6365 results for "11+1双色球多少钱一注"

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• Genome and transcriptome sequence data from a breast cancer patient

  Genome and transcriptome sequence data from a breast cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002030

• Genome and transcriptome sequence data from a breast cancer patient

  Genome and transcriptome sequence data from a breast cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002048

• Genome and transcriptome sequence data from an adrenal cortical carcinoma patient

  Genome and transcriptome sequence data from an adrenal cortical carcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002049

• ChIP-Seq (H3K4me3, H3K4me1, H3K9me3, H3K27ac, H3K27me3, H3K36me3, Input) data for HL60 cell line generated at Centre for Epigenome Mapping Technologies, Genome Sciences Center, B.C. Cancer Agency.

  ChIP-Seq (H3K4me3, H3K4me1, H3K9me3, H3K27ac, H3K27me3, H3K36me3, Input) data for HL60 cell line generated at Centre for Epigenome Mapping Technologies, Genome Sciences Center, B.C. Cancer Agency.

  Dataset EGAD00001002238

• Genome and transcriptome sequence data from a breast cancer patient

  Genome and transcriptome sequence data from a breast cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002531

• Genome and transcriptome sequence data from a breast cancer patient

  Genome and transcriptome sequence data from a breast cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002549

• Genome and transcriptome sequence data from a metastatic endometrial cancer patient

  Genome and transcriptome sequence data from a metastatic endometrial cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002568

• Genome and transcriptome sequence data from a metastatic breast carcinoma patient

  Genome and transcriptome sequence data from a metastatic breast carcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002587

• Genome and transcriptome sequence data from a breast cancer patient

  Genome and transcriptome sequence data from a breast cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002605

• Genome and transcriptome sequence data from a clival chordoma patient

  Genome and transcriptome sequence data from a clival chordoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002640

• Genome and transcriptome sequence data from a metastatic cholangiocarcinoma patient

  Genome and transcriptome sequence data from a metastatic cholangiocarcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002642

• Genome and transcriptome sequence data from a metastatic breast cancer patient

  Genome and transcriptome sequence data from a metastatic breast cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001002643

• Genome and transcriptome sequence data from an ovarian cancer patient

  Genome and transcriptome sequence data from an ovarian cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005829

• Genome and transcriptome sequence data from a cavernous sinus meningioma patient

  Genome and transcriptome sequence data from a cavernous sinus meningioma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005846

• Genome and transcriptome sequence data from a pancreatic cancer patient

  Genome and transcriptome sequence data from a pancreatic cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005864

• Genome and transcriptome sequence data from a pancreatic adenocarcinoma patient

  Genome and transcriptome sequence data from a pancreatic adenocarcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005882

• scTCR-seq from brain metastasis micorenvironment and cerebrospinal fluid

  A total of 9 brain metastasis were sequenced. For 6/9 a matched cerebrospinal fluid sample, prior to surgery and in two cases after surgery (+1 month from surgery) and after treatment (+3 month) were collected. Single-cell T cell receptor clonotypes were produced using the Chromium Single Cell 5’ Library and sequenced on an Illumina NovaSeq 6000.

  Dataset EGAD00001006451

• DNA Whole Exome Sequence for manuscript titled: Evaluation of Endobronchial Ultrasound-Guided Transbronchial Needle Aspiration (EBUS-TBNA) Samples from Advanced Non-Small Cell Lung Cancer for Whole Genome, Whole Exome and Comprehensive Panel Sequencing

  DNA Whole Exome Sequence for manuscript titled: Evaluation of Endobronchial Ultrasound-Guided Transbronchial Needle Aspiration (EBUS-TBNA) Samples from Advanced Non-Small Cell Lung Cancer for Whole Genome, Whole Exome and Comprehensive Panel Sequencing

  Dataset EGAD00001015395

• Genome and transcriptome sequence data from a pancreatic adenocarcinoma patient

  Genome and transcriptome sequence data from a pancreatic adenocarcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001010940

• Genome and transcriptome sequence data from a squamous cell carcinoma patient

  Genome and transcriptome sequence data from a squamous cell carcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001010941

• Genome and transcriptome sequence data from a breast ductal carcinoma patient

  Genome and transcriptome sequence data from a breast ductal carcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001010954

