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Liver tumor/normal pairs

ABSTRACT: A major challenge to the study of tumor DNA copy number (CN) in clinical specimens is the lack of appropriate fresh frozen samples and thus a dependence on Formalin-Fixed Paraffin Embedded (FFPE) banked samples, which typically have more extensive clinical follow up information. However, on most high density CN platforms, DNA from FFPE tissues generally underperforms or suffers high failure rates compared to fresh frozen samples because of DNA degradation and cross-linking. Molecular Inversion Probe (MIP) technology has been applied successfully to obtain high quality CN and genotype data from DNA isolated from cell lines and frozen tumor samples. Since the MIP probes require only a small (~40 bp) target binding site, we reasoned they may be well suited to assess FFPE samples. In this study, we successfully applied MIP technology with a panel of 50,000 markers to CN determination in FFPE samples. Using an input of 37 ng genomic DNA, we demonstrated high quality CN data with MIP technology from 93 FFPE samples from seven diverse collections. We found that the performance of FFPE DNA for CN determination was comparable to that of DNA obtained from matched frozen tumor, with only a modest loss in performance of DNA. Tumor FFPE were analyzed using matched normal FFPE as the reference. Tumor and normal pairs: 01-02, 12-13, 16-17, 08-09, 20-21, 24-25, 28-29, and 35-36. Tumor 32 has no matched normal sample.

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PROVIDER: S-DIXA-D-1022 | biostudies-other |

REPOSITORIES: biostudies-other

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Liver tumor/normal pairs

Project description:A major challenge to the study of tumor DNA copy number (CN) in clinical specimens is the lack of appropriate fresh frozen samples and thus a dependence on Formalin-Fixed Paraffin Embedded (FFPE) banked samples, which typically have more extensive clinical follow up information. However, on most high density CN platforms, DNA from FFPE tissues generally underperforms or suffers high failure rates compared to fresh frozen samples because of DNA degradation and cross-linking. Molecular Inversion Probe (MIP) technology has been applied successfully to obtain high quality CN and genotype data from DNA isolated from cell lines and frozen tumor samples. Since the MIP probes require only a small (~40 bp) target binding site, we reasoned they may be well suited to assess FFPE samples. In this study, we successfully applied MIP technology with a panel of 50,000 markers to CN determination in FFPE samples. Using an input of 37 ng genomic DNA, we demonstrated high quality CN data with MIP technology from 93 FFPE samples from seven diverse collections. We found that the performance of FFPE DNA for CN determination was comparable to that of DNA obtained from matched frozen tumor, with only a modest loss in performance of DNA.

2009-01-23 | GSE14353 | GEO

Liver tumor/normal pairs

2009-01-22 | E-GEOD-14353 | biostudies-arrayexpress

Conpair: concordance and contamination estimator for matched tumor-normal pairs.

Project description:MotivationSequencing of matched tumor and normal samples is the standard study design for reliable detection of somatic alterations. However, even very low levels of cross-sample contamination significantly impact calling of somatic mutations, because contaminant germline variants can be incorrectly interpreted as somatic. There are currently no sequence-only based methods that reliably estimate contamination levels in tumor samples, which frequently display copy number changes. As a solution, we developed Conpair, a tool for detection of sample swaps and cross-individual contamination in whole-genome and whole-exome tumor-normal sequencing experiments.ResultsOn a ladder of in silico contaminated samples, we demonstrated that Conpair reliably measures contamination levels as low as 0.1%, even in presence of copy number changes. We also estimated contamination levels in glioblastoma WGS and WXS tumor-normal datasets from TCGA and showed that they strongly correlate with tumor-normal concordance, as well as with the number of germline variants called as somatic by several widely-used somatic callers.Availability and implementationThe method is available at: https://github.com/nygenome/conpair CONTACT: egrabowska@gmail.com or mczody@nygenome.orgSupplementary information: Supplementary data are available at Bioinformatics online.

| S-EPMC5048070 | biostudies-literature

GNPS - SiTrap proteomics profiling of renal normal/tumor tissue pairs

Project description:These are supporting RAW files for 'Detergent-free simultaneous sample preparation method for proteomics and metabolomics' SiTrap method manuscript. Frozen renal tissue from three matched clear cell renal carcinoma (G2 pT3a, G2 pT1b, G1 pT2) /adjacent normal sample pairs were obtained from The Leeds Multidisciplinary Research Tissue Bank. Approximately 1 cm2 sections with a thickness of 10 um were lysed and processed according to SiTrap protocol using SiTrap cellulose tips. The SiTrap load was normalized by protein concentration. 50 ug of protein was loaded. The collected flow-through fraction, devoid of proteins, was dried down for targeted metabolomics analysis. The captured protein fraction was reduced and alkylated in situ and digested with trypsin according to SiTrap protocol. The resulting peptides were concentrated for proteomics analysis.

2019-10-02 | MSV000084405 | GNPS

Assessing matched normal and tumor pairs in next-generation sequencing studies.

