TRIM28 keeps the time of mitotic gene expression sustaining proliferation and progression of Malignant Pleural Mesothelioma (MPM).
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PROVIDER: PRJNA759144 | ENA |
REPOSITORIES: ENA
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Project description:RNA extracted from tumor samples of 86 patients affected by MPM was analyzed on the nCounter system using a custom panel called MPM_C9073 (Nanostring Technologies).
2022-08-03 | GSE183088 | GEO
Project description:Malignant pleural mesothelioma (MPM) is a highly lethal, poorly understood neoplasm that is typically associated with asbestos exposure. We performed transcriptional profiling using high-density oligonucleotide microarrays containing approximately 22,000 genes to elucidate potential molecular and pathobiological pathways in MPM using discarded human MPM tumor specimens (n=40), normal lung specimens (n=4), normal pleura specimens (n=5), and MPM and SV40-immortalized mesothelial cell lines (n=5). In global expression analysis using unsupervised clustering techniques, we found two potential subclasses of mesothelioma which correlate loosely with tumor histology. We also identified sets of genes with expression levels that distinguish between multiple tumor subclasses, normal and tumor tissues, and tumors with different morphologies. Microarray gene expression data were confirmed using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and protein analysis for three novel candidate oncogenes (NME2, CRI1, and PDGFC) and one candidate tumor suppressor (GSN). Finally, we used bioinformatics tools (i.e. software) to create and explore complex physiological pathways that may be relevant in mesothelioma tumorigenesis, pathobiology, or both. Tissues and cell lines profiled using microarrays. Discarded MPM surgical specimens (n=40), normal pleura specimens (n=5), and normal lung specimens (n=4) were freshly collected (and snap frozen) from patients who underwent surgery at Boston's Brigham and Women's Hospital (BWH) between October 1998 and August 2000. All of these patients underwent extrapleural pneumonectomy with heated intra-pleural cisplatin chemotherapy delivered after the specimens were removed. All normal specimens were obtained from patients who were never diagnosed with MPM. Two human MPM cell lines (MS589 and MS428) were kindly provided by Jonathan A. Fletcher, M.D., Department of Pathology, BWH. The JMN1B MPM cell line19,20 has been described previously. The SV40-immortalized, non-tumorigenic mesothelial cell line (Met-5A)21 and the MPM cell line MSTO-211H22 were purchased from the American Type Culture Collection. Normal tissues were obtained from additional consented patients undergoing treatment for diseases other than MPM. All MPM samples used in these studies contained relatively pure tumor (greater than 50% tumor cells per high power field examined in a section adjacent to the tissue used). The microscopic slides from the patients' resection specimens were reviewed by one of the authors (J.G.), and the diagnosis and histologic subclassification of MPM confirmed in all cases. Linked clinical and pathological data were obtained for all patients who contributed tumor specimens. Specimens and data were rendered anonymous to protect patient confidentiality. Studies utilizing human tissues were approved by and conducted in accordance with the policies of the Institutional Review Board at BWH.
2005-06-01 | GSE2549 | GEO
Project description:For establishing a live-cell biobank of Malignant Pleural Mesothelioma (MPM) samples, cultures of two MPM patients were compared to the original tumor tissue using Affymetrix OncoScan Microarrays for genome-wide CNV and LOH detection.
2018-01-18 | GSE109305 | GEO
Project description:Diagnosis of malignant pleural mesothelioma (MPM) is a challenging task because of its overlap with other neoplasms or even reactive conditions. Recently, DNA methylation analysis proved to be an effective tool for tumor diagnosis. We thus set out to test this approach for MPM diagnosis. A discovery (n=33) and an independent validation cohort (n=46) of MPM samples were subjected to array-based DNA methylation analyses and their DNA methylation patterns were compared to a representative set of both malignant and benign diagnostic mimics. By both unsupervised hierarchical clustering and t-distributed stochastic neighbor embedding analysis, MPM samples of the discovery cohort exhibited a distinct DNA methylation profile, different from that of other neoplastic and reactive mimics.
2021-03-20 | GSE164269 | GEO
Project description:The goal of this experiment was to get deep into TRIM28 biological function in malignant pleural mesothelioma. To this end MSTO-211H cell line was infected by two different sgRNAs targeting TRIM28 and a non-targeting sgRNA as control. Two independent experiments were performed.RNA was collected 7 days after infection and changes in gene expression were analyzed by mRNA-seq.
