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1,746 results for “Oncogenes”
Example of KRAS oncogene mutational regression and HLA haplotype characterization in oligo-metastatic colorectal cancer patient (ID: PAT2)
<p>KRAS oncogene mutational regression from primary tumour to lung metastasis (evaluated through TSO500 panel, Illumina Novaseq 6000 platform) and HLA haplotype characterization (through PCR) in a representative oligo-metastatic colorectal cancer patient (ID: PAT2).</p>
Metabolome analyses of oncogene-induced senescent IMR-90 cells
<p><strong>Methods</strong></p> <p><strong>Cell culture</strong></p> <p>IMR-90 ER:Ras (H-RasG12V) cells were maintained in Dulbecco’s modified Eagle’s medium supplemented with 200 mM L-glutamine, 1 mM sodium pyruvate, 10% (v/v) heat-inactivated fetal bovine serum (FBS), and penicillin/streptomycin (P/S). To induce quiescence, IMR-90 ER:Ras cells were cultured in the above medium containing 0.1% FBS for 2 days. For oncogene-induced senescence, IMR-90 ER:Ras cells were treated with 100 nM 4-hydroxytamoxifen (4-OHT) for 6 days.</p> <p><strong>Metabolite extraction</strong></p> <p>Culture medium was aspirated from the dishes and the cells were washed twice with 5% mannitol solution (10 mL and 2 mL for the first and second washes, respectively). The cells were then treated with 800 µL of methanol and incubated at room temperature for 30 sec to suppress enzyme activity. Next, 550 µL of Milli-Q water containing internal standards (H3304-1002, Human Metabolome Technologies, Inc. (HMT), Tsuruoka, Yamagata, Japan) was added to the cell extract, followed by further incubation at room temperature for 30 sec. The cell extract was then centrifuged at 2,300 × <em>g</em> and 4ºC for 5 min, after which 700 µL of the supernatant was centrifugally filtered through a Millipore 5-kDa cut-off filter (UltrafreeMC-PLHCC, HMT) at 9,100 × <em>g</em> and 4ºC for 120 min to remove macromolecules. Subsequently, the filtrate was evaporated to dryness under vacuum and reconstituted in 50 µL of Milli-Q water for metabolome analysis at HMT.</p> <p><strong>Metabolome analysis</strong></p> <p>Metabolome analysis was conducted using HMT’s Basic Scan package, capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS), and the previously described method <sup>1</sup>. Briefly, CE-TOFMS analysis was carried out using an Agilent CE capillary electrophoresis system equipped with an Agilent 6210 time-of-flight mass spectrometer (Agilent Technologies, Inc., Santa Clara, CA, USA). The systems were controlled by Agilent G2201AA ChemStation software version B.03.01 (Agilent Technologies) and connected by a fused silica capillary (50 μm internal diameter × 80 cm total length) containing commercial electrophoresis buffer (H3301-1001 and I3302-1023 for cation and anion analyses, respectively, HMT) as the electrolyte. The spectrometer scanned from m/z 50 to 1,000 and peaks were identified using MasterHands automatic integration software (Keio University, Tsuruoka, Yamagata, Japan) in order to obtain peak information, including m/z, peak area, and migration time (MT) <sup>2</sup>. Signal peaks corresponding to isotopomers, adduct ions, and other product ions corresponding to known metabolites were excluded, and the remaining peaks were annotated according to HMT’s metabolite database, based on their m/z values and MTs. The areas of the annotated peaks were then normalized to those for internal standards and the amounts of the samples in order to obtain the relative quantity for each metabolite. The absolute quantities of 110 primary metabolites were quantified on the basis of one-point calibrations using their respective standards.</p> <ol> <li>Ohashi, Y., Hirayama, A., Ishikawa, T., Nakamura, S., Shimizu, K., Ueno, Y., Tomita, M., and Soga, T. (2008). Depiction of metabolome changes in histidine-starved Escherichia coli by CE-TOFMS. Mol Biosyst <em>4</em>, 135–147. 10.1039/b714176a.</li> <li> <p>Sugimoto, M., Wong, D.T., Hirayama, A., Soga, T., and Tomita, M. (2010). Capillary electrophoresis mass spectrometry-based saliva metabolomics identified oral, breast and pancreatic cancer-specific profiles. Metabolomics <em>6</em>, 78–95. 10.1007/s11306-009-0178-y.</p> </li> </ol>
Structural Variation Cooperates with Permissive Chromatin to Control Enhancer Hijacking-Mediated Oncogenic Transcription
<p>Dataset required for running leukemia associated structural variants scoring described in Structural Variation Cooperates with Permissive Chromatin to Control Enhancer Hijacking-Mediated Oncogenic Transcription manuscript.</p>
Prognostic Value of Androgen Receptor Expression and Mutations Within Oncogenes and Tumor Suppressor Genes in Patients Treated for High Risk Prostate Cancer With Proton Therapy (PRX32)
ClinicalTrials.gov study NCT03296124. IPD Sharing: NO. Countries: 1. Publications: 17.
Genetic Susceptibility to Oncogenic Viruses
ClinicalTrials.gov study NCT00341484. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Study of Atezolizumab in Advanced Non-oncogene-addicted NSCLC With PD-L1 ≥50%, Including Longitudinal c-FLIP Assessment in Monocytic MDSCs.
ClinicalTrials.gov study NCT07051928. IPD Sharing: NO. Countries: 1. Publications: 1.
Study of the CHK1 Inhibitor BBI-355, an ecDNA-directed Therapy (ecDTx), and the RNR Inhibitor BBI-825, in Subjects With Tumors With Oncogene Amplifications
ClinicalTrials.gov study NCT05827614. IPD Sharing: NO. Countries: 1. Publications: 7.
