Differentially Expressed tRFs in CD5 Positive Relapsed & Refractory Diffuse Large B Cell Lymphoma and the Bioinformatic Analysis for Their Potential Clinical Use
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE140225 | GEO | 2020/04/14
REPOSITORIES: GEO
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Project description:Purpose:In recent years, tRFs(transfer RNA-Derived Fragments) & tiRNAs (transfer RNA-Derived Stress-induced RNAs or tRNA halves) have been shown to have vital roles in cancer biology. We aimed to reveal the expression profile of tRFs&tiRNAs in breast cancer tissues in the study, and to explore their potential as biomarkers of breast cancer. Methods:We characterize tRFs&tiRNAs expression profiles in 6 pairs of breast cancer tissues and adjacent normal samples.Then we selected six tRFs&tiRNAs with significant expression and added 10 pairs of samples to verify the selected genes by qPCR in 16 pairs of breast cancer tissues along with the previous 6 pairs. Results:We found 31 differentially expressed tRFs&tiRNAs across our dataset, out of which 17 were up-regulated, 14 were down-regulated. Compared with 16 breast cancer tissues and healthy controls by qPCR, the results demonstrated that AS-tDR-001430, AS-tDR-001130 and AS-tDR-000779 were significantly expressed in breast cancer tissues (p < 0.001). AS-tDR-000779 was significantly up-regulated, AS-tDR-001430 and AS-tDR-001130 were significantly down-regulated which the expression patterns were similar to the sequencing results. Conclusions:Our studies have demonstrated that there were significantly expressed tRFs&tiRNAs in breast cancer tissues. They are hopefully to become biomarkers and would be valuable researches in this area.
2020-01-21 | GSE123967 | GEO
Project description:CD5-positive (CD5+) diffuse large B-cell lymphoma (DLBCL) has a poor prognosis and high incidence of central nervous system (CNS) relapse, even in the rituximab era. To determine the gene expression profile of CD5+ DLBCL, total RNA from 90 patients with DLBCL, including 33 CD5+ DLBCL and 57 CD5-negative (CD5-) DLBCL patients, was examined using Agilent human oligo microarrays. These cases were separated into 78 activated B-cell-like (ABC) DLBCLs and 12 germinal center B-cell-like (GCB) DLBCLs. All cases of CD5+ DLBCL were classified as ABC DLBCLs. The classifier based on gene expression used in a supervised analysis correctly identified CD5 expression in the DLBCL and ABC DLBCL samples. The gene most relevant to CD5 expression was SH3BP5. The enriched GO categories in the CD5+ ABC DLBCL signature gene set were multicellular organismal signaling, transmission of nerve impulse, and synaptic transmission. This present study, which includes the largest reported number of patients with CD5+ DLBCL, confirmed that most CD5+ DLBCLs are ABC DLBCLs, suggesting that therapeutic strategies for ABC DLBCL may be effective for the treatment of CD5+ DLBCL. Our CD5+ ABC DLBCL signature gene set may provide insights into the cause of the high frequency of CNS relapse in CD5+ DLBCL.
2015-05-19 | GSE66770 | GEO
Project description:Breast cancer is one of the most common cancers in the world and non-triple-negative breast cancer (non-TNBC) accounts for 80-90% of all invasive breast cancers. Early detection of breast cancer is considered as key to successful treatment. Conventionally，breast imaging and needle core biopsy are used for detection and monitoring of disease progression. However, small volume changes may be ignored on imaging and traditional biopsy is spatially and temporally limited, leading to a significant lag time in detecting cancer progression. This thus prompted renewed focus on early and accurate diagnosis. In this article, we committed to investigate whether there exists accurate molecule in peripheral blood which can help diagnose breast cancer. tRNA-derived fragments (tRFs) have been reported to be involved in many pathological processes, but whether it can serve as biomarkers for the diagnosis of breast cancer remains unclear. Using high-throughput sequencing technology, we identified 4021 differentially expressed tRFs in normal breast epithelial cell lines and non-triple-negative breast cancer cell lines and 8 tRFs were selected to construct a signature to predict the non-TNBC. Further, qRT-PCR was conducted to verify its expression and to analyze the correlation between dysregulated tRFs and breast cancer. The results indicated that tDR-7816, tDR-5334, tDR-4733 might be promising biomarkers. Through further bioinformatics analysis, we predicted that tDR-7816 influences xenobiotic metabolic process that support the oncogenesis of breast cancer. Taken together, our results provide a rationale for using circulating tDR-7816 expression as a novel potential biomarker to diagnose early non-TNBC patients.
