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9 results for “usp8”
USP8 and TP53 drivers are associated with CNV in a corticotroph adenoma cohort enriched for aggressive tumors
<p><b>Context:</b> Pituitary corticotroph adenomas are rare tumors that can be associated with excess adrenocorticotropic hormone (ACTH) and adrenal cortisol production, resulting in the clinically debilitating endocrine condition Cushing disease. A subset of corticotroph tumors behave aggressively, and genomic drivers behind the development of these tumors are largely unknown.</p> <p><b>Objective</b><strong>:</strong> To investigate genomic drivers of corticotroph tumors at risk for aggressive behavior.</p> <p><b>Design:</b> Whole-exome sequencing of patient-matched corticotroph tumor and normal DNA from a patient cohort enriched for tumors at risk for aggressive behavior.</p> <p><b>Setting:</b> Tertiary care center.</p> <p><b>Patients:</b> 27 corticotroph tumors from 22 patients analyzed. 12 tumors were macroadenomas, of which 6 were silent ACTH tumors, 2 were Crooke's cell tumors, and 1 was a corticotroph carcinoma.</p> <p><b>Intervention:</b> Whole-exome sequencing.</p> <p><b>Main outcome measure:</b> Somatic mutation genomic biomarkers.</p> <p><b>Results:</b> We found recurrent somatic mutations in USP8 and TP53 genes, both with higher allelic fractions than other somatic mutations. These mutations were mutually exclusive, with TP53 mutations occurring only in USP8-wildtype (WT) tumors, indicating they may be independent driver genes. USP8-WT tumors were characterized by extensive somatic copy number variation compared to USP8-mutated tumors. Independent of molecular driver status, we found an association between invasiveness, macroadenomas, and aneuploidy.</p> <p><b>Conclusions: </b>Our data suggest that corticotroph tumors may be categorized into a USP8-mutated, genome-stable subtype versus a USP8-WT, genome-disrupted subtype, the latter of which has a TP53-mutated subtype with high level of chromosome instability. These findings could help identify high risk corticotroph tumors, namely those with widespread CNV, that may need closer monitoring and more aggressive treatment.</p>
USP8 and TP53 drivers are associated with CNV in a corticotroph adenoma cohort enriched for aggressive tumors
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USP8 mutations determine genes’ expression profile of pituitary corticotroph adenomas, regardless of tumor functional status.
GEO Series GSE132982. Homo sapiens. 20 samples. Type: Expression profiling by high throughput sequencing.
Differential microRNA Expression in USP8-Mutated and Wild-Type Corticotroph Pituitary Tumors Reflect the Difference in Protein Ubiquitination Processes
GEO Series GSE166279. Homo sapiens. 48 samples. Type: Expression profiling by high throughput sequencing.
Targeted Therapy With Gefitinib in Patients With USP8-mutated Cushing's Disease
ClinicalTrials.gov study NCT02484755. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Trancriptome analysis of tumor tissue to search for the associations between USP8 mutation status, molecular markers of pituitary adenomas, and clinical, and diagnostic parametres of Cushing disease
GEO Series GSE263206. Homo sapiens. 16 samples. Type: Expression profiling by high throughput sequencing.
Transcriptome profiling of wild-type (WT) and USP8 knockout (KO) CT26 cell lines
GEO Series GSE164558. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
USP8 coordinates ESCRT-mediated membrane repair, xenophagy, and oxidative stress responses during Mycobacterium tuberculosis infection
GEO Series GSE240372. Mus musculus. 40 samples. Type: Expression profiling by high throughput sequencing.
Targeting USP8 Causes Synthetic Lethality through Degradation of FGFR2 in ARID1A-Deficient Ovarian Clear Cell Carcinoma
GEO Series GSE273150. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
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