Gene expression profile of lung tumors
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE10799 | GEO | 2009/03/11
SECONDARY ACCESSION(S): PRJNA107381
REPOSITORIES: GEO
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Project description:We have investigated whether the early dissemination of tumor cells into bone marrow is associated with a specific molecular pattern in primary lung cancer Experiment Overall Design: two groups of primary lung adenocarcinomas were compared differentiating in the metastatic potential
2009-03-14 | E-GEOD-10799 | biostudies-arrayexpress
Project description:PURPOSE: Bone marrow (BM) is a common homing organ for early disseminated tumor cells (DTC) and their presence can predict the subsequent occurrence of overt metastasis and survival in lung cancer. It is still unclear whether the shedding of DTC from the primary tumor is a random process or a selective release driven by a specific genomic pattern. EXPERIMENTAL DESIGN: DTCs were identified in BM from lung cancer patients by an immunocytochemical cytokeratin assay. Genomic aberrations and expression profiles of the respective primary tumors were assessed by microarrays and FISH analyses. The most significant results were validated on an independent set of primary lung tumors and brain metastases. RESULTS: Combination of DNA copy number profiles (array CGH) with gene expression profiles identified five chromosomal regions differentiating BM-negative from BM-positive patients (4q12-q32, 10p12-p11, 10q21-q22, 17q21 and 20q11-q13). Copy number changes of 4q12-q32 were the most prominent finding, containing the highest number of differentially expressed genes irrespective of chromosomal size (p=0.018). FISH analyses on further primary lung tumor samples confirmed the association between loss of 4q and the BM-positive status. In BM-positive patients 4q was frequently lost (37% vs. 7%), whereas gains could be commonly found among BM-negative patients (7% vs. 17%). The same loss was also found to be common in brain metastases from both small and non-small-cell lung cancer patients (39%). CONCLUSIONS: Thus, our data indicates for the first time that early hematogeneous dissemination of tumor cells might be driven by a specific pattern of genomic changes.
2009-10-05 | GSE13191 | GEO
Project description:MicroRNA expression pattern in 20 pairs of primary lung cancers and their corresponding non cancerous lung tissues. These specimens were obtained from the Nice Hospital Tumor Bio Bank, France. Dye swap-experiment comparing cancerous tissue versus adjacent normal lung tissue.
2010-09-30 | E-GEOD-18692 | biostudies-arrayexpress
Project description:Metastasis is a multi-step process that involves direct cross-talk between cancer cells and their microenvironment. Here we assessed the effect of paired mesenchymal stem cells (MSCs) isolated from the tumor tissue (T-) and normal lung adjacent tissue (N-) on the expression profile of primary lung cancer cells. We observed that MSCs induce the expression of genes in tumor cells associated with an aggressive phenotype and promote early tumor cell dissemination. Our observations provide new insight into mechanisms whereby MSCs promote lung cancer metastasis.
2018-03-31 | GSE104858 | GEO
Project description:Lung tumors, as well as normal tumor-adjacent (NTA) tissue of non-small cell lung cancer (NSCLC) patients, were collected and subjected label-free quantitation shotgun proteomics in data-independent mode to identify differences between the tumors and adjacent tissue. By employing in-depth proteomics, we identified several pathways that are up- or downregulated in the tumors of non-small cell lung cancer patients.
2023-11-27 | PXD046998 | Pride
Project description:Initial screening for potential metastases suppressors down regulated by methylation was performed using lung cancer cell line models specific for site-specific metastasation. Gene expression profiling and qRT-PCR validations were conducted on tumor tissues from primary lung cancer (LC) and brain metastasis. HERC5 was further characterized for the methylation pattern. Three human lung cancer cell lines H1993, H1395 and were compared to the (SV40)-transformed human bronchial epithelial cell line BEAS-2B in order to find genes, which might be specifically involved in brain metastasis formation. The cell lines were treated with 5-Aza-2'-deoxycytidine in order to find genes potentially down regulated by methylation. The non-tumorigenic cell line BEAS-2B was used to control for stress response after the treatment with 5-Aza-2'-deoxycytidine.