2019-10-30 | GSE134992 | GEO
Project description:CD5-positive (CD5+) diffuse large B-cell lymphoma (DLBCL) has a poor prognosis and high incidence of central nervous system (CNS) relapse, even in the rituximab era. To determine the gene expression profile of CD5+ DLBCL, total RNA from 90 patients with DLBCL, including 33 CD5+ DLBCL and 57 CD5-negative (CD5-) DLBCL patients, was examined using Agilent human oligo microarrays. These cases were separated into 78 activated B-cell-like (ABC) DLBCLs and 12 germinal center B-cell-like (GCB) DLBCLs. All cases of CD5+ DLBCL were classified as ABC DLBCLs. The classifier based on gene expression used in a supervised analysis correctly identified CD5 expression in the DLBCL and ABC DLBCL samples. The gene most relevant to CD5 expression was SH3BP5. The enriched GO categories in the CD5+ ABC DLBCL signature gene set were multicellular organismal signaling, transmission of nerve impulse, and synaptic transmission. This present study, which includes the largest reported number of patients with CD5+ DLBCL, confirmed that most CD5+ DLBCLs are ABC DLBCLs, suggesting that therapeutic strategies for ABC DLBCL may be effective for the treatment of CD5+ DLBCL. Our CD5+ ABC DLBCL signature gene set may provide insights into the cause of the high frequency of CNS relapse in CD5+ DLBCL. This present study involved 90 cases (33 patients with CD5+ DLBCL and 57 with CD5- DLBCL) of de novo consecutive DLBCL diagnosed at Mie University Hospital with available frozen biopsy specimens and total RNA samples. Lymphoma tissue RNA from 90 patients was extracted for target preparation and hybridization onto Agilent microarrays. The expression of CD5 in tumor cells was confirmed by means of immunohistochemistry using frozen sections.
2015-05-19 | E-GEOD-66770 | biostudies-arrayexpress
Project description:CD5 is characterized as an inhibitory co-receptor with important regulatory role during T cell development. To study the molecular mechanism by which CD5 operates, we used quantitative mass spectrometry to analyze the components of the CD5 signaling machinery in primary T cells. In a first set of experiments, CD5-containing complexes were immunoprecipitated from thymocytes of wild-type (WT) C57BL/6 mice. Thymocytes were treated with pervanadate to induce widespread activation of protein tyrosine kinases. Corresponding samples prepared from thymocytes of Cd5−/− mice were used as controls, to discriminate CD5-binding molecules from the background of contaminant proteins. Eight biological replicates were prepared for both conditions, and samples were analyzed in duplicate LC-MS runs. This first set of experiment is presented in TableS1 of the paper, and is associated to the MaxQuant result file “Interactome WT” in the present PX dataset. We analyzed the CD5 interactome at different time of stimulation with pervanadate (1min and 10min) using thymocytes from wild-type (WT) C57BL/6 mice. Corresponding samples prepared from thymocytes of Cd5−/− mice were used as controls. Three biological replicates were prepared for both conditions (WT and KO) and each time point (1min and 10min). This set of experiments is presented in TableS2 of the paper and is associated to the MaxQuant result file “Interactome at 1min and 10min” in the present PX dataset. We checked that the activation of CD5 (phosphorylation sites) and the formation of the signaling complex was comparable in different stimulatory conditions (comparison of WT thymocytes stimulated with either pervanadate or anti-CD3+anti-CD4 antibodies). We also analyzed the binding of CD5 interactors in thymocytes from a c-Cbl-/- mouse model (comparison of WT and c-Cbl-/-thymocytes stimulated with pervanadate). These experiments and the associated experimental design of the comparisons are summarized in TableS3 of the paper, and are based on the MaxQuant result file “Comparison of different stimulatory conditions” in this dataset. To check the phosphorylation