Search Results - EGA European Genome-Phenome Archive

Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - 0.25mm punches targeted

Ageing epithelial tissues, including the esophagus, are progressively colonized by somatic mutant clones, some carrying mutations linked to cancer. However, whether normal epithelial mutational landscapes that evolve over decades can be altered by short term interventions such as cancer treatment is not known. Here we sequenced normal esophageal epithelium removed from patients after 5-8 weeks of therapy for esophageal cancer. Some patients had no prior treatment (NT), while others had 8 weeks of 5 Fluorouracil (5-FU) containing chemotherapy (FLOT) or 4 weeks of chemotherapy and radiation directed at the tumor (CROSS). Despite the brief duration of therapy, we observed treatment specific differences in the selection of mutant clones. The median size of mutant TP53 and PPM1D clones in the CROSS group was double that in the other groups. Mutants of the tumor suppressor SPOP were selected in CROSS but not FLOT or NT patients. In FLOT patients we found positive selection of activating MTOR mutations, consistent with the hypothesis that these mutants confer 5-FU resistance. Sequencing densely mutated normal epithelia after cancer reveals treatment specific selection of mutations with potential therapeutic impact.

Dataset EGAD00001011182

Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - nanoseq

Ageing epithelial tissues, including the esophagus, are progressively colonized by somatic mutant clones, some carrying mutations linked to cancer. However, whether normal epithelial mutational landscapes that evolve over decades can be altered by short term interventions such as cancer treatment is not known. Here we sequenced normal esophageal epithelium removed from patients after 5-8 weeks of therapy for esophageal cancer. Some patients had no prior treatment (NT), while others had 8 weeks of 5 Fluorouracil (5-FU) containing chemotherapy (FLOT) or 4 weeks of chemotherapy and radiation directed at the tumor (CROSS). Despite the brief duration of therapy, we observed treatment specific differences in the selection of mutant clones. The median size of mutant TP53 and PPM1D clones in the CROSS group was double that in the other groups. Mutants of the tumor suppressor SPOP were selected in CROSS but not FLOT or NT patients. In FLOT patients we found positive selection of activating MTOR mutations, consistent with the hypothesis that these mutants confer 5-FU resistance. Sequencing densely mutated normal epithelia after cancer reveals treatment specific selection of mutations with potential therapeutic impact.

Dataset EGAD00001011183

Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - 2mm targeted

Ageing epithelial tissues, including the esophagus, are progressively colonized by somatic mutant clones, some carrying mutations linked to cancer. However, whether normal epithelial mutational landscapes that evolve over decades can be altered by short term interventions such as cancer treatment is not known. Here we sequenced normal esophageal epithelium removed from patients after 5-8 weeks of therapy for esophageal cancer. Some patients had no prior treatment (NT), while others had 8 weeks of 5 Fluorouracil (5-FU) containing chemotherapy (FLOT) or 4 weeks of chemotherapy and radiation directed at the tumor (CROSS). Despite the brief duration of therapy, we observed treatment specific differences in the selection of mutant clones. The median size of mutant TP53 and PPM1D clones in the CROSS group was double that in the other groups. Mutants of the tumor suppressor SPOP were selected in CROSS but not FLOT or NT patients. In FLOT patients we found positive selection of activating MTOR mutations, consistent with the hypothesis that these mutants confer 5-FU resistance. Sequencing densely mutated normal epithelia after cancer reveals treatment specific selection of mutations with potential therapeutic impact.

Dataset EGAD00001011184

HiSeq Colorectal Cancer Dataset

Set of 19 patients afflicted with colorectal cancer with matching preoperative and postoperative blood plasma, PBMC, and tumor biopsy sequencing data. Originally referenced by Genome-wide cell-free DNA mutational integration enables ultra-sensitive cancer monitoring. Nat Med. 2020, Zviran et. al.

Dataset EGAD00001011186

Translation of non-canonical open reading frames as a cancer cell survival mechanism in childhood medulloblastoma - RNA-Seq

This study aims to investigate the dysregulation of RNA translation and identify functional non-canonical open reading frames (ORFs) as potential targets for medulloblastoma treatment. The study involves ribosome profiling and RNAseq of medulloblastoma tissues and cell lines to observe the translation of non-canonical ORFs. Multiple CRISPR-Cas9 screens will be used to identify functional non-canonical ORFs implicated in medulloblastoma cell survival.

Dataset EGAD00001011192

Translation of non-canonical open reading frames as a cancer cell survival mechanism in childhood medulloblastoma - Ribo-Seq

This study aims to investigate the dysregulation of RNA translation and identify functional non-canonical open reading frames (ORFs) as potential targets for medulloblastoma treatment. The study involves ribosome profiling and RNAseq of medulloblastoma tissues and cell lines to observe the translation of non-canonical ORFs. Multiple CRISPR-Cas9 screens will be used to identify functional non-canonical ORFs implicated in medulloblastoma cell survival.

Dataset EGAD00001011193

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Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - 0.25mm punches targeted

Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - nanoseq

Cancer treatment re-shapes the somatic mutational landscape of normal esophagus - 2mm targeted

HiSeq Colorectal Cancer Dataset

Translation of non-canonical open reading frames as a cancer cell survival mechanism in childhood medulloblastoma - RNA-Seq

Translation of non-canonical open reading frames as a cancer cell survival mechanism in childhood medulloblastoma - Ribo-Seq

10x Single Cell Gene Expression Library SCRNA10X_SA_CHIP0063_000

Genome and transcriptome sequence data from a metastatic thymic carcinoma patient

Genome and transcriptome sequence data from a colorectal cancer patient

Genome and transcriptome sequence data from a metastatic adenocarcinoma of the salivary gland patient

Genome and transcriptome sequence data from a metastatic lymphoepithelial carcinoma of the parotid gland patient

Genome and transcriptome sequence data from a metastatic lung adenocarcinoma patient

Genome and transcriptome sequence data from a primary unknown patient

Genome and transcriptome sequence data from a metastatic duodenal carcinoma patient

Genome and transcriptome sequence data from a hepatic cholangiocarcinoma patient

Genome and transcriptome sequence data from a pancreatic adenocarcinoma patient

Genome and transcriptome sequence data from a breast invasive ductal adenocarcinoma patient

Genome and transcriptome sequence data from a melanoma patient

Genome and transcriptome sequence data from a metastatic rectal cancer patient

Genome and transcriptome sequence data from a metastatic breast carcinoma (er positive) patient

Genome and transcriptome sequence data from a paget disease of the vulva patient

Genome and transcriptome sequence data from a pancreatic adenocarcinoma patient

Genome and transcriptome sequence data from a metastatic ovarian cancer patient

Genome and transcriptome sequence data from a poorly differentiated adenocarcinoma of the pancreas patient

Genome and transcriptome sequence data from a inflammatory myofibroblastic lung tumor patient