Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

17 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomic landscape of carcinogen induced mouse skin squamous cell carcinoma: whole-exome sequencing

ABSTRACT: Whole-exome sequencing of induced murine squamous cell carcinoma. 26 samples are included.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Bram Boeckx

PROVIDER: E-MTAB-2887 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Genomic landscape of carcinogen-induced and genetically induced mouse skin squamous cell carcinoma.

Nassar Dany D Latil Mathilde M Boeckx Bram B Lambrechts Diether D Blanpain Cédric C

Nature medicine 20150713 8

Mouse models of cancers are routinely used to study cancer biology. However, it remains unclear whether carcinogenesis in mice is driven by the same spectrum of genomic alterations found in humans. Here we conducted a comprehensive genomic analysis of 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced skin cancer, the most commonly used skin cancer model, which appears as benign papillomas that progress into squamous cell carcinomas (SCCs). We also studied genetically induced SCCs that expressed G1 ...[more]

PMID: 26168291

Similar Datasets

Genomic landscape of carcinogen induced mouse skin squamous cell carcinoma: whole-genome sequencing

Project description:Low coverage whole-genome sequencing of induced murine squamous cell carcinoma. 17 samples are included.

2015-04-10 | E-MTAB-2888 | biostudies-arrayexpress

Nkx2.1 represses a latent gastric differentiation program in lung adenocarcinoma

Project description:During cancer evolution, cellular differentiation programs become dysregulated. The transcription factor Nkx2-1 is a master regulator of pulmonary differentiation that is downregulated in poorly differentiated lung adenocarcinoma. Here we use conditional murine genetics to study the fate of lung epithelial cells upon loss of their master cell fate regulator. Nkx2-1 deletion in normal and neoplastic lung causes not only loss of pulmonary identity but also gastric transdifferentiation. Nkx2-1 maintains pulmonary identity by sequestering the Foxa1 transcription factor at lung-specific loci and inhibiting Foxa1 binding to gastrointestinal targets. Murine Nkx2-1-negative lung tumors mimic the mucinous subtype of human lung adenocarcinoma, which also exhibits gastric transdifferentiation. Nkx2-1-negative lung adenocarcinomas are dependent on the gastrointestinal gene Hnf4a for efficient initiation. Thus, loss of Nkx2-1 results in transdifferentiation rather than stable dedifferentiation in vivo, suggesting that inactivation of both active and latent differentiation programs may be required for tumors to reach a primitive, dedifferentiated state. The study was designed to compare the expression profiles of Nkx2-1-positive lung adenocarcinomas with tumors in which Nkx2-1 was deleted at the time of initiation or 6-7 months after initiation.

2013-04-10 | E-GEOD-36473 | biostudies-arrayexpress

Proteogenomics of malignant melanoma cell lines: searching for genetically encoded point mutations in LC-MS/MS data

Project description:In this study we performed proteogenomic analysis for 9 cell lines of malignant melanoma. The main objectives of the study were identifying the variants originating from point mutations and analyzing the effect of exome data filtering on the outcome of variant identification.

2018-12-05 | PXD007662 | Pride

Vav proteins orchestrate a keratinocyte auto/paracrine program critical for skin tumorigenesis.

Project description:Cutaneous squamous tumors rely on autocrine/paracrine loops for proper fitness. Targeting this Achilles’ heel is therefore considered a potential avenue for patient treatment. However, the mechanisms that engage and sustain such programs during tumor ontogeny are poorly understood. Here, we show that two Rho/Rac activators, the exchange factors Vav2 and Vav3, control the expression of an epithelial autocrine/paracrine program that regulates keratinocyte survival and proliferation as well as the creation of an inflammatory microenvironment. Vav proteins are also critically involved in some of the subsequent autocrine signaling loops activated in keratinocytes. The genetic inactivation of both Vav proteins reduces tumor multiplicity without hampering skin homeostasis, thus suggesting that pan-specific Vav therapies may be useful in skin tumor prevention and treatment. The dorsal skin of WT and DKO mice (Vav2-/-;Vav3-/-) were treated with either one or four applications of phorbol ester 12-O-tetradecanoylphorbol-13 acetate (TPA) (6.8 nmol in 200 μl acetone) two days after shaving. As control, we applied 200 μl of acetone. Animals were euthanized 24 hours after treatment.

2013-07-30 | E-GEOD-40849 | biostudies-arrayexpress

Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (papillomas)

Project description:Germline polymorphisms influence gene expression networks in normal mammalian tissues. Analysis of this genetic architecture can identify single genes and whole pathways that influence to complex traits including inflammation and cancer susceptibility. Changes in the genetic architecture during the development of benign and malignant tumours have not been investigated. Here, we document major changes in germline control of gene expression during skin tumour development as a consequence of cell selection, somatic genetic events, and changes in tumour microenvironment. Immune response genes such as Interleukin 18 and Granzyme E are under germline control in tumours but not in normal skin. Gene expression networks linked to tumour susceptibility and hair follicle stem cell markers in normal skin undergo significant reorganization during tumour progression. Our data highlight opposing roles of Interleukin-1 signaling networks in tumour susceptibility and tumour progression and have implications for the development of chemopreventive strategies to reduce cancer incidence. Skin tumors were induced on dorsal back skin from a Mus spretus / Mus musculus backcross ([SPRET/Ei X FVB/N] X FVB/N) mice by treatment of dorsal back skin with dimethyl benzanthracene (DMBA) and tetradecanoyl-phorbol acetate (TPA). This treatment induced multiple benign papillomas as well as malignant squamous cell carcinomas (SCC) and spindle cell carcinomas. Gene expression analysis was performed on mRNA extracted from 68 papillomas: two papillomas from each of 31 FVBBX mice and a single papilloma from six additional FVBBX mice. Papillomas were harvested when mice were sacrificed due to presence of a carcinoma or termination of the experiment.

