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Expression analysis of transgenic embryos carrying the mitf-BRAFV600E allele in the presence or absence of p53 function

ABSTRACT: Investigation of expression differences between melanomas harvested from MiniCoopR-GFP versus MiniCoopR-SETDB1 transgenic zebrafish The embryos described in this study are further analyzed in a manuscript submitted for publication by White, et al.

ORGANISM(S): Danio rerio

PROVIDER: GSE24529 | GEO | 2011/03/30

SECONDARY ACCESSION(S): PRJNA132667

REPOSITORIES: GEO

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Expression analysis of transgenic embryos carrying the mitf-BRAFV600E allele in the presence or absence of p53 function

Project description:Investigation of expression differences between melanomas harvested from MiniCoopR-GFP versus MiniCoopR-SETDB1 transgenic zebrafish The embryos described in this study are further analyzed in a manuscript submitted for publication by White, et al. A 12 chip study comparing gene expression levels in 80hpf animals either WT (Tu), mitf-BRAFV600E, p53-/-, or mitf-BRAFV600E;p53-/- (double)

2011-03-30 | E-GEOD-24529 | biostudies-arrayexpress

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Expression analysis of zebrafish melanoma and skin from the mitf-BRAFV600E;p53-/- line

Project description:Investigation of expression differences between skin and melanomas from a transgenic BRAFV600E zebrafish model of melanoma The embryos described in this study are further analyzed in a manuscript submitted for publication by White, et al. A 15 chip study using RNA extracted from either WT zebrafish skin, mitf-BRAFV600E;p53-/- skin or mitf-BRAFV600E;p53-/- melanoma

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Expression analysis of melanoma harvested from GFP versus SETDB1 transgenic zebrafish (Danio rerio)

Project description:Investigation of expression differences between melanomas harvested from MiniCoopR-GFP versus MiniCoopR-SETDB1 transgenic zebrafish. An eight-chip study using total RNA prepared from four distinct melanomas from zebrafish injected with MiniCoopR-GFP (control) transposon and four distinct melanomas from zebrafish injected with MiniCoopR-SETDB1 transposon. Injected animals carried a p53 loss-of-function mutation, a mutation in nacre, and an mitf:BRAF-V600E transgene. Each chip measures the expression level of 32,292 genes.

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Expression analysis of melanoma harvested from GFP versus SETDB1 transgenic zebrafish (Danio rerio)

Project description:Investigation of expression differences between melanomas harvested from MiniCoopR-GFP versus MiniCoopR-SETDB1 transgenic zebrafish.

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BRAFV600E Mutant Allele Frequency (MAF) Influences Melanoma Clinicopathologic Characteristics.

Project description:Cutaneous melanoma shows high variability regarding clinicopathological presentation, evolution and prognosis. Next generation sequencing was performed to analyze hotspot mutations in different areas of primary melanomas (MMp) and their paired metastases. Clinicopathological features were evaluated depending on the degree of variation of the BRAFV600E mutant allele frequency (MAF) in MMp. In our cohort of 14 superficial spreading, 10 nodular melanomas and 52 metastases, 17/24 (71%) melanomas had a BRAFV600E mutation and 5/24 (21%) had a NRASQ61 mutation. We observed a high variation of BRAFV600E MAF (H-BRAFV600E) in 7/17 (41%) MMp. The H-BRAFV600E MMp were all located on the trunk, had lower Breslow and mitotic indexes and predominantly, a first nodal metastasis. Regions with spindled tumor cells (Spin) and high lymphocytic infiltrate (HInf) were more frequent in the H-BRAFV600E patients (4/7; 57%), whereas regions with epithelial tumor cells (Epit) and low lymphocytic infiltrate (LInf) were predominant (6/10; 60%) and exclusive in the low BRAFV600E MAF variation tumors (L-BRAFV600E). The H-BRAFV600E/Spin/HInf MMp patients had better prognostic features and nodal first metastasis. The H-BRAFV600E MMp were located on the trunk, had better prognostic characteristics, such as lower Breslow and mitotic indexes as well as high lymphocytic infiltrate.

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Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations.

Project description:Patients harboring germline breast cancer susceptibility genes 1 and 2 (BRCA1/2) mutations are predisposed to developing breast, pancreatic, and ovarian cancers. BRCA2 plays a critical role in homologous recombination (HR) DNA repair and deleterious mutations in BRCA2 confer sensitivity to PARP inhibition. Recently, the PARP inhibitors olaparib and rucaparib were FDA approved for the treatment of metastatic breast cancer and patients with recurrent ovarian cancer with mutations in BRCA1/2. Despite their initial antitumor activity, the development of resistance limits the clinical utility of PARP inhibitor therapy. Multiple resistance mechanisms have been described, including reversion mutations that restore the reading frame of the BRCA2 gene. In this study, we generated olaparib- and rucaparib-resistant BRCA2-mutant Capan1 cell lines. We did not detect secondary reversion mutations in the olaparib- or rucaparib-resistant clones. Several of the resistant clones had gene duplication and amplification of the mutant BRCA2 allele, with a corresponding increase in expression of a truncated BRCA2 protein. In addition, HR-mediated DNA repair was rescued, as evidenced by the restoration of RAD51 foci formation. Using mass spectrometry, we identified Disruptor Of Telomeric silencing 1-Like (DOT1L), as an interacting partner of truncated BRCA2. RNAi-mediated knockdown of BRCA2 or DOT1L was sufficient to resensitize cells to olaparib. The results demonstrate that independent of a BRCA2 reversion, mutation amplification of a mutant-carrying BRCA2 contributes to PARP inhibitor resistance.

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Analysis of cisplatin exposure on the kidney cortex proteome in the presence and absence of OCT1/2

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