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Genomic landscape affected by allelic imbalance in the cancerization filed of normal appearing airway

ABSTRACT: Normal appearing airway samples from non-small cell lung (NSCLC) cancer patients were profiled using illumina sequencing arrays. Allelic imbalance was detected in normal-appearing large and small airway samples and affected known lung cancer driver genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE80519 | GEO | 2016/08/10

SECONDARY ACCESSION(S): PRJNA319250

REPOSITORIES: GEO

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Genomic landscape affected by allelic imbalance in the cancerization filed of normal appearing airway

Project description:Normal appearing airway samples from non-small cell lung (NSCLC) cancer patients were profiled using illumina sequencing arrays. Allelic imbalance was detected in normal-appearing large and small airway samples and affected known lung cancer driver genes. Multiple airway samples from 45 patients were analyzed using illumina sequencing arrays in order to comprehensively asses the genomic landscape of airway epithelia adjacent to NSCLC. For each patients there was at least one small airway sample, a tumor samples, as well as germline control sample (blood and/or normal uninvolved lung). In addition to these samples additional samples were analyzed for a subset of patients these included large airway, nasal, and multiple core needle biopsies from the tumor.

2016-08-10 | E-GEOD-80519 | biostudies-arrayexpress

Gene expression profiling of the adjacent airway field cancerization in early stage NSCLC

Project description:Previous work has shown that lung tumors and normal-appearing adjacent lung tissues share specific abnormalities that may be highly pertinent to the pathogenesis of lung cancer. However, the global and molecular adjacent airway field cancerization in non-small cell lung cancer (NSCLC) has not been characterized before. We sought to understand the transcriptomic architecture of the adjacent airway field canerization, in conjunction with tumors, to gain additional insights into the lung cancer biology and oncogenesis. We analyzed the transcriptome, using the Affymetrix Human Gene 1.0 ST platform, of matched NSCLC tumors, multiple normal airway epithelia with differential distance from the tumors as well as uninvolved normal lung tissues. We analyzed the airway field cancerization transcritpome to determine global differentially expressed cancerization profiles in adjacent airways as well as airway profiles that may be modulated by distance from tumors.

2014-03-04 | E-GEOD-44077 | biostudies-arrayexpress

Gene expression profiling of the adjacent airway field cancerization in early stage NSCLC

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Genomic Landscape Established by Allelic Imbalance in the Cancerization Field of a Normal Appearing Airway.

Project description:Visually normal cells adjacent to, and extending from, tumors of the lung may carry molecular alterations characteristics of the tumor itself, an effect referred to as airway field of cancerization. This airway field has been postulated as a model for early events in lung cancer pathogenesis. Yet the genomic landscape of somatically acquired molecular alterations in airway epithelia of lung cancer patients has remained unknown. To begin to fill this void, we sought to comprehensively characterize the genomic architecture of chromosomal alterations inducing allelic imbalance (AI) in the airway field of the most common type of lung tumors, non-small cell lung cancer (NSCLC). To do so, we conducted a genome-wide survey of multiple spatially distributed normal-appearing airways, multiregion tumor specimens, and uninvolved normal tissues or blood from 45 patients with early-stage NSCLC. We detected alterations in airway epithelia from 22 patients, with an increased frequency in NSCLCs of squamous histology. Our data also indicated a spatial gradient of AI in samples at closer proximity to the NSCLC. Chromosome 9 displayed the highest levels of AI and comprised recurrent independent events. Furthermore, the airway field AI included oncogenic gains and tumor suppressor losses in known NSCLC drivers. Our results demonstrate that genome-wide AI is common in the airway field of cancerization, providing insights into early events in the pathogenesis of NSCLC that may comprise targets for early treatment and chemoprevention. Cancer Res; 76(13); 3676-83. ©2016 AACR.

| S-EPMC5393446 | biostudies-literature

Field of Cancerization in Peripheral Airway Epithelium: miRNA

Project description:Field of cancerization in the airway epithelium has been increasing examined to understand early pathogenesis of non-small cell lung cancer. This study uses microarray high-throughput technologies to characterize the molecular aberrations in the terminal airway and bronchoalveolar cells in the context of field cancerization in high-risk smokers and lung cancer patients. We collected peripheral airway brushings from the contral-lateral lung of the tumor from cancer patients (n=17) and smoker controls (n=13); Total RNA were obtained from the peripheral airway epithelium.

2015-01-06 | E-GEOD-54541 | biostudies-arrayexpress

Field of Cancerization in Peripheral Airway Epithelium: Gene Expresssion

2015-01-06 | E-GEOD-54495 | biostudies-arrayexpress

Field of Cancerization in Peripheral Airway Epithelium: miRNA

2015-01-06 | GSE54541 | GEO

Field of Cancerization in Peripheral Airway Epithelium: Gene Expresssion

2015-01-06 | GSE54495 | GEO

Chronic exposure to waterpipe smoke elicits immunomodulatory and carcinogenic effects in the lung

Project description:Previous reports showed that cigarette smoke exposed normal-appearing airways in phenotypically lung cancer-free smokers carry alterations that are characteristic of tumors – suggestive of an airway field of injury. Very little is known of the effects of the chronic consumption of other forms of tobacco, such as waterpipe smoke (WPS), on lung pathobiology. Here we studied normal-appearing airway brushings from waterpipe smokers and those who were not exposed to WPS. We find that WPS elicits a molecular field of injury with gene programs that are pertinent to lung carcinogenesis.

2022-07-13 | GSE197653 | GEO

Comparative Transcriptomic Profiling of Normal-Appearing and Scarred Areas of the Lungs Reveals Pathobiological Clues to Idiopathic Pulmonary Fibrosis

Project description:RATIONALE: Idiopathic pulmonary fibrosis (IPF) is a fatal disease with overtly scarred peripheral and basilar lung regions and macroscopically unaffected central lung areas. OBJECTIVES: To gain better insight into IPF pathobiology by comparing transcriptomic profiles of normal-appearing and scarred regions of IPF lung. METHODS: Lung tissue samples from macroscopically unaffected (normal-appearing, IPFn) and scarred (IPFs) regions of explanted IPF lungs were analyzed by RNASeq and compared with healthy control (HC) lung tissues. RT-qPCR and immunohistochemistry were used to confirm selected findings. MEASUREMENTS AND RESULTS: Numerous previously reported IPF-associated gene expression disturbances as well as additional differentially expressed mRNAs were observed. There were profound transcriptomic changes in IPFn compared with HC tissues, which included elevated expression of extracellular matrix-, immunity- and inflammation-related mRNAs. The magnitude and statistical significance of these changes were comparable or greater than those in the IPFs-to-HC comparison. When directly compared with IPFn, IPFs tissues demonstrated elevated expression of epithelial mucociliary mRNAs. Compared with HC, both IPFn and IPFs tissues demonstrated reduced expression of mRNAs related to solute carrier membrane transport and metabolic processes. Primary fibroblast cultures from IPFn and IPFs tissues were transcriptomically identical. CONCLUSIONS: Macroscopically normal-appearing IPF tissues demonstrate profound disease activity and substantially similar transcriptomic profiles to scarred areas. Differences between these tissues are due to cell types other than fibroblasts and notably include enhanced expression of mucociliary genes in scarred areas. Deranged epithelial homeostasis or possibly non-transcriptomic factors may thus explain the marked architectural differences between normal-appearing and terminally scarred lung in end-stage IPF.

2018-01-24 | GSE99621 | GEO

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