12101 results for "cancer rna-seq"

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• PROstate Cancer Medically Optimized Genome Enhanced ThErapy (PROMOTE) of Castration Resistant Prostate Cancer (CRPC) Patients Treated with Abiraterone Acetate

  The Prostate Cancer Medically Optimized Genome-Enhanced Therapy (PROMOTE) study uses genetic clues in castration-resistant prostate cancer that may identify an individualized treatment approach for men with the disease. Understanding the molecular biology behind castration-resistant prostate cancer has led to more treatment options, but there are still no definite conclusions about which specific drug best treats patients - maximum suppression of cancer growth while minimizing side effects. The PROMOTE study explores the genetic characteristics of each tumor to predict these treatment paradigms for the future, resulting in more effective and less toxic options for patients. Our long-term goal is to improve treatments for men with advanced prostate cancer by using genomic sequencing to increase life span and quality of life. We also will uncover novel vulnerable targets in the cancer genome that may provide new drug therapies. PARTICIPATION Eligible participants are men: With castration-resistant prostate cancer or prostate cancer not responding to hormone treatments About to begin abiraterone acetate therapy Agreeable to undergoing two tumor biopsies During the study, participants travel to Mayo Clinic for an initial biopsy (before beginning abiraterone acetate) and a second biopsy approximately three months later. The cell tissue collected is analyzed to identify gene alterations in the tumor that could eventually be targeted with treatments. Tissue is preserved for future research. Participants can continue to be treated by their local cancer care team during this period and beyond. In addition, the Mayo team carefully monitors participants' cancer via follow-up studies and the genetic signature of tumors that were biopsied so that patients may benefit from future treatments.

  Study phs001141

• The International Consortium for Prostate Cancer Genetics Genome Wide Association Study of Familial Prostate Cancer

  Initially, the ICPCG focused largely on high-risk prostate cancer pedigrees using linkage analysis. However, association studies have also been informative to find prostate cancer susceptibility variants in the genome. We hypothesize that genome-wide (GW) association studies of familial cases of prostate cancer will have the power to identify rarer and perhaps less penetrant risk variants associated with prostate cancer than have been identified to date. Our approach will be to examine evidence for association in selected, independent cases from high-risk pedigrees; we hypothesize that they represent a more homogeneous set of cases with potentially different associations. Use of the 5M plus exome SNP platform will allow us to include in our search more rare variants in our search than have ever been investigated for prostate cancer. Aim 1. Identify a set of independent prostate cancer cases selected from ICPCG high-risk prostate cancer pedigrees that have 3 or more related prostate cancer cases and have an average age at diagnosis ≤ 75 years. Identify appropriate matched controls from participating ICPCG groups/ populations. Aim 2. Perform GW SNP genotyping with the Illumina 5M plus exome SNP set on the set of independent prostate cancer cases and controls described in Aim 1. Aim 3. Perform association analyses appropriately matching controls for different ICPCG populations and groups. There will be a two-stage design for confirmation. Aim 4. Test reported associations using the extensive sample set available to us by collaboration with the PRACTICAL consortium that has access to 50 000 DNA samples from 34 groups internationally (over 7,000 of whom are positive for prostate cancer family history).

  Study phs000733

• Clonal Lineage Tracing of Primary Human Cortical Progenitors, Cell Type Profiles in the Brain Vasculature and Genotyping Data for 22q11DS and Control iPS Lines

  We sought to characterize the cell types produced by individual human cortical progenitors and describe their lineage relationships. We labeled individual human cortical cells with a massively complex lentivirus library encoding a GFP reporter gene and a molecular barcode that could be captured by standard 3' scRNA-seq methodologies. We then cultured the labeled human cells for 6 weeks in either a 1) mouse cortical astrocyte co-culture system or 2) in the mouse cortex as a xenograft. In a separate experiment, we maintained human cortical tissue slices in organotypic slice culture for 12 days. GFP+ cells were then isolated by FACS and then captured on the 10x chromium scRNA-seq platform. An additional sample was labeled by lentivirus and briefly cultured for 3 days prior to being mixed with mouse 3T3 cells in order to perform a cell mixing experiment ("barnyard") to benchmark our methodologies. We found that human individual cortical progenitors gave rise to both excitatory and inhibitory neurons as well as glia.We also sought to characterize the adult brain vasculature in both vascular malformations and non-malformed tissue. We use the 10x chromium scRNA-seq platform across 10 individuals (5 control and 5 arteriovenous malformations). We find broad disregulation across multiple cell types including the immune cells and find a specific monocyte subtype to contribute to a rupture phenotype. We also find a novel population of fibromyocytes in both conditions.Finally, we confirmed the genotype status of iPS lines that were derived from either karyotypically normal control individuals or from DiGeorge Syndrome patients carrying the 22q11.2 deletion using the Illumina Infinium Global Screening Array v3.0.