A Study to Find a Safe and Effective Dose of BI 1701963 Alone and in Combination With BI 3011441 in Patients With Advanced Cancer and a Certain Mutation (Kirsten Rat Sarcoma Viral Oncogene Homologue [
ClinicalTrials.gov study NCT04835714. IPD Sharing: NO. Countries: 1. Publications: 0.
Panitumumab Combination Study With Rilotumumab or Ganitumab in Wild-type Kirsten Rat Sarcoma Virus Oncogene Homolog (KRAS) Metastatic Colorectal Cancer (mCRC)
ClinicalTrials.gov study NCT00788957. IPD Sharing: Not stated. Countries: 0. Publications: 2.
K-RAS Oncogene Mutation in Patients With Advanced Non-Small Cell Lung Cancer Associated With Exposure to Wood Smoke and Tobacco Smoking: Therapeutic Implications
ClinicalTrials.gov study NCT01023828. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Data from: Oncogene inference optimization using constraint-based modelling incorporated with protein expression in normal and tumour tissues
Open the record for dataset details and reuse information.
Data from: Characterization of leukemia-inducing genes using a proto-oncogene/homeobox gene retroviral human cDNA library in a mouse in vivo model
The purpose of this research is to develop a method to screen a large number of potential driver mutations of acute myeloid leukemia (AML) using a retroviral cDNA library and murine bone marrow transduction-transplantation system. As a proof-of-concept, murine bone marrow (BM) cells were transduced with a retroviral cDNA library encoding well-characterized oncogenes and homeobox genes, and the virus-transduced cells were transplanted into lethally irradiated mice. The proto-oncogenes responsible for leukemia initiation were identified by PCR amplification of cDNA inserts from genomic DNA isolated from leukemic cells. In an initial screen of ten leukemic mice, the MYC proto-oncogene was detected in all the leukemic mice. Of ten leukemic mice, 3 (30%) had MYC as the only transgene, and seven mice (70%) had additional proto-oncogene inserts. We repeated the same experiment after removing MYC-related genes from the library to characterize additional leukemia-inducing gene combinations. Our second screen using the MYC-deleted proto-oncogene library confirmed MEIS1and the HOX family as cooperating oncogenes in leukemia pathogenesis. The model system we introduced in this study will be valuable in functionally screening novel combinations of genes for leukemogenic potential in vivo, and the system will help in the discovery of new targets for leukemia therapy.
Oncogenic BRAF V600E induces glial proliferation through ERK and neuronal death through JNK
<p>Background: Activating V600E in BRAF is a common driver mutation in cancers of multiple tissue origins, including melanoma and glioma. BRAF V600E has also been implicated in neurodegeneration. The present study aims to characterize BRAF V600E on cell death and survival in three major cell types of the CNS: neurons, astrocytes, and microglia. Methods : Multiple primary cultures and cell lines of glial cells and neurons were employed. BRAF V600E as well as BRAF WT expression was mediated by lentivirus or retrovirus. Blockage of downstream effectors were achieved by siRNA. Gene expression data from patients with Parkinson’s disease was analyzed. Results : In astrocytes and microglia, BRAF V600E induces cell proliferation, and the proliferative effect in microglia is mediated by activated ERK but not JNK. Conditioned medium from BRAF V600E -expressing microglia induced neuronal cell death. In neuronal cells, BRAF V600E directly induces cell death, through JNK but not ERK. We further show that BRAF-related genes are enriched in pathways in patients with Parkinson’s disease. Conclusions : Our study identifies distinct consequences mediated by distinct downstream effectors in dividing glial cells and in neurons following the same BRAF mutational activation and a causal link between BRAF-activated microglia and neuronal cell death that does not require physical proximity. It provides insight into a possibly important role of BRAF in neurodegeneration as a result of either dysregulated BRAF in neurons or its impact on glial cells.</p>
Oncogenic Role of Engrailed (EN)-2 in Epithelial Ovarian Neoplasms
ClinicalTrials.gov study NCT05553067. IPD Sharing: YES. Countries: 1. Publications: 0.
Effect of Adenovirus E1A Oncogene on DNA Replication Dynamics
ClinicalTrials.gov study NCT03325517. IPD Sharing: UNDECIDED. Countries: 0. Publications: 28.
Study of Panobinostat Monotherapy in Women With v-ERB-B2 Avian Erythroblastic Leukemia Viral Oncogene Homolog 2 (HER2) Positive Locally Recurrent or Metastatic Breast Cancer
ClinicalTrials.gov study NCT00777335. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Tipifarnib in Advanced Squamous NSCLC With Oncogen HRAS MutAtionS
ClinicalTrials.gov study NCT03496766. IPD Sharing: NO. Countries: 1. Publications: 0.
Exploratory Study of TG02-treatment as Monotherapy or in Combination With Pembrolizumab to Assess Safety and Immune Activation in Patients With Locally Advanced Primary and Recurrent Oncogenic RAS Exo
ClinicalTrials.gov study NCT02933944. IPD Sharing: Not stated. Countries: 2. Publications: 0.
Study to Analyze Mutations in V600 BRAF Oncogen in Participants With Metastatic Melanoma
ClinicalTrials.gov study NCT02663232. IPD Sharing: Not stated. Countries: 1. Publications: 0.
A Trial of Integrating SBRT With Targeted Therapy in Stage IV Oncogene-driven NSCLC
ClinicalTrials.gov study NCT02314364. IPD Sharing: Not stated. Countries: 1. Publications: 0.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.