Human Lung Adenocarcinomas (Stage 1 and Stage 2 )
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Williams Jason
PROVIDER: S-ECPF-GEOD-28956 | biostudies-other |
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Comparing Stage 1 and stage 2 lung adenocarcinomas against a standard human reference RNA sample.
2011-05-04 | GSE28956 | GEO
Project description:Comparing Stage 1 and stage 2 lung adenocarcinomas against a standard human reference RNA sample. Two colour design, stage 1 or stage 2 adenocarcinoma vs human reference RNA (Clontech), 5 stage 1 comparisons and 5 stage 2 comparisons
2011-05-04 | E-GEOD-28956 | biostudies-arrayexpress
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).
| S-ECPF-GEOD-10445 | biostudies-other
Project description:BACKGROUND:The prognostic role of epidermal growth factor receptor (EGFR) mutations in patients with lung adenocarcinomas remains controversial and the association between EGFR mutations and stage at the time of the initial diagnosis is debatable. In this study, we evaluated the association of EGFR mutations with stage at diagnosis in lung adenocarcinomas. MATERIALS AND METHODS:We retrospectively analyzed 1004 consecutive patients who were diagnosed with lung adenocarcinomas and tested for EGFR mutations between June 2011 and December 2014. RESULTS:EGFR mutations were detected in 49.2% of 1004 patients with lung adenocarcinomas. In multivariable analysis, EGFR mutations were significantly associated with early stage disease (stage I to II) at diagnosis (odds ratio [OR], 0.65; 95% confidence interval [CI], 0.49-0.87; P = 0.003). When adjusted for age, sex, smoking status, and screening, the adjusted proportion of EGFR mutations significantly decreased according to stage. The adjusted proportions of EGFR mutations were 57.6% (95% CI, 51.7%-63.3%) for stage I, 47.9% (95% CI, 36.9%-59.0%) for stage II, 47.5% (95% CI, 39.6%-55.5%) for stage III, and 43.4% (95% CI, 38.3%-48.6%) for stage IV (P = 0.0082). CONCLUSIONS:The presence of EGFR mutations is significantly associated with early stage disease at initial diagnosis in lung adenocarcinomas after adjusting for age, sex, smoking status, and screening. This finding implies that EGFR mutations may play a role as a positive prognostic marker.
| S-EPMC5115811 | biostudies-literature
Project description:Adenocarcinoma is the predominant histological subtype of lung cancer, the leading cause of cancer deaths in the world. At stage I, the tumor is cured by surgery alone in about 60% of cases. Markers are needed to stratify patients by prognostic outcomes and may help in devising more effective therapies for poor prognosis patients. To achieve this goal, we used an integrated strategy combining meta-analysis of published lung cancer microarray data with expression profiling from an experimental model. The resulting 80-gene model was tested on an independent cohort of patients using RT-PCR, resulting in a 10-gene predictive model that exhibited a prognostic accuracy of approximately 75% in stage I lung adenocarcinoma when tested on 2 additional independent cohorts. Thus, we have identified a predictive signature of limited size that can be analyzed by RT-PCR, a technology that is easy to implement in clinical laboratories.
