Expression data from human lung FFPE samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE211528 | GEO | 2023/05/26
REPOSITORIES: GEO
Similar Datasets
Project description:In this study, we identified the dysregulated ultraconserved regions (UCRs) in Non-small-Cell Lung Cancer patients. We measured the expression profile of UCRs in 18 paired frozen tumor and adjacent non-tumor lung, by microarray analysis. This analysis is performed to identify the most significant dysregulated T-UCRs in tumor compared to the near non-cancerous lung tissue.
2021-12-07 | E-MTAB-11010 | biostudies-arrayexpress
Project description:Lung cancer remains the leading cause of cancer-related death due to poor treatment responses and resistance arising from tumor heterogeneity. Here we show that adverse prognosis associated with epigenetic silencing of the tumour suppressor RASSF1A is due to increased deposition of extracellular matrix (ECM), tumour stiffness and metastatic dissemination in vitro and in vivo. We find that lung cancer cells with RASSF1A promoter methylation display constitutive nuclear YAP1 and expression of collagen prolylhydroxylase (P4HA2) which increases collagen deposition. Furthermore, we identify that elevated collagen creates a stiff-ECM which in turn triggers cancer stem-like programming and metastatic dissemination in vivo. Re-expression of RASSF1A or inhibition of P4HA2 activity reverse these effects and increase markers of lung differentiation (TTF-1, Mucin5B). Our study identifies RASSF1A as a clinical biomarker associated with mechanical properties of ECM which increases levels of cancer stemness and risk of metastatic progression in lung adenocarcinoma. Moreover, we highlight P4HA2 as a potential target for uncoupling ECM signals that support cancer stemness.
2019-05-20 | PXD012694 | Pride
Project description:Detection, treatment, and prediction of outcome for lung cancer patients increasingly depend on a molecular understanding of tumor development and sensitivity of lung cancer to therapeutic drugs. The application of genomic technologies, such as microarray, is widely used to monitor global gene expression and has built up invaluable information and knowledge, which is essential to the discovery of new insights into the mechanisms common to cancer cells, resulting in the identification of unique, identifiable signatures and specific characteristics. It is likely that application of microarray may revolutionize many aspects of lung cancer being diagnosed, classified, and treated in the near future. We used microarrays to detail the global gene expression patterns of lung cancer. Keywords: Disease state analysis
2007-08-30 | GSE7670 | GEO
Project description:Background: The identification of cancer driver genes from sequencing data has been crucial in deepening our understanding of tumor biology and expanding targeted therapy options. However, apart from the most commonly altered genes, the mechanisms underlying the contribution of other mutations to cancer acquisition remain understudied. Leveraging on our whole-exome sequencing of the largest Asian lung adenocarcinoma (LUAD) cohort (n=302), we now functionally assess the mechanistic role of a novel driver, PARP4. Methods: In vitro and in vivo tumorigenicity assays were used to study the functional effects of PARP4 loss and mutation in multiple lung cancer cell lines. Interactomics analysis by quantitative mass spectrometry was conducted to identify PARP4’s interaction partners. Transcriptomic data from cell lines and patient tumors were used to investigate splicing alterations. Results: PARP4 depletion or mutation (I1039T) promotes the tumorigenicity of KRAS- or EGFR-driven lung cancer cells. Disruption of the vault complex, with which PARP4 is commonly associated, did not alter tumorigenicity, indicating that PARP4’s tumor suppressive activity is mediated independently. The splicing regulator hnRNPM is a potentially novel PARP4 interaction partner, the loss of which likewise promotes tumor formation. hnRNPM loss results in splicing perturbations, with a propensity for dysregulated intronic splicing that was similarly observed in PARP4 knockdown cells and in LUAD cohort patients with PARP4 copy number loss. Conclusions: PARP4 is a novel modulator of lung adenocarcinoma, where its tumor suppressive activity is mediated not through the vault complex – unlike conventionally thought, but in association with its novel interaction partner hnRNPM, thus suggesting a role for splicing dysregulation in LUAD tumorigenesis.
2024-04-02 | PXD050844 | Pride
Project description:MS spectrum of lung tissue metabolic analysis in 131 patients with lung cancer or benign lung tumor. These include lung cancer tissues/benign tumor tissues, adjacent normal tissues and distal normal tissues.
2020-06-19 | PXD019969 | iProX
Project description:The target sequecing vcf data of tumor and curculating tumor DNA for non-small cell lung cancer patients.
