7365 results for "canc*"

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• Mutational_burden_in_skin_following_UV_treatment_Nanoseq

  We wish to assess the changes in mutational burden in patients under going UV treatment for psoriasis. Using duplex sequencing we will assess mutational burden in traditionally sun exposed (arm) and non-sun exposed (buttock) skin epidermis both pre and post UV treatment.

  Study EGAS00001007681

• Establishment and characterization of an Epstein-Barr virus-positive cell line from a non-keratinizing differentiated primary nasopharyngeal carcinoma

  Nasopharyngeal carcinoma (NPC), a cancer that is etiologically associated with the Epstein-Barr virus (EBV), is endemic in Southern China and Southeast Asia. The scarcity of representative NPC cell lines owing to the frequent loss of EBV episomes following prolonged propagation and compromised authenticity of previous models underscores the critical need for new EBV-positive NPC models. Herein, we describe the establishment of a new EBV-positive NPC cell line, designated NPC268 from a primary non-keratinizing, differentiated NPC tissue. NPC268 can undergo productive lytic reactivation of EBV and is highly tumorigenic in immunodeficient mice. Whole-genome sequencing (WGS) revealed close similarities with the tissue of origin, including large chromosomal rearrangements, while whole-genome bisulfite sequencing (WGBS) and RNA sequencing demonstrated a hypomethylated genome and enrichment in immune-related pathways, respectively.

  Study EGAS00001007172

• Engineering large chromosomal deletions by CRISPR-Cas9

  Arm-level chromosomal deletions are a prevalent and defining feature of cancer. A high degree of tumor-type and subtype specific recurrencies suggest a selective oncogenic advantage. However, due to their large size it has been difficult to pinpoint the oncogenic drivers that confer this advantage. Suitable functional genomics approaches to study the oncogenic driving capacity of arm-level deletions are limited. Here we present an effective technique to engineer arm-level deletions by CRISPR-Cas9 and create isogenic cell line models. We simultaneously induce double-strand breaks (DSBs) at two ends of a chromosomal arm and select the cells that have lost the intermittent region. Using this technique, we induced arm-level deletions on chromosome 11q (65 MB) and chromosome 6q (53 MB) in neuroblastoma cell lines. Such isogenic models enable further research on the role of arm-level deletions in tumor development and growth, and their possible therapeutic potential.

  Study EGAS00001005134

• Breast Cancer PDTX Encyclopaedia

  Molecular data from the collection of PDTX breast cancer models described in Bruna et al, 2016. Cell. It includes whole exome sequencing, shallow whole genome sequencing, expression arrays and reduced bisulfite representation sequencing (RRBS).

  Study EGAS00001001913

• Molecular analysis of circulating tumour cells identifies distinct profiles in chemosensitive and chemorefractory patients with small cell lung cancer

  In a search for profiles that distinguish chemosensitive versus chemorefractory SCLC disease, we examined copy number aberrations (CNA) in circulating tumour cells (CTCs) from pre-treatment SCLC blood samples. A CNA classifier was generated from 88 CTCs isolated from 13 patients (training set) then verified in 18 additional patients (112 CTC samples) (testing set) and in six SCLC patient-derived CTC explants explant tumours. These data highlight the potential utility of CTCs for molecular profiling and stratification of SCLC patients in future clinical trials.

  Study EGAS00001001951

• SPECTA RP-1759-AYA Sarcoma cohort

  EORTC-SPECTA RP1759 study focuses on cancers in adolescent and young adult (AYA), age 12 to 29 years. This study explicitly recruited AYA patients and therefore collected empirical data to bridge the molecular gap between pediatric and adult oncology. The initial pilot study, activated in February 2019 across Europe, aimed to recruit 100 AYA patients (aged 12-29 years) with newly diagnosed or relapsed high-grade gliomas and high-grade bone and soft tissue sarcomas. The primary objective of the pilot is to determine feasibility and recruitment rates. Here we submit the data from patients with newly diagnosed, recurrent intermediate or high-grade sarcoma that were collected and analyzed during the study. More specifically, we submit raw FASTQ files obtained from whole exome sequencing (WES) of matching tumor and blood samples, tumor RNA sequencing and DNA methylation profiling.

  Study EGAS00001005840

• Melanoma_multi_site_metastases

  Despite multiple large-scale sequencing studies offering substantial insight into the genomic landscape of cutaneous melanoma, the molecular events surrounding disease progression and the resulting molecular heterogeneity between metastases have not been fully elucidated. We have been applying whole genome and transcriptome sequencing across metastases collected during post mortem as well as to multi-site metastases during treatment

  Study EGAS00001001348

• Sequencing of an organoid biobank for childhood soft tissue sarcoma.

  Rhabdomyosarcomas are diverse tumors of mesenchymal origin and the most common childhood soft tissue sarcoma. Patients receive intense treatment with a nevertheless poor prognosis for high-risk patients. New therapy would benefit from additional preclinical models and their rapid establishment. Tumor organoid models (tumoroids) have so far only been established from epithelial cancers. Here, we describe generation and characterization of a collection of pediatric RMS tumoroids comprising all major subtypes.

  Study EGAS00001005912

• OCCAMS_Oesophageal_Cancer_Organoids_1

  ***THIS DATA CAN ONLY BE USED FOR NON-COMMERCIAL CANCER RESEARCH*** Sequencing of organoid cell lines derived from oesophageal tumour sections taken from patients diagnosed with primary oesophageal cancer who underwent tumour resection surgery.

  Study EGAS00001001382

• MutWP1__CRUK_Grand_Challenge__normal_kidney_Nanoseq

  The Mutographs project aims to advance our understanding of the causes of cancer through studies of mutational signatures. Led by Mike Stratton, together with Paul Brennan, Ludmil Alexandrov, Allan Balmain, David Phillips and Peter Campbell, this large-scale international research endeavour was awarded a Cancer Research UK Grand Challenge. Different patterns of somatic mutation are generated by the different environmental, lifestyle and genetic factors that cause cancer, many of them are still unknown. Within Mutographs, the International Agency for Research on Cancer is coordinating the recruitment of 5000 individuals with cancer (colorectal, renal, pancreatic, oesophageal adenocarcinoma or oesophageal squamous cancers) across 5 continents to explore whether different mutational signatures explain marked variation in incidence. In brief, through an international network of collaborators around the world, biological materials are collected, along with demographic, histological, clinical and questionnaire data. Whole genome sequences of tumour-germline DNA pairs are generated at the Wellcome Trust Sanger Institute. Non-tumour DNA is also studied for some cancer types. Somatic mutational signatures are subsequently extracted by non-negative matrix factorisation methods and correlated with risk factors data. Through an enhanced understanding of cancer aetiology, Mutographs unprecedented effort is anticipated to outline modifiable risk factors, lead to new approaches to prevent cancer, and provide opportunities to empower early detection, refine high-risk groups and contribute to further therapeutic development.

  Study EGAS00001005451