| S-EPMC2030461 | biostudies-literature
Project description:To identify patients in whom systematic lymph node dissection would be suitable, preoperative diagnosis of the biological invasiveness of lung adenocarcinomas through the classification of these T1aN0M0 lung adenocarcinomas into several subgroups may be warranted. In this retrospective study, we sought to determine predictive factors of lymph node status in clinical stage T1aN0M0 lung adenocarcinomas.We retrospectively reviewed the records of 273 consecutive patients undergone surgical resection of clinical stage T1aN0M0 lung adenocarcinomas at Shanghai Chest Hospital, from January 2011 to December 2012. Preoperative computed tomography findings of all 273 patients were reviewed and their tumors categorized as pure GGO, GGO with minimal solid components (<5 mm), part-solid (solid parts >5 mm), or purely solid. Relevant clinicopathologic features were investigated to identify predictors of hilar or mediastinal lymph node metastasis using univariate or multiple variable analysis.Among the 273 eligible clinical stage T1aN0M0 lung adenocarcinomas examined on thin-section CT, 103 (37.7%) were pure GGO, 118 (43.2%) GGO with minimal solid components, 13 (4.8%) part-solid (solid parts >5 mm, five GGO predominant and eight solid predominant), and 39 (14.3%) pure solid. There were 18 (6.6%) patients with lymph node metastasis. Incidence of N1 and N2 nodal involvement was 11 (6.6%) and seven (2.6%) patients, respectively. All patients with pure GGO and GGO with minimal solid components (<5 mm) tumors were pathologically staged N0. Multivariate analyses showed that the following factors significantly predicted lymph node metastasis for T1a lung adenocarcinomas: symptoms at presentation, GGO status, and abnormal carcinoembryonic antigen (CEA) titer. Multivariate analyses also showed that the following factors significantly predicted lymph node metastasis for pure solid tumors: air bronchogram sign, tumor size, symptoms at presentation, and abnormal CEA titer.The patients of clinical stage T1aN0M0 lung adenocarcinomas with pure GGO and GGO with minimal solid components tumors were pathologically staged N0 and systematic lymph node dissection should be avoided. But systematic lymph node dissection should be performed for pure solid tumors or part-solid, especially in patients with CEA greater than 5 ng/mL or symptoms at presentation, because of the high possibility of lymph node involvement.
| S-EPMC3945801 | biostudies-other
Project description:Background: A gel-free proteomic approach was utilized to perform in-depth tissue protein profiling of lung adenocarcinoma (ADC) and normal lung tissues from early and advanced stages of the disease. The long-term goal of this study is to generate a large-scale, label-free proteomic data set from histologically well-classified lung ADC that can be used to increase further our understanding of disease progression and aid in identifying novel biomarkers. Methods and Results: Cases of early-stage (I-II) and advanced-stage (III-IV) lung ADCs were selected and paired with normal lung tissues from 22 patients. The histologically and clinically stratified human primary lung adenocarcinomas were analyzed by liquid chromatography tandem mass spectrometry (LC-MS/MS). From the analysis of ADC and normal specimens, 5,933 protein groups were identified. To examine the protein expression profile of ADC, a peak area-based quantitation method was used. In early- and advanced-stage ADC, 33 and 39 proteins were differentially-expressed respectively between normal and tumor tissue (adjusted p-value < 0.01, fold change ≥ 4). For early- and advanced stage ADC tumors compared to normal patient-matched tissue, 11 and 22 proteins and 23 and 16 proteins were identified as down- and up-regulated, respectively. In silico functional analysis of the up-regulated proteins in both tumor groups revealed that most of the enriched pathways are involved in mRNA metabolism. Furthermore, the most over-represented pathways in the proteins that were unique to ADC are related to mRNA metabolic processes. Conclusions: Further analysis of these data may provide an insight into the molecular pathways involved in disease etiology and may lead to the identification of biomarker candidates and potential targets for therapy. Our study provides potential diagnostic biomarkers for lung ADC and novel stage-specific drug targets for rational intervention.
