Project description:Lung cancer is the worldwide leading cause of death from cancer. Tobacco usage is the major pathogenic factor, however, not all lung cancers can be attributable to smoking. The genetic aberrations that differ between smokers' and never-smokersM-bM-^@M-^Y lung carcinomas remain to a large extent unclear. We analyzed 72 early-stage primary lung carcinomas including small cell lung cancers, adenocarcinomas and squamous cell carcinomas by Illumina HT12 gene expression microarrays. Gene expression profiling of 72 lung carcinomas using Illumina HT-12 V3.0 microarrays.
Project description:Lung cancer is the worldwide leading cause of death from cancer. Tobacco usage is the major pathogenic factor, however, not all lung cancers can be attributable to smoking. The genetic aberrations that differ between smokers' and never-smokers’ lung carcinomas remain to a large extent unclear. We analyzed 72 early-stage primary lung carcinomas including small cell lung cancers LCNEC, adenocarcinomas and squamous cell carcinomas by Illumina HT12 gene expression microarrays.
Project description:Primary tumor recurrence occurs commonly after surgical resection of lung squamous cell carcinoma (SCC). The aim of this study was to identify genes involved in recurrence in lung squamous cell carcinoma patients. Array comparative genomic hybridization (aCGH) was performed on DNA extracted from tumour tissue from 62 patients with primary lung squamous cell carcinomas. aCGH data was analysed to identify genes affected by copy number alterations that may be involved in SCC recurrence. Candidate genes were then selected for technical validation based on differential copy number between recurrence and non-recurrence SCC tumour samples. Genes technically validated advanced to tests of biological replication by qPCR using an independent test set of 72 primary lung SCC tumour samples. 18q22.3 loss was identified by aCGH as significantly associated with recurrence (p=0.038). Although aCGH copy number loss associated with recurrence was found for seven genes within 18q22.3, only SOCS6 copy number loss was both technically replicated by qPCR and biologically validated in the test set. DNA copy number profiling using 44K element array comparative genomic hybridization microarrays of 62 primary lung squamous cell carcinomas.
Project description:Lung cancer is still the leading cause of cancer-related deaths in the US and worldwide. Understanding the global molecular profiles or transcriptome of lung cancers would strengthen our understanding of the biology of this malignancy. We performed gene expression profiling using the Human Gene 1.0 ST platform of 80 lung adenocarcinomas and 30 normal lung tissues to better understand the biology of this significant fraction of non-small cell lung carcinomas (NSCLCs)
Project description:The differential diagnosis between head & neck squamous cell carcinomas and lung squamous cell carcinomas is often unresolved because the histologic appearance of these two tumor types is similar. In the development of a gene expression profile test (GEP-HN-LS) that distinguishes these 2 cancer types, a collection of poorly differentiated primary and metastatic tumor specimens were used. Here we describe 76 such tumor specimens that were used for validation of GEP-HN-LS. The specimens are either head & neck squamous cell carcinomas or lung squamous cell carcinomas.
Project description:Series of stage IB lung adenocarcinomas and large cell carcinomas. The aim of the study was to predict outcome using a Copy Number Driven Gene Expression signature. Experiment Overall Design: Homogeneous series of 72 cases of lung primary stage IB adenocarcinomas/large cell carcinomas, analyzed using the Human U133Plus 2.0 oligonucleotide arrays (Affymetrix, Santa Clara, CA).
Project description:Lung cancer is the worldwide leading cause of death from cancer. DNA methylation in gene promoter regions is a major mechanism of gene expression regulation that may promote tumorigenesis. However, whether clinically relevant subgroups based on DNA methylation patterns exist in lung cancer is not well studied. We performed whole-genome methylation analysis using 450K Illumina BeadArrays on 124 tumors including 83 adenocarcinomas, 23 squamous cell carcinomas, one adenosquamous cancer, five large cell carcinomas, nine large cell neuroendocrine carcinomas (LCNEC), three small cell carcinomas (SCLC) and 12 normal lung tissues. Unsupervised class discovery was performed to identify DNA methylation subgroups with clinicopathological and molecular features. Subgroups were validated in two independent NSCLC cohorts. Unsupervised analysis identified five DNA methylation subgroups (epitypes). One epitype was distinctly associated with neuroendocrine tumors (LCNEC and SCLC). For adenocarcinoma, in both discovery and validation cohorts, remaining four epitypes were associated with differences in clinicopathological and molecular features, including global hypomethylation, promoter hypermethylation, copy number alterations, expression of proliferation-associated genes, association with unsupervised and supervised gene expression phenotypes, KRAS, TP53, KEAP1, SMARCA4, and STK11 mutations, smoking history, and patient outcome. Based on a multicohort approach we conducted a comprehensive survey of genome-wide DNA methylation in lung cancer, identifying a distinct neuroendocrine epitype and four adenocarcinoma epitypes associated with molecular and clinicopathological characteristics, and patient outcome. Our results bring further understanding of the epigenetic characteristics and molecular diversity in lung cancer generally and in adenocarcinoma specifically. Genome-wide DNA methylation analysis of 124 lung carcinomas and 12 normal lung tissues using Illumina Human Methylation 450K v1.0 Beadchips.