2023-09-16 | E-MTAB-10942 | biostudies-arrayexpress
Project description:We characterized tumor and immune microenvironment (TiME) of malignant pleural mesothelioma (MPM) using immunoproteomic approach to comprehensively understand the landscape to affect prognosis and possibly to predict response to immunotherapy. Time-of-Flight Mass Cytometry (CyTOF) was performed on the tumors of 12 MPM patients. We comprehensively analyzed TiME by developing intuitive models for visualizing single-cell data with statistical inference and performed unsupervised clustering of cell frequency. A clinically relevant protein signature through mass spectrometry and mRNA transcriptome array was tested for its ability to reflect prognosis in three independent cohorts (n=330) and to predict response to immune checkpoint inhibitor therapy in publicly available data and in 10 patients of MPM treated with anti-PD1 therapy. A systematic understanding of antitumor immunity by immunoproteomic characterization of TiME envisions significant progress in developing rational immunotherapeutic strategies in MPM.
2018-04-05 | GSE99070 | GEO
Project description:Malignant pleural mesothelioma (MPM) is an asbestos-related lethal malignancy refractory to conventional therapies. Since its symptoms are not specific, MPM can be easily confused with other chest diseases, especially metastatic lung adenocarcinomas (ADCA), and diagnosis is often established late when the disease is at an advanced stage. Classically, a reliable diagnosis requires histological analysis of multiple pleural biopsies. However, there is still no absolute marker for MPM. Thus, with the aim of identifying novel markers with higher specificity and sensitivity, gene expression profiling studies have been conducted using tumor specimens. Because of the cell heterogeneity of tumor samples, we decided to apply counterflow centrifugal elutriation to isolate cancer cells from pleural effusions, which are a common feature of MPM and ADCA. We profiled a total of 54 biological samples corresponding to triplicates of 13 MPM and 4 ADCA as well as the SV40-immortalized cell line MeT-5A. Our microarray results confirmed some of the existing markers which are currently used to distinguish MPM from ADCA by immunostaining of pleural biopsies and which have also been proposed for use in a PCR-based assay. Of particular interest, we also identified novel cellular markers (including predominantly COL3A1, OSAP, OCIAD2, XAGE1), which we validated by real time RT-PCR, and novel soluble markers, such as osteonectin and galectin-3, whose clinical utility as molecular targets remains to be determined. Keywords: cell type comparison three-condition experiment: ADCA vs MPM vs Met5A cells 13 MPM, 4 ADCA and Met5A were independantly grown and harvested 3 biological replicates per cell line, one replicate per array
2010-05-16 | E-GEOD-17310 | biostudies-arrayexpress
Project description:Malignant pleural mesothelioma (MPM) is a deadly pleural malignancy with over 90% mortality within five years and a median survival of approximately 7 months without treatment. The current first-line chemotherapy, a combination of pemetrexed and cisplatin, modestly extends survival, with the addition of bevacizumab offering a further 2-month benefit. Radiation therapy, while not effective as a primary treatment due to the extensive field required, plays a role in multimodal approaches or as localized therapy. The diversity in patient outcomes and responses to treatments indicates significant tumor heterogeneity in MPM, underscoring the need for therapies that consider this variability and target the molecular specifics of individual MPM cases. Tumor heterogeneity is observed at both intertumor and intratumor levels, encompassing tumor cells and their microenvironments. Molecular profiling studies have further highlighted this heterogeneity, complicating the identification of a unique biomarker for MPM.
2024-01-04 | GSE247203 | GEO
Project description:To identify regions that display DNA copy number alterations in malignant pleural mesothelioma (MPM), we carried out array comparative genomic hybridization (CGH) analysis with 14 MPM cell lines. Regions of genomic aberrations observed in >20% of individuals were 9p21.3, 13q12.11, 16p13, and 22q12.2 of losses. The most frequent alteration was 9p21.3, which include the p16INK4/p14ARF. The loss of 22q12.2 regions include the NF2 was observed in 3 out of 14 cell lines. In 3 cell lines, loss of 13q12.11 region which contains Large Tumor Suppressor, homolog 2 (LATS2) was detected. Human malignant pleural mesothelioma cell lines were profiled on Agilent 244K aCGH arrays according to manufacturer’s instructions. Pooled normal human genomic DNA was used as the reference.
2010-06-15 | E-GEOD-22237 | biostudies-arrayexpress
Project description:To identify regions that display DNA copy number alterations in malignant pleural mesothelioma (MPM), we carried out array comparative genomic hybridization (CGH) analysis with 14 MPM cell lines. Regions of genomic aberrations observed in >20% of individuals were 9p21.3, 13q12.11, 16p13, and 22q12.2 of losses. The most frequent alteration was 9p21.3, which include the p16INK4/p14ARF. The loss of 22q12.2 regions include the NF2 was observed in 3 out of 14 cell lines. In 3 cell lines, loss of 13q12.11 region which contains Large Tumor Suppressor, homolog 2 (LATS2) was detected.
2010-06-15 | GSE22237 | GEO