15169 results for "cancer studies using rna-seq"

in 31.79 milliseconds.

• Accelerated single cell seeding in relapsed multiple myeloma

  Study EGAS00001004404

• AUBTRG - Whole Exome Sequencing of Diffuse Glioma Samples

  Study EGAS00001003035

• Molecular analysis of inflammatory myofibroblastic tumor (WGS and WES)

  Study EGAS00001005081

• Molecular characterization of a renal cell carcinoma PDX cohort

  Study EGAS00001006249

• Validation of a targeted sequencing panel for multiple myeloma

  Study EGAS00001006164

• Study of the microenvironment of angioimmunoblastic T-cell lymphoma

  Study EGAS00001006401

• RNAseq analysis on primary sites Colorectal Cancer xenografts (PRX) samples

  Study EGAS00001007051

• Characterization of alternative promoter usage in advanced prostate cancer

  Study EGAS00001006275

• GBM stem cell lines and PRMT5 inhibitor

  Study EGAS00001004397

• Elucidating the molecular landscape of KRAS/BRAF mutant colorectal cancers

  Study EGAS00001007459

• Yale Policy for head and neck cancer and HPV clinical trials

  Dac EGAC00001003519

• Aberrant EZHIP Expression Drives Tumorigenesis in Osteosarcoma

  Study EGAS00001007531

• Integrated genetic analysis of primary CNS lymphoma

  Study EGAS00001007222

• SickKids_Cancer Molecular Diagnostics

  Cancer Molecular Diagnostics at Hospital for Sick Children

  Dac EGAC50000000375

• Fasting-mimicking diet reshapes antitumor immunity in cancer patients

  Study EGAS00001004944

• Whole genome sequencing to identify structural variants in early-stage breast cancer

  Dac EGAC50000000461

• Hepatoblastoma tumoroid biobank as a key resource for tumour genetics

  Study EGAS00001008251

• Intercepting Progression from Pre-Invasive to Invasive Lung Adenocarcinoma

  An improved understanding of the biology of lung cancer is needed to intercept the disease at an early point in its progression. In this project we have used multidimensional methods to profile the tumor microenvironment (TME) and to determine the crosstalk between cancer cells and the TME in pre-invasive to invasive human lung non-solid adenocarcinomas. Comparative analysis of the cellular and molecular events associated with the distinct histological stages will lead to identification of the critical events triggering progression and thereby identify targets to intercept disease progression. The data being submitted represents the genomic profiles of patient samples with pre-invasive and invasive human lung adenocarcinomas.

  Study phs002818

• Somatic Copy Number Analysis of Endometrial Carcinomas

  Endometrial cancer (EC) is the most commonly diagnosed gynecologic malignancy in the United States and is the sixth leading cause of cancer death amongst American women. The purpose of this study was to identify somatic (tumor-specific) copy number alterations in 7 clear cell ECs, 31 serous ECs, 17 endometrioid ECs, and the clear cell components of 2 endometrioid/clear cell ECs. To this end, DNAs from de-identified primary endometrial tumors and matched non-tumor tissues or blood were hybridized to high-density Illumina Infinium HumanHap650Y Beadchips or to high-density Human660W-Quad Beadchips and the data analyzed to annotate somatic copy number alterations throughout the genome.

  Study phs001690

• Longitudinal copy number variation analysis from plasma DNA of head and neck cancer patients under re-radiotherapy

  Recurrent locally advanced head and neck cancer (HNC) patients, receiving re-radiotherapy (re-RT), are presented with short progression-free (PFS) and overall survival. Hence, biomarkers predicting therapy failure are urgently needed. We analyzed copy number variations (CNVs) in blood plasma of HNC patients collected before, during and after re-RT. Detectable CNVs after five and ten fractions of re-irradiation as well as at the end of re-RT were associated with short PFS. Furthermore, we found that CNV kinetics in longitudinally collected plasma reflected therapy response and could detect disease progression in advance of radiographic tumor assessments.

  Study EGAS50000000163

• Targeted DNA sequencing and mRNA sequencing data from patients with peritoneal metastasis from colorectal cancer

  Patients with peritoneal metastasis from colorectal cancer (PM-CRC) have inferior prognosis and respond particularly poorly to chemotherapy. This study aims to identify the molecular explanation for the observed clinical behavior and suggest novel treatment strategies in PM-CRC. Tumor samples (230) from a Norwegian national cohort undergoing surgery and hyperthermic intraperitoneal chemotherapy (HIPEC) with mitomycin C (MMC) for PM-CRC were subjected to targeted DNA sequencing, and associations with clinical data were analyzed. mRNA sequencing was conducted on a subset of 30 samples to compare gene expression in tumors harboring BRAF or KRAS mutations and wild-type tumors.

  Study EGAS50000000404

• Tissue-specific cell-free DNA degradation quantifies circulating tumor DNA burden

  Profiling of circulating tumor DNA (ctDNA) may offer a non-invasive approach to monitor disease progression. Here, we developed a quantitative method, exploiting local tissue-specific cell-free DNA (cfDNA) degradation patterns, that accurately estimates ctDNA burden independent of genomic aberrations. Nucleosome-dependent cfDNA degradation at promoters and first exon-intron junctions was strongly associated with differential transcriptional activity in tumors and blood. A quantitative model, based on just 6 regulatory regions, could accurately predict ctDNA levels in colorectal cancer patients. Strikingly, a model restricted to blood-specific regulatory regions could predict ctDNA levels across both colorectal and breast cancer patients.

  Study EGAS00001004657

• Spatial and temporal genomic evolution in glioblastoma

  Tumor heterogeneity is a challenging barrier to successful targeted therapy in glioblastoma. Identifying the mechanisms that drive cancer cells as they genetically evolve and adapt in response to treatment is a vital goal of modern cancer research. Analysis of sequencing data provides a method for uncovering the mechanisms sustaining tumor heterogeneity and driving evolution. Here, we analyzed genomic profiles of GBM biopsies taken from pre- and post-treatment GBMs (with matched germline controls), to understand 1) the intratumoral clonal compositions of primary GBM and 2) how GBM responds to therapeutic intervention. Our results provide a molecular portrait of GBM recurrence.

  Study EGAS00001001033

• Reconstruction of complex rearrangement patterns causing the initiation of clear cell renal cell carcinoma.

  The genomic hallmark of clear cell renal cell carcinoma is the loss of the short arm of chromosome three. This appears to be the earliest genomic event in the formation of these cancers. Often chromosome 3 is lost at the same time as part of chromosome 5 is duplicated via an unbalanced translocation, often with features consistent with focal chromothripsis. In this study, we sought to reconstruct the chromothriptic event that underlies the initiation of kidney cancer. We used long read sequencing (promethION, Oxford Nanopore Technologies) of patient tumour-derived DNA to elucidate how a single cell division error can generate cancer genome complexity.

  Study EGAS00001004015

• Combination Therapies for Personalised Cancer Medicine in drug resistant EGFR mutant lung cancer

  This study involves mutagenizing a range of different cell lines with ENU to identify those mutations which engender resistance to targeted treatment. In the last decade we have begun to move towards the use of targeted therapeutics in the clinic, often resulting in dramatic response rates in cancer patients. However, clinical experience has demonstrated time and time again that such responses are invariably followed by the development of drug resistance. Identification of the underlying mechanisms may enable us to reverse such resistance. Traditional methods of modelling this resistance in vitro can lead to a plethora of potential resistance mechanisms that can be difficult to decipher.

  Study EGAS00001002509