• Genome and transcriptome sequence data from a metastatic ovarian cancer patient

  Genome and transcriptome sequence data from a metastatic ovarian cancer patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001011005

• Genome and transcriptome sequence data from a rectal adenocarcinoma patient

  Genome and transcriptome sequence data from a rectal adenocarcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001011040

• RNASeq data from one small cell prostate cancer patient (4 samples from 3 time points)

  RNASeq data from one small cell prostate cancer patient - 4 cancer samples (FFPE) from Patient 1 collected at 3 different time points. mRNA was selected using the Magnetic mRNA Isolation Module (NEB) and sequenced on the Illumina NextSeq 500 as 75bp paired end reads (total read length 150bp).

  Dataset EGAD00001011154

• RNA-seq dataset: Short-term fasting before living kidney donation has an immune-modulatory effect

  This dataset contains 13 RNA-seq samples in CRAM format, generated using the Illumina NovaSeq 6000 platform. The Roche_mRNA_UniversalAdapterUniquePrime protocol was used for library preparation. The aim of the study is to determine the effect of Short-Term Fasting on the abundance and phenotype of different immune cell populations.

  Dataset EGAD00001015472

• WXS dataset of Oncogenic and immunological targets for matched therapy of pediatric blood cancer patients: Dutch iTHER study experience

  WXS dataset of Oncogenic and immunological targets for matched therapy of pediatric blood cancer patients: Dutch iTHER study experience

  Dataset EGAD00001015638

• Induction of HIV-1 Env-Specific Peripheral Blood Plasmablasts and Clonal Persistence as Bone Marrow Plasma Cells Following Vaccination in Humans

  Induction of persistent HIV-1 Envelope (Env) specific antibody (Ab) is a primary goal of HIV vaccine strategies, however, it is unclear if HIV Env immunization in humans induces bone marrow plasma cells, the presumed source of long-lived systemic Ab. To define the features of Env-specific plasma cells after vaccination, samples were obtained from HVTN 105, a phase I trial testing the same gp120 protein immunogen, AIDSVAX B/E, as used in RV144, along with a DNA immunogen in various prime/boost strategies. Boosting regimens that included AIDSVAX B/E induced robust peripheral blood plasmablast responses. The Env-specific immunoglobulin repertoire of the plasmablasts was dominated by VH1 gene usage and targeting of the V3 region. Numerous plasmablast-derived immunoglobulin lineages persisted in the bone marrow greater than eight months after immunization, including in the CD138+ long-lived plasma cell compartment. These findings identify a cellular linkage for the development of sustained Env-specific Ab following vaccination in humans.

  Study phs002027

• HSC_population_dynamics___KX004_samples___WGS

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001003768

• HSC_population_dynamics___CB002_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001003743

• HSC_population_dynamics___KX007_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004193

• HSC_population_dynamics___KX008_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004490

• HSC_population_dynamics_CBD_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001003091

• HSC_population_dynamics___KX003_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001003550

• HSC_population_dynamics___TG001_2_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001003688

• PGRN/PAT: The genomic basis for susceptibility to drug-induced long QT syndrome (diLQTS)

  The goal of this study was to search for genetic variants that could be responsible for modifying the risk of drug-induced long QT syndrome (diLQTS). diLQTS is a relatively common adverse drug event and has been a leading cause for drug relabeling and withdrawal from the market. Our hypothesis, that variants in genes which regulate electrical properties in the heart modify the risk of diLQTS, was tested by sequencing approximately 225 patients of European descent using next-generation targeted captured or whole exome sequencing. Data from cases and controls (1:2) were analyzed to identify both rare and common genetic variation.

  Study phs000808

• Gene Expression Signatures in CATHGEN

  Case control cohort: The details have been previously published: American Heart Journal. 2010;160:371-379 e372. Briefly, a nested case:control cohort of CATHGEN participants who had experienced death or MI (n = 250) after their index catheterization and age-, sex-, and race-matched controls (n = 250) who were free of death/MI > 2 years after cardiac catheterization was identified as part of the MURDOCK Horizon 1 Cardiovascular Disease Study.21 Sufficient RNA for microarray analysis was available in 447 members of this cohort. Observational cohort: 224 sequential CATHGEN samples were selected for whole blood RNA analysis, of which, 191 had sufficient RNA for microarray analysis.

