Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene signature driving invasive mucinous adenocarcinoma of the lung

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE86959 | GEO | 2017/03/02

SECONDARY ACCESSION(S): PRJNA343081

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene signature driving invasive mucinous adenocarcinoma of the lung.

Project description:Though invasive mucinous adenocarcinoma of the lung (IMA) is pathologically distinctive, the molecular mechanism driving IMA is not well understood, which hampers efforts to identify therapeutic targets. Here, by analyzing gene expression profiles of human and mouse IMA, we identified a Mucinous Lung Tumor Signature of 143 genes, which was unexpectedly enriched in mucin-producing gastrointestinal, pancreatic, and breast cancers. The signature genes included transcription factors FOXA3, SPDEF, HNF4A, mucins MUC5AC, MUC5B, MUC3, and an inhibitory immune checkpoint VTCN1/B7-H4 (but not PD-L1/B7-H1). Importantly, induction of FOXA3 or SPDEF along with mutant KRAS in lung epithelium was sufficient to develop benign or malignant mucinous lung tumors, respectively, in transgenic mice. FOXA3 and SPDEF induced MUC5AC and MUC5B, while HNF4A induced MUC3 in human mucinous lung cancer cells harboring a KRAS mutation. ChIP-seq combined with CRISPR/Cas9 determined that upstream enhancer regions of the mucin genes MUC5AC and MUC5B, which were bound by SPDEF, were required for the expression of the mucin genes. Here, we report the molecular signature and gene regulatory network driving mucinous lung tumors.

| S-EPMC5376761 | biostudies-literature

Mucinous colorectal adenocarcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-28 | GSE236698 | GEO

Gene signature driving invasive mucinous adenocarcinoma of the lung

Project description:Gene signature driving invasive mucinous adenocarcinoma of the lung

| PRJNA343081 | ENA

Lung adenocarcinoma subtypes definable by lung development-related miRNA expression profiles in association with clinicopathologic features

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-19 | E-GEOD-51855 | biostudies-arrayexpress

Epigenetic screen of metastasis-driving genes in osteosarcoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-08-25 | E-GEOD-56255 | biostudies-arrayexpress

Druggable oncogene fusions in invasive mucinous lung adenocarcinoma.

Project description:PurposeTo identify druggable oncogenic fusions in invasive mucinous adenocarcinoma (IMA) of the lung, a malignant type of lung adenocarcinoma in which KRAS mutations frequently occur.Experimental designFrom an IMA cohort of 90 cases, consisting of 56 cases (62%) with KRAS mutations and 34 cases without (38%), we conducted whole-transcriptome sequencing of 32 IMAs, including 27 cases without KRAS mutations. We used the sequencing data to identify gene fusions, and then performed functional analyses of the fusion gene products.ResultsWe identified oncogenic fusions that occurred mutually exclusively with KRAS mutations: CD74-NRG1, SLC3A2-NRG1, EZR-ERBB4, TRIM24-BRAF, and KIAA1468-RET. NRG1 fusions were present in 17.6% (6/34) of KRAS-negative IMAs. The CD74-NRG1 fusion activated HER2:HER3 signaling, whereas the EZR-ERBB4 and TRIM24-BRAF fusions constitutively activated the ERBB4 and BRAF kinases, respectively. Signaling pathway activation and fusion-induced anchorage-independent growth/tumorigenicity of NIH3T3 cells expressing these fusions were suppressed by tyrosine kinase inhibitors approved for clinical use.ConclusionsOncogenic fusions act as driver mutations in IMAs without KRAS mutations, and thus represent promising therapeutic targets for the treatment of such IMAs.

| S-EPMC6329293 | biostudies-literature

ADAM9 Up-regulates N-Cadherin via MiR-218 Suppression in Lung Adenocarcinoma Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-03 | E-GEOD-52051 | biostudies-arrayexpress

Human lung adenocarcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-05-17 | GSE36471 | GEO

Molecular portraits of epithelial, mesenchymal and hybrid states in lung adenocarcinoma and their relevance to survival

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series.

2014-12-09 | E-GEOD-63977 | biostudies-arrayexpress

A high dimensional deep sequencing study of non-small cell lung adenocarcinoma in never-smoker Korean females

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series