2022-05-09 | PRJEB52694 | EVA
Project description:Early detection of small cell lung cancer crucially demands highly reliable markers. Growing evidence suggests that extracellular vesicles carry tumor cell-specific cargo suitable as protein markers in cancer. Therefore, we isolated plasma-derived exosomes from newly diagnosed small cell lung cancer patients and investigated proteome dynamics of these exosomes aiming at improving the detection of small cell lung cancer. A total of 1,016 proteins were initially identified. After data processing and statistical analysis, several proteins were found to be differentially expressed in comparing small cell lung cancer patients and healthy individuals, indicating that circulating exosomes may encompass specific proteins with potential diagnostic attributes for small cell lung cancer. Furthermore, our data may indicate a novel tumor-suppressing role of blood coagulation and involvement of complement activation in small cell lung cancer pathogenesis.
2022-04-04 | PXD028885 | Pride
Project description:Lung cancer remains the most common cause of cancer deaths worldwide, yet there is currently a lack of diagnostic noninvasive biomarkers that could guide treatment decisions. Small molecules (<1500 Da) were measured in urine collected from 469 lung cancer patients and 536 population controls using unbiased liquid chromatography-mass spectrometry. Clinical putative diagnostic and prognostic biomarkers were validated by quantitation and normalized to creatinine levels at two different time points and further validated in an independent sample set, which comprises 80 cases and 78 population controls, with similar demographic and clinical characteristics when compared to the training set. Creatine riboside (IUPAC name: 2-{2-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)-oxolan-2-yl]-1-methylcarbamimidamido}acetic acid), a novel molecule identified in this study, and N-acetylneuraminic acid (NANA), were each significantly (P <0.00001) elevated in non–small cell lung cancer (NSCLC) and associated with worse prognosis (hazard ratio (HR) =1.81 [P =0.0002], and 1.54 [P =0.025], respectively). Creatine riboside was the strongest classifier of lung cancer status in all and stage I–II cases, important for early detection, and also associated with worse prognosis in stage I–II lung cancer (HR =1.71, P =0.048). All measurements were highly reproducible with intraclass correlation coefficients ranging from 0.82 – 0.99. Both metabolites were significantly (P <0.03) enriched in tumor tissue compared to adjacent non-tumor tissue (N =48), thus revealing their direct association with tumor metabolism. Creatine riboside and NANA may be robust urinary clinical metabolomic markers that are elevated in tumor tissue and associated with early lung cancer diagnosis and worse prognosis.
2014-05-06 | MTBLS28 | MetaboLights
Project description:Tumor-infiltrating myeloid cells (TIMs) comprise monocytes, macrophages, dendritic cells and neutrophils, and have emerged as key regulators of cancer growth. These cells can diversify into a spectrum of states, which may promote or limit tumor outgrowth, but remain poorly understood. Here, we used single-cell RNA sequencing to map TIMs in non-small cell lung cancer patients. We uncovered 25 TIM states, most of which were reproducibly found across patients. To facilitate translational research of these populations, we also profiled TIMs in mice. In comparing TIMs across species, we identified a near-complete congruence of population structures among dendritic cells and monocytes; conserved neutrophil subsets; and species differences among macrophages. By contrast, myeloid cell population structures in patients’ blood showed limited overlap with those of TIMs. This study determines the lung TIM landscape and sets the stage for future investigations into the potential of TIMs as immunotherapy targets.
2019-04-09 | GSE127465 | GEO
Project description:Pulmonary fibrosis develops as a consequence of environmentally induced lung injury and/or an inherent disease susceptibility causing fibroblast activation, proliferation and extracellular matrix deposition. The study was undertaken to characterise global gene expression in pulmonary fibroblasts to better understand the mechanisms underlying the fibrotic fibroblast phenotype. Gene expression was evaluated in lung fibroblasts derived from ten controls (normal periphery of resected tumor), open lung biopsies from eight patients with interstitial lung disease associated with systemic sclerosis (fibrotic non specific interstitial pneumonia pattern on biopsy), and from three patients with usual interstitial pneumonia. Lung fibroblasts were grown to confluence in DMEM with 10% fetal calf serum. At confluence, lung fibroblasts were serum-deprived for 44 hours in the presence of fibroblast growth medium with the addition of 0.1% bovine serum albumin (Sigma).
2013-08-05 | E-GEOD-40839 | biostudies-arrayexpress