  Study phs000551

• Genetics of Pigmentation in Eastern and Southern African Populations Study

  The goal of this study was to identify genes and loci associated with pigmentation in African populations. It comprises 1,593 participants from Ethiopia, Tanzania, and Botswana. Sexes are evenly represented (768 males and 825 females) and self reported ages ranged from 18 to 103. Mean age was used for individuals without ages. For each participant, a DSM II color meter was used to measure underarm skin reflectance in triplicate. These measures averaged and converted to a melanin index (MI = 100 x log10(1/(x/255)). All individuals were included in a genome wide scan that accounted for age, sex, and genetic relatedness.

  Study phs001396

• Phase I Study of the Oral PI3kinase Inhibitor BKM120 or BYL719 and the Oral PARP Inhibitor Olaparib in Patients with Recurrent Triple Negative Breast Cancer or High Grade Serous Ovarian Cancer

  We analyzed massive parallel sequence data from patients with breast and ovarian cancer and identified single base substitution mutational signature 3 (Sig3) - extracted using SigMA - as a biomarker of homologous recombination deficiency (HRD) and predictive for response to PARP inhibitors. Participants were patients enrolled in clinical trials as 2 independent datasets: (1) high-grade serous ovarian cancer and triple-negative breast cancer (TNBC) from a Phase 1b trial of the PARP inhibitor olaparib in combination with the PI3K inhibitor buparlisib (BKM120) (NCT01623349), and (2) TNBC patients who received neoadjuvant olaparib in the Phase II PETREMAC trial (NCT02624973).

  Study phs003019

• Integrative Analysis of Lung Adenocarcinoma in EAGLE (Version 2)

  We performed a comprehensive analysis of intratumor heterogeneity of somatic mutations in cancer driver genes, copy number aberrations and DNA methylation in 292 tumor samples from 84 lung adenocarcinoma (LUAD) patients from the Environment And Genetics in Lung cancer Etiology (EAGLE) study. SNVs of 37 established lung cancer driver genes were profiled by deep target sequencing in 180 tumor samples and 55 blood samples and 1 buccal sample from 56 subjects. Somatic copy number alterations were profiled using SNP arrays in 268 tumor samples from 80 subjects. DNA methylation levels were profiled with methylation arrays in 205 tumor samples and 74 normal tissue samples from 68 subjects.

  Study phs001169

• A Phase I/IB Study of Ipilimumab or Nivolumab in Patients With Relapsed Hematologic Malignancies After Allogeneic Hematopoietic Cell Transplantation

  Relapse after allogeneic hematopoietic stem cell transplantation (HSCT) is characterized by poor outcomes and novel therapeutic options are urgently needed. Immune checkpoint blockade using CTLA-4 and PD-1 blocking antibodies are a potential concept for reinstating a dormant graft-versus-leukemia (GvL) effect.This study investigated transcriptomic changes in biopsies obtained from patients who received immune checkpoint blockade for relapsed hematologic malignancy post-HSCT and elucidated transcriptional programs associated with successful reinvigoration of GvL. Differential gene expression analysis showed evidence of increased T cell infiltration in biopsies of responders to ipilimumab treatment and demonstrated shared gene programs between GvL and GvHD.

  Study phs002377

• Collaborative Cohort of Cohorts for COVID-19 Research (C4R): Severe Asthma Research Program (SARP)

  Cohort Description The Severe Asthma Research Program (SARP) has been investigating the clinical, physiologic and molecular phenotypes of asthma since 2000. It is currently following ~400 deeply phenotyped asthma patients. Data Being Submitted Wave 1 questionnaire data includes 397 variables for up to 375 SARP participants in C4R.Wave 2 questionnaire data includes 448 variables for up to 289 SARP participants in C4R.Dried Blood Spot/Serosurvey data includes 7 variables for up to 290 SARP participants in C4R.Derived data includes 43 variables for up to 463 SARP participants in C4R.Phenotype data includes 113 variables for up to 463 SARP participants in C4R.

