7083 results for "canc*"

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• scRNA-seq from lung cancer organoids and immune cells

  15 scRNA-seq samples were multiplexed, and 5' 10X Chromium scRNA-seq was performed. This dataset provides the FASTQ files for the multiplexed data, as well as the BAM files for the demultiplexed samples.

  Dataset EGAD50000000845

• Multimodal cell-free DNA whole-genome TAPS is sensitive and reveals specific cancer signals

  This study presents a methodology for detecting circulating tumor DNA (ctDNA) using deep whole-genome TET-Assisted Pyridine Borane Sequencing (TAPS), a less destructive alternative to bisulphite sequencing. The method enables simultaneous analysis of genomic and methylomic data for multi-cancer detection and monitoring minimal residual disease. In a diagnostic accuracy study across various cancer types, it achieved 85.3% sensitivity and 88.8% specificity, with validation done using matched tumour biopsies. Additionally, in silico validation showed strong discrimination at low ctDNA levels. The approach also successfully tracks tumour burden and ctDNA shedding from precancerous lesions post-treatment, making it ready for further clinical testing.

  Study EGAS50000000715

• 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

• cfDNA whole-genome TAPS data for cancer detection DAC

  80x whole-genome sequencing data from circulating tumour DNA pre-treated with TAPS from 91 patients

  Dac EGAC50000000440

• Transcriptomics for the ALTTO study

  Transcriptomics for the ALTTO study by high-throughput sequencing. 386 HER2+ breast cancers treated by trastuzumab were sequenced. Two fastq files are given for each sample.

  Dataset EGAD50000000746

• WES in muscle-invasive bladder cancer (MIBC) treated with durvalumab plus olaparib in the neoadjuvant setting: NEODURVARIB trial

  This submission contains the metadata derived from the whole exome sequencing of 70 samples from 26 patients who developed advanced urothelial carcinomas. The patients were enrolled in the Neodurvarib clinical trial, which compares the molecular profiles at diagnosis and after neoadjuvant treatment with Durvalumab and Olaparib. In this regard, the analyzed samples include: normal tissue and tumoral tissue obtained from the transurethral resection of the bladder (TURBT, a procedure performed prior to neoadjuvant therapy) from the 26 patients (52 samples), as well as tissue obtained from the radical cystectomy (a procedure performed after treatment with the aforementioned drugs; 18 samples).

  Study EGAS50000000791

• Uncovering Principles of Adaptive Regulation in Cancer Resistance Through Deep Evolutionary Profiling

  A comprehensive understanding of the emergence of therapy resistance in cancer requires new approaches capable of generating and characterizing drug resistant cell lines at scale. Here, we present the EVolution Of Lineages in Vitro (EVOLV) platform, a high-throughput approach for generating diverse libraries of viable, drug-resistant cell lines from a common progenitor. EVOLV enables deeper insights into the genomics of drug resistance as well as into the complex interplay among genomic, transcriptomic, and functional layers during cancer evolution.

  Study phs003851

• Melanoma Genome Sequencing Project

  Melanoma is the most prevalent cause of skin cancer morbidity and mortality. In order to characterize the full range of somatic mutations that may drive the growth of melanoma, we are sequencing tumor and normal DNA from a set of roughly 150 melanomas. For the majority of samples (approximately 90% of the cases), mutations in protein coding genes will be assessed in the exonic DNA of tumor-normal pairs using hybrid capture and paired-end DNA sequencing. For a few of DNA samples (approximately 10% of the cases), the entire genomes will be analyzed to assess the possible contribution of complex structural rearrangements contributing to oncogenesis. The sequencing data are supplemented by copy number profiling on the same tumors using high-density SNP arrays. Integration of these approaches will enable the unbiased and comprehensive characterization of both known and novel recurrent DNA alterations that arise in melanoma.Versions 1-4 contain whole exome and bulk RNA sequencing data for patients with melanoma.Version 5 - We compared somatic genomic profiles from matched pre-treatment and post-resistance tumor biopsies in patients with metastatic melanoma who exhibited heterogeneous responses to immune checkpoint inhibitors (ICIs). This version includes whole exome sequencing (WES) data from 14 patients.

  Study phs000452

• Patient-derived xenograft models of head and neck cancers

  Establishment and characterization of two patient-derived xenograft models from HNSCC patients , initiatlly treatment-naive, and for which cetuximab-acquired resistant model couterparts have been generated. All models have been characterized at genomic level. HNSCC tissues were obtained from surgical resections at Cliniques universitaires St Luc in Brussels (Belgium).

  Dac EGAC50000000502

• Subclonal diversification of primary breast cancer

  Cancers are ecosystems of genetically related clones, competing across space and time for limited resources. To understand the clonal structure of primary breast cancer, we applied genome and targeted sequencing to 295 samples from 49 patients’ tumors. The extent of subclonal diversification varied considerably among patients and encompassed many spatial patterns, including local growth, intraductal dissemination and clonal intermixture. Landmarks of disease progression, such as acquiring invasive or metastatic potential, arose within detectable subclones of antecedent lesions, suggesting that subclonal mutations could be relevant if actionable. No defined temporal order of mutation was evident, with the commonest genes, including PIK3CA, TP53, BRCA2, PTEN and MYC, mutated early in some, late in others, often exhibiting parallel evolution across subclones. Signatures of homologous recombination deficiency correlated with response to neoadjuvant chemotherapy. Thus, the interplay of mutation, growth and competition drives clonal structures of breast cancer that are complex, variable across patients and clinically relevant.

  Dataset EGAD00001000898