From GEO Summary and overall design: Gene fusions arising from chromosomal translocations are key oncogenic drivers in soft tissue sarcomas but little is known about how they exert their oncogenic effects. Our study explores the molecular mechanisms by which the SS18-SSX fusion oncoprotein subverts epigenetic mechanisms of gene regulation to drive synovial sarcoma. Using functional genomics, we identify...

From GEO Summary and overall design: Gene fusions arising from chromosomal translocations are key oncogenic drivers in soft tissue sarcomas but little is known about how they exert their oncogenic effects. Our study explores the molecular mechanisms by which the SS18-SSX fusion oncoprotein subverts epigenetic mechanisms of gene regulation to drive synovial sarcoma. Using functional genomics, we identify...

From GEO Summary and overall design: Gene fusions arising from chromosomal translocations are key oncogenic drivers in soft tissue sarcomas but little is known about how they exert their oncogenic effects. Our study explores the molecular mechanisms by which the SS18-SSX fusion oncoprotein subverts epigenetic mechanisms of gene regulation to drive synovial sarcoma. Using functional genomics, we identify...

Summary from the GEO: "The RNA modification N6-methyladenosine (m6A) regulates gene expression through various transcript-specific effects. The overall goal of these experiments was to determine the effects of the m6A methyltransferase complex proteins METTL3 and METTL14 on the expression of interferon stimulated genes. First, we depleted METTL3 and METTL14 in Huh7 cells using siRNAs and treated with...

Summary from the GEO: "The RNA modification N6-methyladenosine (m6A) regulates gene expression through various transcript-specific effects. The goal of this experiment was to identify m6A-modified transcripts during the type I interferon response, with interest in determining which interferon-stimulated genes are modified by m6A. We found that a high percentage of ISGs are m6A-modified, and in follow-up...

Summary from the GEO: "The biological role of PSMA, a biomarker expressed in prostate cancer and by the neovasculature of solid tumors, remains unknown. Although PSMA processes folates in our duodenum, and in the brain cleaves NAAG to control neuronal signaling, little is known about its role in cancer. We used microarrays to detail the glonal perturbations in gene expression in the absence of PSMA,...

Summary from the GEO: " The biological role of PSMA, a biomarker expressed in prostate cancer and by the neovasculature of solid tumors, remains unknown. Although PSMA processes folates in our duodenum, and in the brain cleaves NAAG to control neuronal signaling, little is known about its role in cancer. We used microarrays to detail the glonal perturbations in gene expression in the absence of PSMA,...

Summary from the GEO: "While breast cancer patients with tumors that express estrogen receptor α (ER) generally respond well to hormone therapies that block ER’s actions, a significant number relapse. Approximately 30% of these recurrences harbor activating mutations in ER’s ligand binding domain. ER mutations have been shown to confer ligand-independent function to ER; however, much is still unclear...

Summary from the GEO: "While breast cancer patients with tumors that express estrogen receptor α (ER) generally respond well to hormone therapies that block ER’s actions, a significant number relapse. Approximately 30% of these recurrences harbor activating mutations in ER’s ligand binding domain. ER mutations have been shown to confer ligand-independent function to ER; however, much is still unclear...

This superseries is composed of the subseries: GSE148276, GSE148277, and GSE148278. Breast cancer patients with tumors that express estrogen receptor α (ER) at times harbor activating mutations in ER’s ligand binding domain. To investigate mutant ER’s molecular effects, multiple isogenic ER mutant cell lines for the two most common ER ligand binding domain mutations, Y537S and D538G, were developed....