status of the CD5 tyrosine residues at different time of stimulation, we analyzed samples immunoprecipitated from thymocytes of wild-type (WT) C57BL/6 mice, following stimulation with anti-CD3+anti-CD4 antibodies for 1min, 3min and 10min. This set of experiment is presented in TableS4 of the paper and is associated to the MaxQuant result file “CD5 pY kinetics” in the present PX dataset. To determine the role of Y429 in the context of CD5 signaling, we expressed a wild-type (CD5tgWt) or a mutated form of CD5, containing a tyrosine to phenylalanine substitution at position 429 (CD5tgY429F) in transgenic mice. We analyzed the CD5 interactome by comparing samples immunoprecipitated from thymocytes of these 2 mice models (following pervanadate stimulation, 6 and 5 biological replicates respectively) with samples prepared in the same way from Cd5−/− mice as controls (6 biological replicates). The results are shown in TableS5 of the paper, and correspond to the MaxQuant result file “interactome CD5tgWt_CD5tgY429F”.
2020-05-18 | PXD017343 | Pride
Project description:Purpose: The goals of this study are to confirm whether CD5-2 works through VE-cadherin Methods: mRNA profiles of HUVEC and VE-cadherin-/- EC treated with either control or CD5-2 were generated by deep sequencing using Illumina Hiseq4000 platform and 150 bp paired-end reads were generated. Reference genome and gene model annotation files were downloaded from genome website browser (NCBI/UCSC/Ensembl) directly. Indices of the reference genome were built using Bowtie (v2.2.3) and paired-end clean reads were aligned to the reference genome using TopHat (v2.0.12). Differentially expressed genes were then determined using DESeq R package (v1.12.0). The resulting P-values were adjusted using the Benjamini and Hochberg’s approach for controlling the False Discovery Rate (FDR). Genes with an adjusted P-value<0.05 and FDR<0.005 were assigned as differentially expressed. Results: 585 differentially expressed genes (DEGs) in CD5-2 treated ECs compared with control treated ECs (P < 0.05; false discovery rate [FDR] ≤ 0.005). In stark contrast to that seen in normal ECs, in VE-cadherin-/- ECs, no gene was significantly differently expressed between control and CD5-2 treated group when using the same cut-off criteria, Conclusions: Our study suggests VE-cadherin is essential for the CD5-2 mediated gene changes
2020-05-07 | GSE149948 | GEO
Project description:We have previously observed that regulatory B cells expressing the apoptosis-inducing surface molecule Fas ligand were enriched in the B cell fraction denoted by a surface phenotype of CD5+CD1dhigh. To identify potential growth factors, transcriptional regulators, or surface markers that might better characterize regulatory B cells, we compared global gene expression by microarray in two B cells subsets isolated by FACS. Splenocytes from 20 DBA/1 male mice were harvested, pooled, and CD19+ B cells were isolated by positive selection using MACS. B cells were then stained for CD5 and CD1d and sorted by FACS into CD5+CD1dhigh and CD5-CD1dhigh populations.
2013-06-30 | GSE46245 | GEO
Project description:We have previously observed that regulatory B cells expressing the apoptosis-inducing surface molecule Fas ligand were enriched in the B cell fraction denoted by a surface phenotype of CD5+CD1dhigh. To identify potential growth factors, transcriptional regulators, or surface markers that might better characterize regulatory B cells, we compared global gene expression by microarray in two B cells subsets isolated by FACS. Splenocytes from 20 DBA/1 male mice were harvested, pooled, and CD19+ B cells were isolated by positive selection using MACS. B cells were then stained for CD5 and CD1d and sorted by FACS into CD5+CD1dhigh and CD5-CD1dhigh populations. Single replicates of both CD5+CD1dhigh and CD5-CD1dhigh B cells from pooled mouse splenocytes were isolated and assay using the Affymetrix GeneChip Mouse 430 2.0 Array.