2010-12-22 | E-GEOD-21263 | biostudies-arrayexpress

Expression data from sorted epithelial CD34+ expressing cells from DMBA/TPA induced skin tumors

Project description:Transcriptional profile of control and VEGF overexpressing FACS-isolated CD34+ Cancer stem cells from DMBA/TPA induced skin tumours Tumours were digested in collagenase I (Sigma) for 2 hours at 37°C on a rocking plate. Collagenase I activity was blocked by addition of EDTA (5mM) and then rinced in PBS supplemented with 2%FCS. After tumour digestion, cells were first incubated in PBS complemented with 30% FCS to block Fc receptors for 15 min at room temperature. Immunostaining was performed using biotin-conjugated anti-CD34 (clone RAM34; BD Pharmingen), FITC-conjugated anti-α6-integrin (clone GoH3; BD Pharmingen), PE-conjugated anti-CD45 (clone 30F11, eBiosciences), PE-conjugated anti CD31 (clone MEC13.3; BD Pharmingen), PE-conjugated anti-CD140a (clone APA5; eBiosciences), APC-Cy7-conjugated anti-Epcam (clone G8.8; Biolegend) by incubation for 30min on ice. Cells were washed and stained using APC-conjugated Streptavidin (BD Pharmingen) for 20min on ice. Living tumour cells were selected by forward scatter, side scatter and by Hoechst dye exclusion. Fluorescence-activated cell sorting analysis was performed using FACSAria and FACSDiva software (BD Biosciences). Sorted cells were collected in the lysis buffer provided by the manufacturer (Microprep kit, RNeasy, Stratagene) and RNA extraction was performed according to the manufacturer's protocol. Total RNA was analysed using Mouse whole genome 430 2.0 array from Affymetrix at the VIB microarray facility (KU – Leuven, Belgium). We analyzed CD34+ TECs isolated by FACS from a K14CreER:Rosa-VEGF-164 and control mice. Analysis of the microarray was perfored by the VIB microarray facility (KU – Leuven, Belgium).

2011-09-06 | E-GEOD-31465 | biostudies-arrayexpress

Inflammation and tumor susceptibility in skin cancer

Project description:This SuperSeries is composed of the following subset Series: GSE12248: Genetic architecture of murine skin inflammation and tumor susceptibility GSE21247: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (carcinomas) GSE21263: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (papillomas) GSE26273: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (aCGH) Refer to individual Series

2010-12-22 | E-GEOD-21264 | biostudies-arrayexpress

Proliferation and Tumorigenesis of a Murine Sarcoma Cell Line in the Absence of Dicer

Project description:MicroRNAs are a class of short ~22 nucleotide RNAs predicted to regulate nearly half of all protein-coding genes, including many involved in basal cellular processes and organismal development. Although both increases and decreases in the levels of specific miRNAs have been shown to promote tumor development, a global reduction in miRNAs is commonly observed in various human tumors. However, complete loss has not been documented, suggesting an essential function for miRNAs in tumorigenesis. Here we present the finding that transformed or immortalized Dicer-null somatic cells can be isolated readily in vitro, maintain the characteristics of Dicer-expressing controls and remain stably proliferative. Furthermore, Dicer-null cells from a sarcoma cell line, though depleted of miRNAs, are competent for tumor formation. Hence, miRNA levels in cancer may be maintained in vivo by a complex stabilizing selection in the intratumoral environment. Small RNAs from tumor cell lines (murine sarcoma KrasG12D, p53 -/-) with and without Dicer (Dicer f/-, Dicer -/-) were analyzed.

2012-08-20 | E-GEOD-34825 | biostudies-arrayexpress

In vivo SILAC-based proteomics reveals phosphoproteome changes during mouse skin carcinogenesis

Project description:Cancer progresses through distinct stages and mouse models recapitulating traits of this progression are frequently used to explore genetic, morphological and pharmacological aspects of tumor development. To complement genomic investigations of this process, here we quantify phosphoproteomic changes in skin cancer development using the SILAC mouse technology coupled to high resolution mass spectrometry. We distill protein expression signatures from our data that distinguish between skin cancer stages. A distinct phosphoproteome of the two stages of cancer progression is identified which correlates with perturbed cell growth and implicates cell adhesion as a major driver of malignancy. Importantly, integrated analysis of phosphoproteomic data and prediction of kinase activity revealed PAK4-PKC/SRC network to be highly deregulated in SCC but not in papilloma. This detailed molecular picture, both at the proteome and phosphoproteome level, will prove useful for the study of mechanisms of tumor progression.

2013-03-13 | PXD000821 | Pride

Massive parallel sequencing uncovers actionable FGFR2-PPHLN1 fusion and ARAF mutations in intrahepatic cholangiocarcinoma

Project description:Intrahepatic cholangiocarcinoma (iCCA) is a fatal bile duct cancer with dismal prognosis and limited therapeutic options. By performing RNA- and exome sequencing analyses we have discovered a novel fusion event, FGFR2-PPHLN1 (16%), and damaging mutations in the ARAF oncogene (11%). Methods: mRNA and gDNA were exctracted from fresh frozen tumor tissues and corresponding normal tissue (n=8 pairs) from patients with iCCA who underwent surgical resection. RNA-seq was performed using Illumina HiSeq 2500 System with 100 nucleotide single-end reads. One sample and its paired non-tumoral tissue were eliminated from the subsequent analysis because of bad RNa quality. The same 8 paired tumors were also analyzed by whole-exome seq. Submitter confirms there are no patient privacy concerns with these data. This dataset is part of the TransQST collection.

2015-01-22 | E-GEOD-63420 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data