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Whole Micro-RNA transcriptome profiling of relapsed /refractory and remission Diffuse Large B cell Lymphoma cases to identify differentially expressed micro RNA

ABSTRACT: Whole Micro-RNA transcriptome profiling of relapsed /refractory and remission Diffuse Large B cell Lymphoma cases to identify differentially expressed micro RNA

PROVIDER: PRJNA744910 | ENA |

REPOSITORIES: ENA

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Whole Micro-RNA transcriptome profiling of relapsed /refractory and remission Diffuse Large B cell Lymphoma cases to identify differentially expressed micro RNA

Project description:Purpose: high throughput sequencing technique has revolutionalized research. The aim is to compare the mi-RNA transcriptome expression between Diffuse Large B cell Lymphoma patients who are in complete remission to those who had relpase or were refractory to first line treatment Methods-mi-RNA profiles of primary biopsies of complete remission(n=3) and refractory(n=3)/relapsed(n= 4) diffuse large b cell lymphoma cases were generated, using S5 Ion Torrent. The sequencing reads that passed quality filters were analyzed for differential micro-RNA expression in refractory/relapsed cohort using DESeq2. qRT–PCR validation was performed using SYBR Green assays. Results- we analysed 1.5 million reads mapped to human genome (hg19) per sample, two samples had less than threshold reads reads but micro-RNA having > 10 counts in the same cohort was selected .Reads less than 17 bp were removed using Fastx, then aligned to reference genome hg19 using Bowtie. Differentially expressing micro-RNA in the non responder cohort compared to complete response was found by Dseq . Altered micro-RNA with fold change ≥2.0 and p value 0.001 was selected. Downregulation of three shortlisted mi-RNA was validated with q-RT-PCR. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

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Phase II Study of Immune Checkpoint Blockade with Pembrolizumab after High Dose Cytarabine in Relapsed/Refractory Acute Myeloid Leukemia

Project description:To address the role of immune dysregulation in AML, we conducted a phase II study of high-dose cytarabine followed by pembrolizumab 200 mg IV on day 14 to examine whether programmed death-1 inhibition improves clinical responses in relapsed/refractory (R/R) AML. Overall responders could receive pembrolizumab maintenance up to two years. Among thirty-seven patients enrolled, the overall response rate, composite complete remission rate (CRc; primary endpoint), and median overall survival (OS) were 46%, 38% and 11.1 months, respectively. Patients with refractory/early relapse and those receiving treatment as first salvage had encouraging outcomes (median OS 13.2 and 11.3 months, respectively). Grade >3 immune-related adverse events were rare (14%) and self-limiting. Patients who achieved CRc had a higher frequency of progenitor exhausted CD8+ T-cells in the bone marrow prior to treatment and a non-significant increase in baseline T-cell diversity.

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Altered Expression Profiles of tRNA-derived fragments in relapsed/refractory multiple myeloma

Project description:tRNA related fragments(tRF) and tRNA halves(tiRNA) are novel class of short non-coding RNA derived from tRNAs. Using RNA sequencing, we evaluated the tRFs/tiRNAs expression profiles in relapsed/refractory multiple myeloma and multiple myeloma patients. Bioinformatics analyses indicated that tRFs/tiRNAs may be involved in the progression and drug-resistance of multiple myeloma.

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Chidamide triggers BTG1-mediated autophagy and reverses the chemotherapy resistance in the relapsed/refractory B cell lymphoma

Project description:Rituximab/chemotherapy relapsed and refractory B cell lymphoma patients have a poor overall prognosis, and it is urgent to develop novel drugs for improving the therapies of these patients. A new oral histone deacetylase inhibitor, chidamide shows anti-tumor activity by activating the pro-apoptosis pathway in some other hematological malignancies, suggesting its potential application to the relapsed and refractory B cell lymphoma. In this study, we examined the therapeutic effects of chidamide on the cell and mouse models of the rituximab/chemotherapy resistant B cell lymphoma, as well as the primary B cell lymphoma cells. In Raji-4RH and RL-4RH cells, the rituximab/chemotherapy resistant B cell lymphoma cell lines (RRCL), chidamide treatment induced growth inhibition and G0/G1 cell cycle arrest, which were associated with E2F1/2 inactivation and CDK2 degradation. The primary B cell lymphoma cells from Rituximab/chemotherapy relapsed and refractory patients were also very sensitive to chidamide treatment. Interestingly, chidamide triggered the cell death via the autophagy pathway instead of the activation of apoptosis in Raji-4RH and RL-4RH cells, likely due to the lack of the pro-apoptotic proteins in these resistant cells. In the RNA-seq and chromatin immunoprecipitation (ChIP) analysis, we identified BTG1 and FOXO1 as the direct target genes of chidamide, which control the autophagy and cell cycle respectively in RRCL treated with chidamide. Moreover, the combination of chidamide with the chemotherapy drug Cisplatin sensitized the RRCL to growth inhibition in a synergistic manner. Chidamide-Cisplatin combination significantly reduced the tumor burden of a mouse lymphoma model established with engraftment of RRCL. Taken together, our studies provides a theoretic and mechanistic basis for further evaluation of the chidamide-based clinical trial for rituximab/chemotherapy relapsed and refractory B cell lymphoma patients.

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