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Pancreatic endocrine tumours: expression profiling evidences a rold for AKT-mTOR pathway

ABSTRACT: We investigated the global gene expression in a large panel of pancreatic endocrine tumours (PETs) aimed at identifying new potential targets for therapy and biomarkers to predict patient outcome.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73338 | GEO | 2015/10/30

SECONDARY ACCESSION(S): PRJNA296799

REPOSITORIES: GEO

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Pancreatic endocrine tumours: expression profiling evidences a rold for AKT-mTOR pathway

Project description:We investigated the global gene expression in a large panel of pancreatic endocrine tumours (PETs) aimed at identifying new potential targets for therapy and biomarkers to predict patient outcome. Total RNA was extracted from frozen tissue and hybridized on a custom 18.5K human oligo microarrays obtained from the Ohio State University Cancer Center.

2015-10-30 | E-GEOD-73338 | biostudies-arrayexpress

MicroRNA expression abnormalities in pancreatic endocrine and acinar tumours are associated with distinctive pathologic features and clinical behavior

2015-10-30 | GSE73350 | GEO

MicroRNA expression abnormalities in pancreatic endocrine and acinar tumours are associated with distinctive pathologic features and clinical behavior

Project description:We investigated the global microRNA expression patterns in normal pancreas, pancreatic endocrine tumours and acinar carcinomas to evaluate their involvement in transformation and malignant progression of these tumour types. A neoplastic cellularity higher than 90% was obtained by cryostat enrichment. RNA was extracted with Trizol (Invitrogen, Carlsbad, CA) from 10 20-Î¼m thick cryostat sections, checking the cell composition of the sample every five sections. RNA integrity was confirmed using the Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). microRNA microarray (Ohio State University Comprehensive Cancer Center, version 2.0) contains probes for 460 mature microRNAs spotted in quadruplicate (235 homo sapiens, 222 mus musculus, and three Arabidopsis thaliana) with annotated active sites. Often, more than one probe set exists for a given mature microRNA.

2015-10-30 | E-GEOD-73350 | biostudies-arrayexpress

Pancreatic endocrine tumour (PET)_Affymetrix 500K SNP arrays

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EUROPEAN SURGICAL REGISTRY FOR RARE ENDOCRINE TUMOURS

Project description:Interventions: Group 1: Survey of surgical treatment of benign and malignant endocrine and neuroendocrine tumors as well as associated complications. Primary outcome(s): Frequency of disease Study Design: Allocation: ; Masking: ; Control: ; Assignment: ; Study design purpose: health services research

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Proteomics of thyroid tumours - Proteomics of thyroid tumours provides new insights into their molecular composition and changes associated with malignancy

Project description:Although most thyroid tumours are benign, thyroid cancer represents the most common malignancy of the endocrine system, comprising mainly follicular and papillary thyroid carcinomas (FTC and PTC, respectively). Previous studies have shed some light on the molecular pathogenesis of thyroid cancer but there have not been any comprehensive mass spectrometry-based proteomic studies to reveal protein expression differences between thyroid tumours and the molecular alterations associated with tumour malignancy. We applied a label-free quantitative mass spectrometry analysis to compare normal thyroid tissue with the three most common tumours of the thyroid gland: follicular adenoma, follicular carcinoma and papillary carcinoma.

2017-05-03 | PXD002732 | Pride

PI3K/AKT/mTOR pathway in pulmonary carcinoid tumours.

Project description:The present study examined the expression of mammalian target of rapamycin (mTOR) and mutations in the phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway in 54 patients with typical carcinoid tumours (TC) or atypical carcinoid tumours (AC). In total, 54 bronchopulmonary neuroendocrine tumour (NET) surgical specimens, consisting of 17 TC, 8 AC, 17 large-cell neuroendocrine carcinoma (LCNEC), and 12 small-cell lung carcinoma (SCLC) samples, were tested for mTOR by immunohistochemistry, and 104 exon sites were tested in the PI3K/AKT/mTOR pathway by nested polymerase chain reaction. It was found that the positive rates for mTOR expression in TC/AC and LCNEC/SCLC were 60 (15/25) and 55.2% (16/29), respectively. In total, 4 missense mutations were found in 3 patients with TC/AC, including mutations in exon 48 of mTOR (c.6667C>T), exon 21 of tuberous sclerosis complex (TSC) 1 (c.2765G>A), and exons 12 (c.1265C>T) and 19 (c.2148C>T) of TSC2. To the best of our knowledge, mutations in exon 48 of mTOR and exon 21 of TSC1 have not been previously reported. Tissues from patients with single mutations exhibited strong positive mTOR immunohistochemical staining, and tissues from patients with double mutations were weakly positive. The same mutations were not observed in SCLC or LCNEC. In conclusion, gene mutations were observed and an association between the gene mutations and mTOR expression were indicated in the PI3K/AKT/mTOR pathway in TC/AC tumours. Those mutations may be driver genes and treatment targets.

