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Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes

ABSTRACT: Purpose: The goal of this study is to compare transcriptome profiling (RNA-seq) between tumors of mammary tumor bearing mice treated with a vehicle control or FDA approved Hedgehog signaling inhibitor, Vismodegib.

ORGANISM(S): Mus musculus

PROVIDER: GSE146222 | GEO | 2023/02/01

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes II

Project description:Purpose: The goal of this study is to compare transcriptome profiling (RNA-seq) between tumors of mammary tumor bearing mice treated with a vehicle control or FDA approved Hedgehog signaling inhibitor, Vismodegib.

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Transcriptomic analysis of early-stage basal cell carcinomas in murine skin following ablative fractional laser and vismodegib treatment

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Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes

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Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes II

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes II

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Expression profile of Rhabdomyosarcoma (RMS) cells after Vismodegib treatment

Project description:A cDNA microarray was performed to identify pathways differentially regulated between untreated and Vismodegib-treated cells.

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Next Generation Sequencing Facilitates Quantitative Analysis of Hedgehog Signaling Blockade on Macrophage Transcriptomes

Project description:Purpose: The goal of this study is to compare transcriptome profiling (RNA-seq) between macrophages inhibited for Hedgehog signaling and vehicle control.

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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.

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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.

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ATAC sequencing of sorted BCC cells after vismodegib treatment

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