2014-11-18 | E-GEOD-57492 | biostudies-arrayexpress
Project description:Tumor tissue of lung carcinoid tumors (pulmonary neuroendocrine tumors) and adjacent normal lung tissue was profiled using scRNA-seq
2022-02-08 | GSE196303 | GEO
Project description:The leading cause of death in human patients with metastatic renal cell carcinoma (RCC) and malignant cancer in general is the dissemination of the primary tumor to secondary sites. The mechanisms by which RCC colonize the lung microenvironment during metastasis remain largely unknown. To investigate the mechanisms of lung colonization by tumor cells, we grafted human RCC cells with different lung metastatic activities in mice. Gene expression profiling of the mouse lung stromal compartment revealed a gene signature enriched for neutrophil-specific functions, induced preferentially by poorly metastatic cells. Analysis of the gene expression patterns in tumor cells and clinical specimens showed an inverse correlation between metastatic activity and the levels of a number of chemokines, including CXL5 ad IL8. Enforced depletion of CXCL5 and IL8 in tumor cells allowed us to establish a functional link between lung neutrophil infiltration, the secretion of chemokines by cancer cells and metastatic activity. Finally, we showed that human neutrophils displayed a higher cytotoxic activity toward poorly metastatic cells relative to highly metastatic cells. Together, these results support a model in which neutrophils recruited to the lung by tumor-secreted chemokines build an antimetastatic barrier and loss of those neutrophil chemokines in tumor cells is a critical rate-limiting step during lung metastatic seeding. Total 12 samples are analysed from two cell lines (SN12C and LM2) and Normal tissue. There are four biological replicates for each cell line and four biological replicates from normal lung tissue (as reference).
2012-05-29 | E-GEOD-29688 | biostudies-arrayexpress
Project description:Disseminated cancer cells (DCCs) that escape the primary site can seed in distal tissues, but may take several years, or even decades to grow out into overt metastases, a phenomenon termed tumor dormancy. Despite its importance in metastasis and residual disease, few studies have been able to successfully model or characterize dormancy within melanoma. Here, we show that age-related changes in the lung microenvironment facilitate a permissive niche for efficient outgrowth of disseminated dormant tumor cells, in contrast to the aged skin, where age-related changes suppress melanoma growth but drive dissemination. A model of melanoma progression that addresses these microenvironmental complexities is the phenotype switching model, which argues that melanoma cells switch between a proliferative cell state and a slower-cycling, invasive state1-3. We have previously shown that dermal fibroblasts are key orchestrators of promoting phenotype switching in primary melanoma tumors via changes in the secretion of soluble factors during aging4-8. Our new data identifies Wnt5A as a master regulator of activating melanoma DCC dormancy within the lung, which initially enables efficient dissemination and seeding of melanoma cells in metastatic niches. Age-induced reprogramming of lung fibroblasts increases their secretion of the soluble Wnt antagonist sFRP1, which inhibits Wnt5A, enabling efficient metastatic outgrowth. Further, we have identified the tyrosine kinase receptors AXL and MER as promoting a dormancy-toreactivation axis respectively. Overall, we find that age-induced changes in distal metastatic microenvironments promotes efficient reactivation of dormant melanoma cells in the lung.
2022-03-03 | MSV000088977 | MassIVE
Project description:We used a proteogenomic approach combining RNA-sequencing and mass spectrometry to study the MHC I-immunopeptidome of cutaneous melanoma and non-small cell lung cancer (NSCLC) samples. The RNA-sequencing of each sample was used to construct sample-specific databases for the mass spectrometry-based identification of MHC I-associated peptides (MAPs). MAPs were then filtered based on their RNA expression in the respective cancer types from The Cancer Genome Atlas (TCGA-SKCM for melanoma MAPs, or TCGA-LUSC and TCGA-LUAD for NSCLC MAPs) vs. benign tissues (from the Genotype-Tissue Expression (GTEx) Project, medullary thymic epithelial cells, purified blood and bone marrow cells, and normal melanocytes for melanoma or bronchial brushing samples for NSCLC). MAPs were classified as mutated tumor-specific antigens (mTSAs, derived from non-synonymous mutations expressed in the sample of origin), or unmutated tumor antigens: aberrantly expressed tumor-specific antigens (aeTSAs, no/low expression in benign tissues and at least two times higher expression in TCGA), tumor-associated antigens (TAAs, significant expression in benign tissues and at least two times higher expression in TCGA), lineage-associated antigens (LSAs, specific expression to cancer and normal tissue of origin, i.e., lung and bronchial brushing samples for NSCLC or skin and melanocytes for melanoma). The tumor antigens described here represent attractive targets for immunotherapy of melanoma and NSCLC.
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