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ATAC sequencing of sorted BCC cells after vismodegib treatment

ABSTRACT: ATAC sequencing of sorted BCC cells after vismodegib treatment

PROVIDER: PRJNA480705 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7511801_1.fastq.gz	Fastqsanger.gz
	SRR7511801_2.fastq.gz	Fastqsanger.gz
	SRR7511802_1.fastq.gz	Fastqsanger.gz
	SRR7511802_2.fastq.gz	Fastqsanger.gz
	SRR7511803_1.fastq.gz	Fastqsanger.gz

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ATAC sequencing of sorted BCC cells after vismodegib treatment

Project description:K14Cre-ER; Ptch1fl/fl; p53fl/fl;Lgr5GFP mice were aged until the appropriate tumor density was achieved. Skin samples were taken from control mice (untreated) or mice treated for 6 days or 14 days at twice a day dosing with vismodegib (75mg/kg body weight). RNA was extracted from freshly FACS sorted tumor cells based on GFP intensity. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech.

2018-08-08 | GSE116965 | GEO

Sorted BCC timecourse after Vismo treatment - MCT, 6d, 14d

Project description:Sorted BCC timecourse after Vismo treatment - MCT, 6d, 14d

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Sorted BCC timecourse after Vismo treatment - MCT, 6d, 14d

2018-08-08 | GSE116961 | GEO

Identification of anaplastic lymphoma kinase as a candidate of new therapeutic target for BCC

Project description:Background; Basal cell carcinoma (BCC) is the most common cancer in humans. The pathogenesis of BCC is associated with the sonic hedgehog (SHH) signaling pathway. Vismodegib, a smoothened inhibitor, that targets this pathway is now in clinical use for advanced BCC patients, but its efficacy is limited. Therefore, new therapeutic options for this cancer are required. Methods; We studied gene expression profiling of BCC tumour tissue coupled with laser capture microdissection to identify tumor specific receptor tyrosine kinase expression that can be targeted by small molecule inhibitors. The expression of selected molecules was confirmed by quantitative RT-PCR (qRT-PCR) and by immunohistochemistry. The action of kinase inhibitors was examined on primary normal human epidermal keratinocytes. Results; We found a >250 fold change increase (false discovery rate <10-4) of the oncogene, anaplastic lymphoma kinase (ALK) as well as its ligands, pleiotrophin and midkine in BCC compared to microdissected normal epidermis. qRT-PCR confirmed increased expression of ALK (p<0.05). Stronger staining of phosphorylated ALK in BCC tumour nests than normal skin was observed by immunohistochemistry. Additionally, Crizotinib, an FDA-approved ALK inhibitor, reduced keratinocyte proliferation in culture, whereas a c-Met, another receptor tyrosine kinase, inhibitor did not. Crizotinib significantly reduced the expression of GLI1 and CCND2 mRNA by approximately 60% and 20%, respectively (p<0.05). Conclusions; Our data suggest that ALK may increase GLI1 expression in parallel with the conventional SHH-pathway and promotes keratinocyte proliferation. Furthermore, an ALK inhibitor alone or in combination with targeting SHH-pathway molecules may be a potential treatment for BCC patients. Laser capture microdissection was performed on 5 cases of nodular/superficial BCC, 5 cases of infiltrative BCC.

2013-01-30 | E-GEOD-42109 | biostudies-arrayexpress

Basal-to-inflammatory transition enhances basal cell carcinoma (BCC) therapy resistance via crosstalk with a pro-inflammatory stromal niche [ATAC-Seq]

Project description:The goal of these ATAC-seq experiments was to determine changes in chromatin accesiblity caused by Il1a and Osm ligand treatment of mouse BCC cells at 48h timepoint versus PBS control

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Identification of anaplastic lymphoma kinase as a candidate of new therapeutic target for BCC

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Metarhizium sp. BCC 4849 isolate:BCC 4849

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Single-cell ATAC-Seq (scATAC-Seq) of mouse basal cell carcinoma (BCC) immune cells.

Project description:We used scATAC-Seq to examine BCC immune cell heterogeneity.

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Expression data from mouse basal cell carcinoma (BCC) and normal epidermis, and BCC cell line treated with cyclopamine

Project description:Activation of the Sonic hedgehog (Shh) signaling pathway due to Patched 1 (PTCH1) mutation is a key event in sporadic and familial basal cell carcinoma (BCC) development. To find out the specific pathway for therapeutic intervention, we developed a mouse BCC model by skin specific Ptch1 inactivation, and sought to identify novel Shh targets. We used microarrays to identify up-regulated genes in mouse BCC. We used microarrays to identify down-regulated genes in mouse BCC cell line by cyclopamine.

2018-01-15 | GSE20065 | GEO

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