Gene expression profile of lung tumors
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE10799 | GEO | 2009/03/11
SECONDARY ACCESSION(S): PRJNA107381
REPOSITORIES: GEO
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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.
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Project description:2 normal lung parenchyma SAGE libraries, generated from 2 pools of 4 individuals each Discussed in the study: IDENTIFICATION OF NOVEL LUNG GENES IN BRONCHIAL EPITHELIUM BY SERIAL ANALYSIS OF GENE EXPRESSION Kim M. Lonergan1, Raj Chari1, Ronald J. deLeeuw1, Ashleen Shadeo1, Bryan Chi1, Ming-Sound Tsao2, Steven Jones3, Marco Marra3, Victor Ling1, Raymond Ng1,4, Calum MacAulay5, Stephen Lam5 and Wan L. Lam1 From the 1Department of Cancer Genetics & Developmental Biology, 5Department of Cancer Imaging, 3Canada's Michael Smith Genome Sciences Centre, British Columbia Cancer Research Centre, Vancouver, BC, Canada, 2Ontario Cancer Institute / Princess Margaret Hospital, Toronto, ON, Canada, 4the Department of Computer Science, University of British Columbia, Vancouver, BC, Canada A description of the transcriptome of human bronchial epithelium should provide a basis for studying lung diseases including cancer. We demonstrate here that minute epithelial specimens obtained by bronchial brushings afford reliable profiling by serial analysis of gene expression (SAGE) leading to lung gene discovery. We have deduced global gene expression profiles of bronchial epithelium and lung parenchyma, based upon a vast data set of nearly two million sequence tags from 21 SAGE libraries generated from individuals with a history of smoking. Cluster and linear regression analysis demonstrate the repeatability and reproducibility of bronchial SAGE libraries, and suggest that the transcriptome of the bronchial epithelium is distinct from that of lung parenchyma and other tissue types. This distinction is highlighted by the abundant expression of signature genes that reflect tissue-specific and region-specific functions. Through our analysis we have identified novel bronchial-enriched genes and a novel transcript variant for surfactant, pulmonary-associated protein B in lung parenchyma. Conspicuously, gene expression associated with ciliogenesis is evident in bronchial epithelium. Additionally, it is noted that a large number of unmapped tags awaits further investigation. This study represents a comprehensive delineation of the bronchial and parenchyma transcriptomes, identifying more than 20,000 known and hypothetical genes expressed in the human lung, constituting one of the largest human SAGE studies reported to date. Keywords: lung parenchyma 2 normal lung parenchyma SAGE libraries, generated from 2 pools of 4 individuals each
2006-11-20 | E-GEOD-3708 | 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:A description of the transcriptome of human bronchial epithelium should provide a basis for studying lung diseases including cancer. We demonstrate here that minute epithelial specimens obtained by bronchial brushings afford reliable profiling by serial analysis of gene expression (SAGE) leading to lung gene discovery. We have deduced global gene expression profiles of bronchial epithelium and lung parenchyma, based upon a vast data set of nearly two million sequence tags from 21 SAGE libraries generated from individuals with a history of smoking. Cluster and linear regression analysis demonstrate the repeatability and reproducibility of bronchial SAGE libraries, and suggest that the transcriptome of the bronchial epithelium is distinct from that of lung parenchyma and other tissue types. This distinction is highlighted by the abundant expression of signature genes that reflect tissue-specific and region-specific functions. Through our analysis we have identified novel bronchial-enriched genes and a novel transcript variant for surfactant, pulmonary-associated protein B in lung parenchyma. Conspicuously, gene expression associated with ciliogenesis is evident in bronchial epithelium. Additionally, it is noted that a large number of unmapped tags awaits further investigation. This study represents a comprehensive delineation of the bronchial and parenchyma transcriptomes, identifying more than 20,000 known and hypothetical genes expressed in the human lung, constituting one of the largest human SAGE studies reported to date. Keywords: SuperSeries This reference Series links data in the following related Series: GSE3707 Expression profiling of bronchial epithelium GSE3708 Expression profiling of normal lung parenchyma
2006-11-20 | E-GEOD-3754 | biostudies-arrayexpress
Project description:To examine whether the local carbon ion radiotherapy affects the characteristics of the metastatic tumors, the expression profiles of the primary tumors and the lung metastases were studied in a mouse squamous cell carcinoma model by applying local radiotherapy with no irradiation (negative control), gamma-ray irradiation (reference beam), and carbon-ion irradiation. Keywords: mouse, squamous cell carcinoma, primary tumor, lung metastases, radiotherapy, carbon ion, gamma ray A highly metastatic mouse squamous cell carcinoma NR-S1 was implanted into the hind leg of synergetic C3H/HeNrs mice and irradiated with 5 Gy of carbon ion beam. 8 Gy of gamma ray was used as a reference beam. At 2 weeks after the irradiation, the lung tissue was sampled. In order to collect samples of primary tumors, the tumors were implanted in other mice and irradiated in the same manner, and the primary tumors were collected at 1 week after the irradiation. The tumor cells of the primary and metastatic tumors were collected by laser microdissection, and oligonucleotide microarray analysis of the irradiated primary tumors and the metastatic tumors were all performed in comparison to the non-irradiated primary tumor by two-color methods.
2009-04-22 | E-GEOD-9305 | biostudies-arrayexpress