The RNA sequencing results revealed the expression of different genes and signaling pathways during chemotherapy resistance in peripheral T-cell lymphoma
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ABSTRACT:
PROVIDER: PRJNA1051666 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27193453_1.fastq.gz | Fastqsanger.gz | |||
| SRR27193453_2.fastq.gz | Fastqsanger.gz | |||
| SRR27193454_1.fastq.gz | Fastqsanger.gz | |||
| SRR27193454_2.fastq.gz | Fastqsanger.gz | |||
| SRR27193455_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: NK/T cell lymphoma (NKTCL) is a type of non-Hodgkin's lymphoma that occurs primarily extra nodal. The main treatment methods are radiotherapy and chemotherapy. The 5-year recurrence rate is still high, and there is currently no standard treatment for relapse-resistant patients. Compared with other lymphoid tumors, its malignancy is relatively strong, and the prognosis is not very good. Here, we try to identify the key genes and signaling pathways related to chemotherapy resistance in extra nodal NK/T cell lymphoma. Methods: Firstly, we collect white blood cells from 5 healthy controls and 7 different clinical patients,4 patients were chemotherapy sensitive while 3 patients were chemotherapy resistant. Secondly, after total RNA extraction from those white blood cells, RNA sequence was performed on the Illumina HiSeq platform. Finally, we used qRT-PCR to confirm the expression patterns of different expression genes(DEGs) from the mostly enriched signaling pathways, especially the cancer related genes on the NK/T cell lymphoma clinical individuals. Results: The RNA sequence results displayed 4063 DEGs, including 1128 up regulated and 2935 down regulated genes in the chemotherapy resistance cases of extra nodal NK/T cell lymphoma specimens. Further quantitative gene expression analysis was performed to identify the differential expression pattern in all libraries. And 9 down regulated genes and 10 up regulated genes were confirmed by quantitative real time PCR comparison of chemotherapy resistance in extra nodal NK/T cell lymphoma from 6 clinical specimens. KEGG analysis revealed significant pathway changes, including 6 down regulated and 9 up regulated gene enrichment pathways. The TNF signaling pathway, one of the most extensively regulated, was among the pathways. DEGs and the TNF signaling pathway may be essential in the resistance to chemotherapy in extra nodal NK/T cell lymphoma. Conclusion:Our finding indicated that different genes expression may be important for chemotherapy resistance in extra nodal NK/T cell lymphoma, particularly TNFRSF1B, TRADD2 and MAP3K7.The TNF signaling pathway, a critical signaling pathway, was pinpointed as a potential factor in the emergence of chemotherapy resistance in extra nodal NK/T cell lymphoma.
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Project description:BackgroundPeripheral T-cell lymphoma (PTCL) is a subtype of non-Hodgkin's lymphoma that occurs primarily at extranodal sites and is commonly treated using chemotherapy and radiotherapy. PTCL is more malignant than other lymphoid tumors, resulting in a poor prognosis.The 5-year recurrence rate remains high, and there is a lack of standard treatment for patients with relapse-resistant disease. However, the molecular mechanisms underlying the resistance of peripheral T-cell lymphoma cells to chemotherapeutic drugs, as well as identifying strategies to overcome drug resistance remains unclear. In this study, we aimed to identify pivotal genes and signaling pathways associated with chemotherapy resistance in PTCL.MethodsIn this study, a total of 5 healthy controls and 7 clinical patients were enrolled; 4 patients were classified as chemotherapy sensitive, and 3 patients were classified as chemotherapy resistant. Peripheral blood samples were collected from each participant, and total RNA was extracted from the white blood cells. RNA sequencing was conducted on the Illumina HiSeq platform to obtain comprehensive gene expression profiles. Subsequently, the expression patterns of the DEGs associated with the most enriched signaling pathways, with a special focus on cancer-related genes, were validated using quantitative real-time polymerase chain reaction (qRT-PCR) in peripheral TCL patients.ResultsRNA sequencing (RNA-seq) analysis revealed 4063 differentially expressed genes (DEGs) in peripheral T-cell lymphoma specimens from patients with chemotherapy resistance, of which 1128 were upregulated and 2935 were downregulated. Subsequent quantitative gene expression analysis confirmed a differential expression pattern in all the libraries, with 9 downregulated genes and 10 upregulated genes validated through quantitative real-time PCR in 6 clinical specimens from patients with chemotherapy resistance. KEGG pathway analysis revealed significant alterations in several pathways, with 6 downregulated pathways and 9 upregulated pathways enriched in the DEGs. Notably, the TNF signaling pathway, which is extensively regulated, was among the pathways that exhibited significant changes. These findings suggest that DEGs and the TNF signaling pathway may play crucial roles in chemotherapy resistance in peripheral T-cell lymphoma.ConclusionOur study revealed that the expression of specific genes, including TNFRSF1B, TRADD2, and MAP3K7, may play an important role in chemotherapy resistance in peripheral T-cell lymphoma. Moreover, we identified the downregulation of the TNF signaling pathway, a crucial pathway involved in cell survival, death, and differentiation, as a potential contributor to the development of chemotherapy resistance in peripheral T-cell lymphoma. These findings provide valuable insights into the molecular mechanisms underlying chemotherapy resistance and highlight potential targets for overcoming treatment resistance in this challenging disease.
