different arrays of expression data, including DNA copy number, mRNA and microRNA. The prostate tumor samples originated from 218 patients.
Each dataset in the SubSeries share the same description: "Current knowledge of prostate cancer genomes is largely based on relatively small patient cohorts using single modality analysis platforms. Here we report concordant assessment of DNA copy number, mRNA and microRNA expression and focused exon resequencing in prostate tumors from 218 patients with primary or metastatic prostate cancer with a median of 5 years clinical follow-up, now made available as a public resource. Mutations in known, commonly mutated oncogenes and tumor suppressor genes such as PIK3CA, KRAS, BRAF and TP53 are present but generally rare. However, integrative analysis of mutations with copy number alterations (CNAs) and expression changes reveal alterations in the PI3K, RAS/RAF and androgen receptor (AR) pathways in nearly all metastatic samples and in a higher frequency of primary samples than previously suspected based on single-gene studies. Other new findings include evidence that the nuclear receptor coactivator NCOA2 functions as a driver oncogene in ~20 percent of primaries. Tumors with the androgen-driven TMPRSS2-ERG fusion were significantly associated with a small, previously unrecognized, prostate-specific 3p14 deletion that, through mRNA expression and resequencing analysis, implicates FOXP1, RYBP and SHQ1 as candidate cooperative tumor suppressors. Comparison of transcriptome and DNA copy number data from primary tumors for prognostic impact revealed that CNAs robustly define clusters of low- and high-risk disease beyond that achieved by Gleason score. In sum, this integrative genomic analysis of a substantial cohort of tumors clarifies the role of several known cancer pathways in prostate cancer, implicates several new ones, reveals a previously unappreciated role for CNAs in prognosis and provides a blueprint for clinical development of pathway inhibitors."