2021-09-09 | PXD019259 | Pride
Project description:ObjectivesThyroid transcription factor 1 (TTF-1) is routinely tested in the diagnostic evaluation of suspected lung cancers, is commonly expressed by lung adenocarcinomas, and may modulate lung cancer biology. We examined the role of TTF-1 as a predictive and prognostic marker in patients with advanced lung adenocarcinomas.Materials and methodsWe analyzed clinical, pathologic, and molecular features, treatments received, and overall survival obtained from the medical records of 479 consecutive patients at a single site with stage IV lung adenocarcinomas and evaluable TTF-1 expression. TTF-1 expression was determined by immunohistochemistry using antibody 8G7G3/1.Results and conclusionTTF-1 expression was evaluable in 479 (75%) of all patients reviewed, and was positive in 383 (80%, 95% CI 76-83%). Clinicopathologic features were similar between TTF-1 positive and TTF-1 negative tumors, except EGFR mutations were more common in TTF-1 positive cases (24% vs 6%, p<0.001). In univariate analysis, overall survival was significantly longer in patients with TTF-1 positive versus TTF-1 negative tumors (18 months vs 9 months, p<0.0001). In multivariate analysis, TTF-1 positivity remained associated with better overall survival (HR=0.38, p<0.0001), exceeding the prognostic impact of Karnofsky performance status >/=80% (HR 0.62, p=0.0003) and receipt of first-line combination chemotherapy or targeted therapy (HR relative to first-line single agent chemotherapy 0.59, p=0.05 and 0.51, p=0.05 respectively). Both patients with TTF-1 positive and TTF-1 negative cancers had longer durations of initial therapy when treated with pemetrexed-based chemotherapy. In patients with advanced lung adenocarcinomas, TTF-1 expression is associated with better survival but is not predictive of distinct benefit from pemetrexed-based chemotherapy.
| S-EPMC6423973 | biostudies-literature
Project description:BACKGROUND:Discovery of the progression-associated genes and pathways in lung adenocarcinoma (LAD) has important implications in understanding the molecular mechanism of tumor development. However, few studies had been performed to focus on the changes of pathways in lung adenocarcinoma development using microarray expression profile. RESULT:We performed a meta-analysis of 4 LAD microarray datasets encompassing 353 patients to reveal differentially expressed genes (DEGs) between normal lung tissues and LAD of different stages. Overall, 1 838 genes were found to be dys-regulated, and the adipogenesis, circadian rhythm, and Id pathways were significantly changed. Interestingly, most of the genes from the same gene family (such as Interleukin receptor, Matrix metallopeptidase, Histone cluster and Minichromosome maintenance complex component families) were found to be up-regulated (or down-regulated). Real-time PCR (qRT-PCR) was applied to validate the expression of randomly selected 18 DEGs in LAD cell lines. In the pathway analysis among stages, Oxidative stress, Glycolysis/Gluconeogenesis and Integrin-mediated cell adhesion pathways, which were involved in cancer cell proliferation and metastasis, were showed to be significantly regulated in stages other than IA. CONCLUSION:Genes involved in adipogenesis and Id pathways might play important roles in development of LADs. The similar trend of expression of the gene family members suggested coordinate regulation in tumor progression. Three pathways (Oxidative stress, Glycolysis/Gluconeogenesis and Integrin-mediated cell adhesion pathways) significantly regulated in stages other than stage IA suggested that genes and pathways conferring invasive character might be activated in the preinvasive stage IB, while the Oxidative stress and the Glycolysis/Gluconeogenesis pathways might have strong connections to cisplatin-based chemotherapy. The insignificantly regulated three pathways in stage IA might be used in early-stage detection of LAD.
| S-EPMC3088877 | biostudies-other
Project description:Analysis of gene expression patterns in normal tissues and their perturbations in tumours can help to identify the functional roles of oncogenes or tumour suppressors and identify potential new therapeutic targets. Here, gene expression correlation networks were derived from 92 normal human lung samples and patient-matched adenocarcinomas. The networks from normal lung show that NKX2-1 is linked to the alveolar type 2 lineage, and identify PEBP4 as a novel marker expressed in alveolar type 2 cells. Differential correlation analysis shows that the NKX2-1 network in tumours includes pathways associated with glutamate metabolism, and identifies Vaccinia-related kinase (VRK1) as a potential drug target in a tumour-specific mitotic network. We show that VRK1 inhibition cooperates with inhibition of poly (ADP-ribose) polymerase signalling to inhibit growth of lung tumour cells. Targeting of genes that are recruited into tumour mitotic networks may provide a wider therapeutic window than that seen by inhibition of known mitotic genes.
| S-EPMC4450149 | biostudies-literature