Project description:Next generation sequencing technology has revolutionized the study of cancers. Through matched normal-tumor pairs, it is now possible to identify genome-wide germline and somatic mutations. The generation and analysis of the data requires rigorous quality checks and filtering, and the current analytical pipeline is constantly undergoing improvements. We noted however that in analyzing matched pairs, there is an implicit assumption that the sequenced data are matched, without any quality check such as those implemented in association studies. There are serious implications in this assumption as identification of germline and rare somatic variants depend on the normal sample being the matched pair. Using a genetics concept on measuring relatedness between individuals, we demonstrate that the matchedness of tumor pairs can be quantified and should be included as part of a quality protocol in analysis of sequenced data. Despite the mutation changes in cancer samples, matched tumor-normal pairs are still relatively similar in sequence compared to non-matched pairs. We demonstrate that the approach can be used to assess the mutation landscape between individuals.

| S-EPMC3060821 | biostudies-literature

SiTrap proteomics profiling of renal normal/tumor tissue pairs

2019-10-02 | MSV000084405 | MassIVE

Reversion of tumor hepatocytes to normal hepatocytes during liver tumor regression in an oncogene-expressing transgenic zebrafish model.

Project description:Tumors are frequently dependent on primary oncogenes to maintain their malignant properties (known as 'oncogene addiction'). We have previously established several inducible hepatocellular carcinoma (HCC) models in zebrafish by transgenic expression of an oncogene. These tumor models are strongly oncogene addicted, as the induced and histologically proven liver tumors regress after suppression of oncogene expression by removal of a chemical inducer. However, the question of whether the liver tumor cells are eliminated or revert to normal cells remains unanswered. In the present study, we generated a novel Cre/loxP transgenic zebrafish line, Tg(fabp10: loxP-EGFP-stop-loxP-DsRed; TRE: CreERT2) (abbreviated to CreER), in order to trace tumor cell lineage during tumor regression after crossing with the xmrk (activated EGFR homolog) oncogene transgenic line, Tg(fabp10: rtTA; TRE: xmrk; krt4: EGFP) We found that, during HCC regression, restored normal liver contained both reverted tumor hepatocytes (RFP+) and newly differentiated hepatocytes (GFP+). RNA sequencing (RNA-seq) analyses of the RFP+ and GFP+ hepatocyte populations after tumor regression confirmed the conversion of tumor cells to normal hepatocytes, as most of the genes and pathways that were deregulated in the tumor stages were found to have normal regulation in the tumor-reverted hepatocytes. Thus, our lineage-tracing studies demonstrated the potential for transformed tumor cells to revert to normal cells after suppression of expression of a primary oncogene. This observation may provide a basis for the development of a therapeutic approach targeting addicted oncogenes or oncogenic pathways.

| S-EPMC6826027 | biostudies-literature

RNA-seq data of 20 pairs of colorectal tumor with matched adjacent normal colorectal tissue

Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of gene expression. The goals of this study is to compare gene expressions in colorectal tumor versus adjacent normal colorectal tissue.

2022-12-16 | GSE142279 | GEO

Tumor Liver vs Normal Liver: ChIP-chip and RNA expression

Project description:There is widespread interest in efficient characterization of differences between tumor and normal samples. Here, we demonstrate an effective methodology for genome-scale characterization of tumors. Using matched normal and tumor samples from liver cancer patients, as well as non-cancer-related normal liver tissue, we first determined changes in gene expression as monitored on RNA expression arrays. We identified several hundred mRNAs that were consistently changed in the tumor samples. To characterize the mechanisms responsible for creation of the tumor-specific transcriptome, we performed ChIP-chip experiments to assay binding of RNA polymerase II, H3me3K27, and H3me3K9 in 25,000 promoter regions. These experiments identified changes in active and silenced regions of the genome in the tumor cells. Finally, we used a “virtual comparative genomic hybridization” (vCGH) method to identify copy number alterations in the tumor samples. Through comparison of RNA Polymerase II binding, chromatin structure, and copy number changes, we suggest that the major contributor to creation of the liver tumor transcriptome was changes in gene copy number. Keywords: ChIP-chip, gene expression, CGH

2008-06-04 | GSE10842 | GEO

Identification of tumor suppressor microRNAs by integrative miRNA and mRNA sequencing of matched tumor normal pairs in lung adenocarcinoma

Project description:Roles of microRNAs (miRNAs) have not yet been explored systematically at the genome scale in lung cancer biology despite their important regulatory functions. Here, we report an integrative analysis of microRNA and mRNA sequencing data for the matched tumor and normal samples from 109 Korean female patients with non-small-cell lung adenocarcinoma. We produced miRNA-Seq and RNA-Seq data for 48 patients and RNA-Seq data only for additional 61 patients. Differential expression analysis with stringent criteria yielded 44 miRNAs and 2,322 genes. Integrative gene set analysis of differentially expressed miRNAs and genes using miRNA-target information yielded several processes related to cell cycle regulation that were targeted by tumor suppressor miRNAs. We performed the colony formation assay in A549 and NCI-H460 cell lines to test the tumor suppressive activity of down-regulated miRNAs in cancer and identified 7 novel tumor suppressor miRNAs. Two miRNAs showed differential survival characteristics in the TCGA LUAD patient cohort, suggesting their prognostic value. Our study not only provides a massive dataset of miRNA and mRNA sequencing from the matched tumor-normal samples but also reports several novel tumor suppressor miRNAs that could be further developed into prognostic biomarkers or RNA therapeutic targets.

2019-02-20 | GSE110907 | GEO

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