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Identification of intrinsically immunogenic small cell lung carcinoma (SCLC) subpopulations

ABSTRACT: Identification of intrinsically immunogenic small cell lung carcinoma (SCLC) subpopulations

PROVIDER: PRJNA706431 | ENA |

REPOSITORIES: ENA

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Identification of intrinsically immunogenic small cell lung carcinoma (SCLC) subpopulations

Project description:Identification of intrinsically immunogenic small cell lung carcinoma (SCLC) subpopulations

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Identification of intrinsically immunogenic small cell lung carcinoma (SCLC) subpopulations

Project description:This SuperSeries is composed of the SubSeries listed below.

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Quantitative Proteomics Analysis of Extracellular Vesicles from mouse-derived SCLC cell lines

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The RNAseq of 79 small cell lung cancer (sclc) and 7 normal control

Project description:Even though small cell lung cancer (SCLC) has entered the age of broad genomic analysis, platinum-based chemotherapy remains the standard care for SCLC. Topotecan is the only approved agent for recurrent or progressive SCLC (1). In the absence of well-defined genomic biomarkers, clinical efficacy signals in genomically distinct subsets of SCLC could have been missed. Serine/Arginine Splicing Factor 1 (SRSF1) is a member of SR protein family. The deleterious consequences of overexpression of the SRSF1 proto-oncogene in human cancers suggest that there are complex mechanisms and pathways underlying SRSF1-mediated transformation (2). Whole exome and transcriptome sequencing of primary tumor SCLC from 99 Chinese patients has identified SRSF1 DNA amplification and mRNA over-expression which predicts poor survival in Chinese SCLC patients. In vitro and in vivo studies have demonstrated that SRSF1 is essential for tumorigenecity of SCLC and plays a key role in DNA repair and chemo-sensitivity. We did RNAseq on 79 small cell lung cancer patients' tumor sample and 7 normal lung tissue. We normalized the RNAseq data and did differential expression analysis. The deleterious consequences of overexpression of the SRSF1 proto-oncogene in human cancers suggest that there are complex mechanisms and pathways underlying SRSF1-mediated transformation.

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