  Study phs002913

• Primary central nervous system lymphoma (PCNSL) biopsies show heterogeneity in gene expression profiles, genetic subtypes, and in vitro drug sensitivity to kinase inhibitors

  Primary central nervous system lymphoma (PCNSL) is an aggressive large B-cell lymphoma, most often of the activated B cell (ABC) subtype, but with limited tumor biology studies due to small biopsy size and lack of strict cohort definition. Here we examined the genetic heterogeneity of 29 HIV- EBV- PCNSL tumors using whole exome sequencing (WES). We compared these tumors to 5 cell lines comprised of two human PCNSL cell lines (TK and HKBML) and three systemic activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL) (OCI-Ly3, TMD-8, HBL-1).

  Study EGAS50000000312

• HSC_population_dynamics___PX001_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004146

• HSC_population_dynamics___KX009_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004580

• HSC_population_dynamics___KX010_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001004581

• Understanding Rare Variant Contributions to autism: Lessons from Dystrofin-Deficient Model

  This project generated a whole-exome sequencing (WES) dataset of 83 boys with a pathogenic variant in the DMD gene, along with WES data from the parents of 38 of them, totaling 159 samples. Pathogenic DMD variants, besides causing dystrophinopathies, are also known risk factors for neurodevelopmental disorders (NDDs). However, the low penetrance of NDDs in individuals with dystrophinopathies suggests that additional factors contribute to their manifestation. This study aimed to: (1) characterize ASD in males with dystrophinopathies; (2) determine the relevance of additional de novo and inherited rare risk variants for their neurodevelopmental phenotype; and (3) clinically and functionally characterize the identified risk variants.

  Study EGAS50000000754

• Targeting EGFR in NF1 Mutant Melanoma

  Our study focused on melanoma patients with driver mutations in the neurofibromin 1 (NF1) tumor suppressor gene, a subset of melanoma patients that have not benefitted from recent treatment advances. We have leveraged patient-derived short-term cultures (STCs) and multiomics approaches to identify molecular features that could be developed into therapies for NF1 mutant melanoma patients. Our studies revealed that the epidermal growth factor receptor (EGFR) is highly expressed and active in NF1 mutant melanoma cells, and that genetic or pharmacological EGFR inhibition impaired tumor cell proliferation, survival, and cell growth in patient-derived NF1 mutant but not NF1 wild-type melanoma models.

  Study phs003906

• Immune Checkpoint Blockade for Relapsed Hematologic Malignancy Post-HSCT

  Relapse after allogeneic hematopoietic stem cell transplantation (HSCT) is characterized by poor outcomes and novel therapeutic options are urgently needed. Immune checkpoint blockade using CTLA-4 and PD-1 blocking antibodies are a potential concept for reinstating a dormant graft-versus-leukemia (Gvl) effect. This study investigated transcriptomic changes in biopsies obtained from patients who received immune checkpoint blockade for relapsed hematologic malignancy post-HSCT and elucidated transcriptional programs associated with successful reinvigoration of GvL. Differential gene expression analysis showed evidence of increased T cell infiltration in biopsies of responders to ipilimumab treatment and demonstrated shared gene programs between GvL and GvHD.

  Study phs003291

• HSC_population_dynamics_KSP_samples

  My research project aims to use the clonal dynamics of spontaneously occurring somatic mutations to answer fundamental questions about human haematopoietic stem cell (HSC) biology. The four major questions I will address are: 1. How do age and aging affect normal human HSC dynamics in vivo? 2. How do in vivo perturbations, particularly chemotherapy and increased levels of reactive oxygen species, affect HSC population dynamics? 3. Is response to in vitro perturbation heritable and/or correlated with other features such as age of individual and contribution of the lineage to peripheral blood? 4. How are HSC dynamics altered in people with early driver mutations (clonal haematopoiesis)?

  Study EGAS00001002762

• Amplicon sequencing of melanoma samples

  The types of biomarkers for skin tumors have been 1) biochemical markers in blood, urine, and body fluid, 2) histopathological markers, 3) genetic examination of tumor tissue, 4) tumor-susceptibility assessed by germ_x0002_line genetic examination. Biomarkers in a blood are frequently used in the treatment of cutaneous malignancies, but are not suitable for early detection of malignancies. Research on circulating tumor cells, cell free DNA, exosomes has been promoted in recent years, but clinical application is halfway. Based on these circumstances, the purpose of this study is to search for biomarkers for diagnosis, therapeutic effect, and follow-up of skin tumors, and to verify their usefulness.

  Study JGAS000351