2013-06-30 | E-GEOD-46245 | biostudies-arrayexpress
Project description:Diffuse large B-cell lymphoma (DLBCL) comprises molecularly distinct subgroups such as activated B-cell-like (ABC) and germinal center B-cell-like (GCB) DLBCLs. We previously reported that CD5(+) and CD5(-)CD10(+) DLBCL constitute clinically relevant subgroups. To determine whether these 2 subgroups are related to ABC and GCB DLBCLs, we analyzed the genomic imbalance of 99 cases (36 CD5(+), 19 CD5(-)CD10(+), and 44 CD5(-)CD10(-)) using array-based comparative genomic hybridization (CGH). Forty-six of these cases (22 CD5(+), 9 CD5(-)CD10(+), 1 CD5 (-), and 14 CD5(-)CD10(-)) were subsequently subjected to gene-expression profiling, resulting in their division into 28 ABC (19 CD5(+) and 9 CD5(-)CD10(-)) and 18 GCB (3 CD5(+), 7 CD5(-)CD10(+), and 8 CD5(-)CD10(-)) types. A comparison of genome profiles of distinct subgroups of DLBCL demonstrated that (1) ABC DLBCL is characterized by gain of 3q, 18q, and 19q and loss of 6q and 9p21, and GCB DLBCL is characterized by gain of 1q, 2p, 7q, and 12q; (2) the genomic imbalances characteristic of the CD5(+) and CD5(-)CD10(+) groups were similar to those of the ABC and GCB types, respectively. These findings suggest that CD5(+) and CD5(-)CD10(+) subgroups are included, respectively, in the ABC and GCB types. Finally, when searching for genomic imbalances that affect patients' prognosis, we found that 9p21 loss (p16(INK4a) locus) marks the most aggressive type of DLBCL.
2009-07-10 | GSE16920 | GEO
Project description:Diffuse large B-cell lymphoma (DLBCL) comprises molecularly distinct subgroups such as activated B-cell-like (ABC) and germinal center B-cell-like (GCB) DLBCLs. We previously reported that CD5(+) and CD5(-)CD10(+) DLBCL constitute clinically relevant subgroups. To determine whether these 2 subgroups are related to ABC and GCB DLBCLs, we analyzed the genomic imbalance of 99 cases (36 CD5(+), 19 CD5(-)CD10(+), and 44 CD5(-)CD10(-)) using array-based comparative genomic hybridization (CGH). Forty-six of these cases (22 CD5(+), 9 CD5(-)CD10(+), 1 CD5 (-), and 14 CD5(-)CD10(-)) were subsequently subjected to gene-expression profiling, resulting in their division into 28 ABC (19 CD5(+) and 9 CD5(-)CD10(-)) and 18 GCB (3 CD5(+), 7 CD5(-)CD10(+), and 8 CD5(-)CD10(-)) types. A comparison of genome profiles of distinct subgroups of DLBCL demonstrated that (1) ABC DLBCL is characterized by gain of 3q, 18q, and 19q and loss of 6q and 9p21, and GCB DLBCL is characterized by gain of 1q, 2p, 7q, and 12q; (2) the genomic imbalances characteristic of the CD5(+) and CD5(-)CD10(+) groups were similar to those of the ABC and GCB types, respectively. These findings suggest that CD5(+) and CD5(-)CD10(+) subgroups are included, respectively, in the ABC and GCB types. Finally, when searching for genomic imbalances that affect patients' prognosis, we found that 9p21 loss (p16(INK4a) locus) marks the most aggressive type of DLBCL. Expression profiles in 46 patients with DLBCL and 8 for normal lymph node biopsy samples.
2009-07-10 | E-GEOD-16920 | biostudies-arrayexpress