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Project description:Analysis of gene expression levels in non-Hodgkin lymphoma (NHL) cells exposed to neutrophils and chemotherapy. We aimed to see the impact of normal peripheral blood neutrophils on the sensitivity of lymphoma B cells to anticancer agents. The results provide insight into the genes that may be involved in the mechanism by which neutrophils attenuate the sensitivity of lymphoma B cell to chemotherapy.
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Project description:Chimeric antigen receptor (CAR) T cell therapy depends on T cells that are genetically modified to recognize and attack cancer cells. Their effectiveness thus hinges on the functionality of a patient’s own T cells. However, CAR T cell therapy is currently only approved for advanced cancers after at least one line of chemotherapy. To evaluate the potential negative effects of prior exposure to chemotherapy on T cell functionality we studied T cells of two B cell Non-Hodgkin’s lymphoma (B-NHL) patient cohorts, one collected before treatment (pre-therapy) and the other after one or more (median 3) lines of chemotherapy (post-therapy). Leveraging advanced multi-parameter flow cytometry and single-cell RNA sequencing (scRNAseq), we elucidated significant modifications in T cell subsets and their transcriptional profiles post-therapy. Our analysis revealed a discernible shift towards phenotypically more differentiated T cells and an upregulation of markers indicative of T cell exhaustion. Additionally, scRNAseq and DNA methylation analyses revealed gene expression and epigenetic changes associated with diminished functionality in post-therapy T cells. Cytotoxicity assays demonstrated superior killing efficacy of CAR T cells derived from treatment-naïve patients compared to those with chemotherapy history. These findings corroborate that employing T cells collected prior to frontline chemotherapy could enhance the effectiveness of CAR T cell therapy and improve patient outcomes.
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Project description:The survival of patients with diffuse large-B-cell lymphoma after chemotherapy is influenced by molecular features of the tumors. We used the gene-expression profiles of these lymphomas to develop a molecular predictor of survival. METHODS: Biopsy samples of diffuse large-B-cell lymphoma from 240 patients were examined for gene expression with the use of DNA microarrays and analyzed for genomic abnormalities. Subgroups with distinctive gene-expression profiles were defined on the basis of hierarchical clustering. A molecular predictor of risk was constructed with the use of genes with expression patterns that were associated with survival in a preliminary group of 160 patients and was then tested in a validation group of 80 patients. The accuracy of this predictor was compared with that of the international prognostic index. RESULTS: Three gene-expression subgroups--germinal-center B-cell-like, activated B-cell-like, and type 3 diffuse large-B-cell lymphoma--were identified. Two common oncogenic events in diffuse large-B-cell lymphoma, bcl-2 translocation and c-rel amplification, were detected only in the germinal-center B-cell-like subgroup. Patients in this subgroup had the highest five-year survival rate. To identify other molecular determinants of outcome, we searched for individual genes with expression patterns that correlated with survival in the preliminary group of patients. Most of these genes fell within four gene-expression signatures characteristic of germinal-center B cells, proliferating cells, reactive stromal and immune cells in the lymph node, or major-histocompatibility-complex class II complex. We used 17 genes to construct a predictor of overall survival after chemotherapy. This gene-based predictor and the international prognostic index were independent prognostic indicators.
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