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Oxidative phosphorylation is a metabolic vulnerability of endocrine therapy and palbociclib resistant metastatic breast cancers

Project description:Resistance to endocrine treatments and CDK4/6 inhibitors is considered a near-inevitability in most patients with estrogen receptor positive breast cancers (ER + BC). By genomic and metabolomics analyses of patients' tumours, metastasis-derived patient-derived xenografts (PDX) and isogenic cell lines we demonstrate that a fraction of metastatic ER + BC is highly reliant on oxidative phosphorylation (OXPHOS). Treatment by the OXPHOS inhibitor IACS-010759 strongly inhibits tumour growth in multiple endocrine and palbociclib resistant PDX. Mutations in the PIK3CA/AKT1 genes are significantly associated with response to IACS-010759. At the metabolic level, in vivo response to IACS-010759 is associated with decreased levels of metabolites of the glutathione, glycogen and pentose phosphate pathways in treated tumours. In vitro, endocrine and palbociclib resistant cells show increased OXPHOS dependency and increased ROS levels upon IACS-010759 treatment. Finally, in ER + BC patients, high expression of OXPHOS associated genes predict poor prognosis. In conclusion, these results identify OXPHOS as a promising target for treatment resistant ER + BC patients.

2023-06-27 | MTBLS3342 | MetaboLights

Long-term acquired everolimus resistance in pancreatic neuroendocrine tumours can be overcome with novel PI3K-AKT-mTOR inhibitors.

Project description:BackgroundThe mTOR-inhibitor everolimus improves progression-free survival in advanced pancreatic neuroendocrine tumours (PNETs). However, adaptive resistance to mTOR inhibition is described.MethodsQGP-1 and BON-1, two human PNET cell lines, were cultured with increasing concentrations of everolimus up to 22 weeks to reach a dose of 1??M everolimus, respectively, 1000-fold and 250-fold initial IC50. Using total DNA content as a measure of cell number, growth inhibitory dose-response curves of everolimus were determined at the end of resistance induction and over time after everolimus withdrawal. Response to ATP-competitive mTOR inhibitors OSI-027 and AZD2014, and PI3K-mTOR inhibitor NVP-BEZ235 was studied. Gene expression of 10 PI3K-Akt-mTOR pathway-related genes was evaluated using quantitative real-time PCR (RT-qPCR).ResultsLong-term everolimus-treated BON-1/R and QGP-1/R showed a significant reduction in everolimus sensitivity. During a drug holiday, gradual return of everolimus sensitivity in BON-1/R and QGP-1/R led to complete reversal of resistance after 10-12 weeks. Treatment with AZD2014, OSI-027 and NVP-BEZ235 had an inhibitory effect on cell proliferation in both sensitive and resistant cell lines. Gene expression in BON-1/R revealed downregulation of MTOR, RICTOR, RAPTOR, AKT and HIF1A, whereas 4EBP1 was upregulated. In QGP-1/R, a downregulation of HIF1A and an upregulation of ERK2 were observed.ConclusionsLong-term everolimus resistance was induced in two human PNET cell lines. Novel PI3K-AKT-mTOR pathway-targeting drugs can overcome everolimus resistance. Differential gene expression profiles suggest different mechanisms of everolimus resistance in BON-1 and QGP-1.

| S-EPMC4800296 | biostudies-literature

Peptidomic analysis of pancreatic neurodendocrine tumours (Glucagonoma)

Project description:A peptidomic analysis of plasma from patients with well characterised pancreatic neuroendocrine tumours (PNET) was performed. A nano LC-MS analysis identified a number of peptides from the glucagon gene, which were idenfiried in a previous case study using multiple immunoassays. Peptides to other proteins involved in peptide secretion were also identified. Plasma from a second glucagonoma patient was analysed using a high flow approach, and this identified similar peptides to the nano analysis. In order to demonstrate the potential clinical application of LC-MS to characterising neuroendocrine tumours, a large cohort of plasma samples were analysed to demonstrate the ability of this approach to identify glucagonoma patients, and differentiate from a single insulinoma patient

2018-08-31 | MSV000082880 | MassIVE

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