5495 results for "*oma"

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• Transcriptomics analysis of biopsy and resected material from HCC and matched non-tumor

  We hypothesize that pre-analytical handling such as surgery procedure and cold ischemia have significant effects on omics data derived from liver and liver tumor tissue that may confound classification of tumor subtypes of hepatocellular carcinoma. This study is aimed at revealing such effects by comparing resection samples with patient matched biopsy samples in a multi-omics analysis.

  Study EGAS50000001602

• FGFR2b Prevalence in Biliary Tract Cancers

  Patients with intrahepatic cholangiocarcinoma (iCCA) often have limited effective treatment options after first-line therapy. Actionable driver mutations are present in only a small subset of patients with iCCA; therefore, therapeutic strategies such as antibody–drug conjugates (ADCs) that do not exclusively rely on presence of specific oncogenic mutations may be particularly attractive. However, there is a critical lack of knowledge regarding prevalent and actionable cell-surface targets in iCCA. We applied a novel isoform-resolved proteogenomic discovery framework for profiling cell surface targets and identified FGFR2b, a splicing isoform of FGFR2, as a therapeutic target in iCCA that is highly-expressed, tumor-enriched, localized to the membrane, and associated with prognosis. FGFR2b is the dominant isoform in iCCA, and it was present in all patients with FGFR2 fusions. These findings provide a strong rationale for further research and therapeutic development of FGFR2b-targeted biologics, including therapeutic antibodies and ADCs, in iCCA.

  Study EGAS50000002012

• Tumoral immune microenvironment profiling in B-cell non-Hodgkin lymphoma stratifies patients in different prognostic groups

  Dac EGAC50000001065

• RNAseq and WES of CHC patients years before HCC development

  We conducted a nested case–control study within a prospective liver biopsy biobank at the University Hospital Basel. Patients with chronic hepatitis C (CHC) who developed hepatocellular carcinoma (HCC) during follow-up (index cases, CHC-HCC) were identified and 1:2 propensity score-matched to CHC controls without HCC (controls, CHC-nonHCC). Matching included clinical, demographic, and virological risk factors for HCC. Liver biopsies were analyzed using RNA and whole-exome sequencing.

  Dataset EGAD50000001591

• Targeted DNA sequencing of 60 non-Hodgkin lymphoma biopsies using a custom gene panel for hematological malignancies: raw (FASTQ) data

  Targeted DNA sequencing was performed on 60 non-Hodgkin lymphoma (NHL) samples using a custom next-generation sequencing panel targeting the coding regions of 190 genes recurrently mutated in hematological malignancies. Libraries were sequenced on an Illumina NovaSeq 6000 platform using 2 × 150 bp paired-end reads. The dataset includes the raw sequencing data (FASTQ files) for all 60 samples.

  Dataset EGAD50000002845

• scRNAseq and spatial transcriptomics data of melanoma samples

  Paired-end 10x single-cell RNA sequencing and Visium spatial transcriptomics data from samples derived from 11 melanoma patients. Sequencing was performed on the Illumina NovaSeq 6000 using 10xGenomics Chromium Next GEM Single-Cell 5 Reagent Kits v2 or 10xGenomics Visium Gene Expression kit.

  Dataset EGAD50000002902

• RNA-seq of adult T-cell leukemia-lymphoma patient-derived xenograft (PDX) models treated with the MALT1 protease inhibitor CRD-1441551

  To elucidate the therapeutic effect of MALT1 protease inhibition in adult T-cell leukemia/lymphoma (ATL), we performed RNA-seq on tumor tissues from five ATL patient-derived xenograft (PDX) models. NOG mice engrafted with each PDX model were treated with the MALT1 protease inhibitor CRD-1441551 or vehicle for 21 days, in biological triplicate (n = 3 per condition; 30 samples in total). Mouse-derived reads were removed and the remaining human reads were aligned to the human reference genome (hg19). These data underlie the gene-expression analyses reported in the associated publication.

  Study JGAS000921

• Impact of Mutated CTCF DNA binding sites of Topologically associating domains on nearby Cancer Gene Regulation: A Multi-Omics Analysis

  Cutaneous squamous cell carcinoma (cSCC) is the most common lethal malignancy world-wide. Due in most part to the extremely high mutational burden (TMB) in cSCC, making sense of it’s non-coding and regulatory regional genomic variation has lagged that of other far less common cancers. This study presents the first investigation of mutations at CCCTC-binding factor binding sites (CTCFbs) of Topologically associating domains (TAD) across defined cSCC progression stages—primary non-metastatic (PNM), primary metastat-ic (PM), and lymph node metastasis (LNM).

  Study EGAS50000001686

• CTCF Binding Site Mutations: Linking Topologically Associated Domains Dysregulation to Cutaneous Squamous Cell Carcinoma Progression

  Fresh tumor tissue from nodal metastases (n = 41) was harvested during surgery and immediately snap-frozen. A total of 72/75 cSCC, WGS samples were included in the analysis (refer to QC section), comprising primary tumors (both metastatic (PM (n = 16)) and non-metastatic (PNM (n = 15)), as well as lymph node metastases (LNM (n = 41)). The metastatic cohort included matched PM and LNM samples for 13 patients. The PNM group had to meet the following criteria: absence of metastases at > 24 months follow-up after resection of the primary or negative sentinel lymph node biopsy at time of resection or histologically negative neck dissection. Somatic variant analysis was performed using DRAGEN pipeline version 4.3.6 on the Illumina Connected Analytics (ICA) v2 environment using in house shell scripting. Tumor-normal paired analyses were carried out in three stages: alignment, variant calling, and integrative somatic analysis. Further information on the somatic calling is available at https://help.dragen.illumina.com/product-guides/dragen-v4.3/dragen-dna-pipeline/small-variant-calling/somatic-mode.

  Dataset EGAD50000002416

• IMC-F106C-101 dose escalation

  Brenetafusp is an ImmTAC bispecific (PRAME×CD3) targeting the cancer testis antigen PRAME. In this phase 1 study (NCT04262466), 126 HLA-A*02:01+ patients with advanced solid tumors received weekly IV doses from 0.3-320 mcg. The primary objective was to identify the maximum tolerated dose (MTD) or recommended phase 2 dose (RP2D); additional objectives included pharmacokinetics, pharmacodynamics, and preliminary anti-tumor activity. Brenetafusp demonstrated manageable safety and preliminary efficacy in PRAME+ tumors. A phase 3 trial in metastatic cutaneous melanoma is ongoing

  Study EGAS50000001976