  Study phs002624

• Whole-genome cfDNA TAPS sequencing data from 91 people with various types of cancer and from non-cancer controls

  TAPS data in the form of BAM files from 214 samples: plasma (at 80x) and matched germline (at 30x) pairs from 61 cancer and 30 non-cancer subjects, fresh-frozen matched tumour biopsies (at 80x) from 16 subjects, as well as several follow-up plasma samples (at 80x) from 10 subjects with colorectal cancer.

  Dataset EGAD50000000996

• Metastatic_Breast_Cancer_Whole_Genome

  We propose to definitively characterise the somatic genetics of Metastatic breast cancer through generation of comprehensive catalogues of somatic mutations in Metastatic breast cancer cases by high coverage genome sequencing coupled with integrated transcriptomic and methylation analyses.

  Study EGAS00001000902

• Breast_Cancer_FRT_RNA_seq

  We propose to definitively characterise the somatic genetics of ER+ve, HER2-ve breast cancer through generation of comprehensive catalogues of somatic mutations in breast cancer cases by high coverage genome sequencing coupled with integrated transcriptomic and methylation analyses.

  Study EGAS00001000420

• Triple_Negative_Breast_Cancer_RNA_Sequencing

  We propose to definitively characterise the somatic genetics of triple negative breast cancer through generation of comprehensive catalogues of somatic mutations in breast cancer cases by high coverage genome sequencing coupled with integrated transcriptomic and methylation analyses.

  Study EGAS00001000377

• San Francisco Bay Area Latina Breast Cancer Study

  The genome-wide association study (GWAS) includes participants enrolled into two different studies. The first study, the San Francisco Bay Area Cancer Study (SFBCS) is a population-based case-control study of breast cancer conducted in the San Francisco Bay Area and included women ages 35-79 years from three racial/ethnic groups: Non-Hispanic whites, African Americans, and Hispanics/Latinas. For the GWAS, only Hispanic/Latina women were included. Women diagnosed with invasive breast cancer between 1995 and 2002 were identified through the Greater Bay Area Cancer Registry. Controls were identified by random digit dialing and were frequency-matched to cases by age in 5 year increments and by race/ethnicity. Hispanic/Latina ethnicity was assessed by self-report. 175 Hispanic/Latina cases and 307 Hispanic/Latina controls from the SFBCS had given adequate consent and provided biospecimens that were used in the GWAS to be included in this data submission. The second study is the Northern California site of the Breast Cancer Family Registry (NC-BCFR). This population-based family study recruited breast cancer cases ages 18-64 years diagnosed from 1995-2009 that were identified through the Greater Bay Area Cancer Registry. Cases included all women at increased genetic susceptibility for breast cancer who met one or more of the following criteria: (a) being diagnosed with breast cancer at age <35 years; b) having a personal history of ovarian cancer or childhood cancer; (c) being diagnosed with two different breast cancers (bilateral breast cancers), with the first one diagnosed at age <50 years; and d) having one or more first-degree relatives with breast cancer, ovarian cancer or childhood cancer. Cases not meeting these criteria were randomly sampled and racial/ethnic minorities were oversampled. Controls were recruited by random digit dialing and were matched by 5-year age increments and by race/ethnicity. For the current GWAS only Latina/Hispanic cases and controls were included. Latina/Hispanic ethnicity was assessed by self-report. 631 Hispanic/Latina cases and 61 Hispanic/Latina controls from the NC-BCFR had given adequate consent and provided biospecimens that were used in the GWAS to be included in this data submission.

  Study phs000912

• Chugai_colorectal_organoid_sequencing

  Genomic and transcriptomic characterization of drug-resistant colon cancer stem cell lines.

  Study EGAS00001000872

• The impact of CCR8+ regulatory T cells on cytotoxic T cell function in human lung cancer

  Regulatory T cells (Tregs) suppress the host immune response and maintain immune homeostasis. Tregs also promote cancer progression and are involved in resistance to immune checkpoint inhibitor treatments. Recent studies identified selective CCR8 expression on tumor-infiltrating Tregs; CCR8+ Tregs have been indicated as a possible new target of cancer immunotherapy. Here, we investigated the features of CCR8+ Tregs in lung cancer patients. CCR8+ Tregs were highly activated and infiltration of CCR8+ Tregs in tumors was associated with poor prognosis in lung cancer patients. We also investigated their immune suppressive function, especially the influence on cytotoxic T lymphocyte cell function. The Cancer Genome Analysis revealed that CD8 T cell activities were suppressed in high CCR8-expressing tumors. Additionally, depletion of CCR8+ cells enhanced CD8 T cell function in an ex vivo culture of lung tumor-infiltrating cells. Moreover, CCR8+ Tregs, but not CCR8��� Tregs, induced from human PBMCs markedly suppressed CD8 T cell cytotoxicity. Finally, we demonstrated the therapeutic effect of targeting CCR8 in a murine model of lung cancer. These findings reveal the significance of CCR8+ Tregs for immunosuppression in lung cancer, especially via cytotoxic T lymphocyte cell suppression, and suggest the potential value of CCR8-targeted therapy for cancer treatment.

  Study JGAS000454