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Gene expression changes detected in mouse melanomas after conditional genetic inactivation of ezh2 using tyr:Cre-ERT2 on a braf;pten genetic background

ABSTRACT: We use RNAseq to examine gene expression changes in braf;pten mouse melanomas after arising after conditional genetic inactivation of ezh2

ORGANISM(S): Mus musculus

PROVIDER: GSE192491 | GEO | 2021/12/29

REPOSITORIES: GEO

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Gene expression changes detected in mouse melanomas after conditional genetic inactivation of ezh2 using tyr:Cre-ERT2 on a braf pten genetic background

Project description:Gene expression changes detected in mouse melanomas after conditional genetic inactivation of ezh2 using tyr:Cre-ERT2 on a braf pten genetic background

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Beta-catenin Controls Metastasis in Braf-activated Pten-inactivated Melanomas

Project description:Malignant melanoma is characterized by frequent metastasis, however specific changes that regulate this process have not been clearly delineated. Although it is well known that Wnt signaling is frequently dysregulated in melanoma, the functional implications of this observation are unclear. By modulating beta-catenin levels in a mouse model of melanoma that is based on melanocyte-specific Pten loss and BrafV600E mutation, we demonstrate that beta-catenin is a central mediator of melanoma metastasis to lymph node and lung. In addition to altering metastasis, beta-catenin levels control tumor differentiation and regulate both MAPK/Erk and PI3K/Akt signaling. Highly metastatic tumors with beta-catenin stabilization are very similar to a subset of human melanomas; together these findings establish Wnt signaling as a metastasis regulator in melanoma. MoGene-1_0-st-v1: Four samples total. Two biological replicates of uncultured Pten/Braf murine melanomas and two biological replicates of uncultured Pten/Braf/Bcat-STA murine melanomas. MoEx-1_0-st-v1: Two samples total. Dissociated tumor and FACS-enriched Pten/Braf and Pten/Braf/Bcat-STA murine melanoma.

2011-10-12 | E-GEOD-32907 | biostudies-arrayexpress

Beta-catenin Controls Metastasis in Braf-activated Pten-inactivated Melanomas

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?-catenin signaling controls metastasis in Braf-activated Pten-deficient melanomas.

Project description:Malignant melanoma is characterized by frequent metastasis, however, specific changes that regulate this process have not been clearly delineated. Although it is well known that Wnt signaling is frequently dysregulated in melanoma, the functional implications of this observation are unclear. By modulating ?-catenin levels in a mouse model of melanoma that is based on melanocyte-specific Pten loss and Braf(V600E) mutation, we demonstrate that ?-catenin is a central mediator of melanoma metastasis to the lymph nodes and lungs. In addition to altering metastasis, ?-catenin levels control tumor differentiation and regulate both MAPK/Erk and PI3K/Akt signaling. Highly metastatic tumors with ?-catenin stabilization are very similar to a subset of human melanomas. Together these findings establish Wnt signaling as a metastasis regulator in melanoma.

| S-EPMC3241928 | biostudies-literature

Transcriptomic profiling of melanomas treated with BRAF inhibitor

Project description:Transcriptomic profiling of melanomas treated with BRAF inhibitor

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CGH analysis of melanomas and germline samples from Braf mutant mouse model

Project description:We investigated copy number alterations in melanomas from two cohorts of Braf mutant mice (UV exposed and no UV exposure) by comparing tumour DNA to germline DNA by array CGH

2014-06-11 | GSE58265 | GEO

CGH analysis of melanomas and germline samples from Braf mutant mouse model

Project description:We investigated copy number alterations in melanomas from two cohorts of Braf mutant mice (UV exposed and no UV exposure) by comparing tumour DNA to germline DNA by array CGH There were 15 tumour samples in each cohort (UV exposed and no UV exposure)

2014-06-11 | E-GEOD-58265 | biostudies-arrayexpress

Gene expression profile in melanomas from Pdk1-inactivated BrafV600E::Pten-/- mice

Project description:Gene expression profiling was performed to access the changes in gene expression in melanomas from Pdk1-inactivated Brafv600E::Pten-/- mice. The expression profiles of the BrafV600E::Pten-/-::Pdk1-/- were compared to the BrafV600E::Pten-/-::Pdk+/+ genotypes. The analysis has identified several important signaling pathways in Pdk1-dependent melanomagenesis.

2013-09-17 | GSE42187 | GEO

The Genetic Germline Background of Single and Multiple Primary Melanomas.

Project description:Background: Melanoma has a complex molecular background and multiple genes are involved in its development and progression. The advent of next generation sequencing platforms has enabled the evaluation of multiple genes at a time, thus unraveling new insights into the genetics of melanoma. We investigated a set of germline mutations able to discriminate the development of multiple primary melanomas (MPM) vs. single site primary melanomas (SPM) using a targeted next generation sequencing panel. Materials and Methods: A total of 39 patients, 20 with SPM and 19 with MPM, were enrolled in our study. Next generation analysis was carried out using a custom targeted sequencing panel that included 32 genes known to have a role in several carcinogenic pathways, such as those involved in DNA repair, pigmentation, regulation of kinases, cell cycle control and senescence. Results: We found a significant correlation between PIK3CA:p.I391M and MPMs, compared to SPMs, p = 0.031 and a trend for the association between CYP1B1: p.N453S and SPMs, compared to MPMs (p = 0.096). We also found that both subgroups shared a spectrum of 9 alterations in 8 genes (CYP1B1: p.N453S, BAP1: p.C39fs, PIK3CA: p.I391M, CDKAL1: c.1226_1227TG, POLE: p.V1161fs, OCA2: p.R419Q, OCA2: p.R305W, MC1R: p.V60L, MGMT: p.L115F), which suggested that these genes may play a role in melanoma development. Conclusions: In conclusion, despite the small cohort of patients, we found that germline mutations, such as those of PIK3CAand CYP1B1, might contribute to the differential development of SPM and MPM.

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Tumor genetic heterogeneity analysis of chronic sun-damaged melanomas

Project description:Chronic sun-damaged (CSDhigh) melanoma represents 10-20% of cutaneous melanomas and is characterized by infrequent BRAF V600E mutations and high mutational load. However, the order of genetic events, or the extent of intra-tumor heterogeneity (ITH) in CSDhigh melanoma is still unknown. Ultra-deep targeted sequencing of 40 cancer-associated genes was performed in 73 in situ or invasive CMM, including 23 CSDhigh cases. In addition, we performed whole-exome and RNA sequencing on multiple regions of primary tumor and multiple in-transit metastases from one CSDhigh melanoma patient. We found no significant difference in mutation frequency in melanoma-related genes or in mutational load between in situ and invasive CSDhigh lesions while this difference was observed in CSDlow lesions. In addition, increased frequency of BRAF V600K, NF1 and TP53 mutations (P < 0.01, Fisher’s Exact Test) was found in CSDhigh melanomas. Sequencing of multiple specimens from one CSDhigh patient revealed strikingly limited ITH with > 95% shared mutations. Our results provide evidence that CSDhigh and CSDlow melanomas are distinct molecular entities that progress via different genetic routes.

2020-05-19 | GSE139362 | GEO

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