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61 results for “RAS mutant”
RAS-mutant AML LSCs originate from GMPs and drive clinical resistance to BH3 mimetics [ATAC-Seq]
GEO Series GSE253696. Homo sapiens. 12 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Expression data from salivary tumor tissues derived from MMTV-ras transgenic mice with wild-type p53, no p53 or gain-of-function mutant p53
GEO Series GSE59452. Mus musculus. 12 samples. Type: Expression profiling by array.
Mechanisms of Therapy Driven Clonal Evolution in Oncogenic RAS Mutant Relapsed Acute Lymphoblastic Leukemia
Although multi-agent combination chemotherapy is curative in a significant fraction of childhood acute lymphoblastic leukemia (ALL) patients, 20% of cases relapse and most die due to chemo-refractory disease. Here we used whole-exome and whole-genome sequencing to analyze the mutational landscape and pattern of clonal evolution at relapse in pediatric ALL cases. These analyses showed that ALL relapses originate from a common ancestral precursor clone of the diagnosis and relapsed populations and frequently harbor mutations implicated in chemotherapy resistance. RAS-MAPK pathway activating mutations in NRAS, KRAS and PTPN11 were present in 24/55 (44%) cases in our series. Notably, while some cases showed emergence of RAS mutant clones at relapse, in others, RAS mutant clones present at diagnosis were replaced by RAS wild type populations. Mechanistically, functional dissection of mouse and human wild type Kras and mutant Kras (Kras G12D) isogenic leukemia cells demonstrated induction of methotrexate resistance, but also improved response to vincristine, in mutant Kras- expressing lymphoblasts. These results identify chemotherapy driven selection as a central mechanism of leukemia clonal evolution and pave the road for the development of tailored personalized therapies for the treatment of relapsed ALL.
Gene expression profiles of spontaneous metastasis in a K-ras/p53 mutant mouse model
GEO Series GSE14449. Mus musculus. 16 samples. Type: Expression profiling by array.
CAPOX and Bevacizumab With or Without Primary Tumor Radiotherapy and Iparomlimab and Tuvonralimab as First-line Treatment for RAS-Mutant/MSS Metastatic Rectal Cancer
ClinicalTrials.gov study NCT07383285. IPD Sharing: Not stated. Countries: 0. Publications: 0.
The Prediction Model of Avastin Plus Chemotherapy in Unresectable Ras Mutant CRLM Patients
ClinicalTrials.gov study NCT04525313. IPD Sharing: UNDECIDED. Countries: 0. Publications: 0.
Efficacy of FOLFOX Versus FOLFOX Plus Aflibercept in K-ras Mutant Patients With Resectable Liver Metastases
ClinicalTrials.gov study NCT01646554. IPD Sharing: Not stated. Countries: 0. Publications: 0.
SBRT Combined With CAPEOX, Bevacizumab, and PD-1 Inhibitor for the Treatment of RAS-Mutant, MSS-Type, Unresectable Metastatic Colorectal Cancer.
ClinicalTrials.gov study NCT06835179. IPD Sharing: NO. Countries: 0. Publications: 0.
Fruquintinib Versus Bevacizumab Plus Chemotherapy in Second-Line RAS-Mutant Metastatic Colorectal Cancer (FRU-RAS)
ClinicalTrials.gov study NCT07362836. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Gene expression changes with inducible expression of activated ras and ras effector domain mutants
GEO Series GSE8916. Homo sapiens. 16 samples. Type: Expression profiling by array.
Transactivation-deficient p53 Mutants in Ras-induced Cellular Senescence
GEO Series GSE27901. Mus musculus. 23 samples. Type: Expression profiling by array.
Keap1 deletion-based Nrf2 activation accelerates mutant K-ras/p53-driven cholangiocarcinoma
GEO Series GSE138101. Mus musculus. 8 samples. Type: Expression profiling by array.
Prognostic Values of Immune Landscape in Ras-Mutant Colorectal Cancer Peritoneal Metastases
GEO Series GSE198085. Homo sapiens. 21 samples. Type: Other.
Regorafenib monotherapy as second-line treatment of patients with RAS-mutant advanced colorectal cancer (STREAM): an academic, multicenter, single-arm, two-stage, phase 2 study
<p><strong>Background</strong></p> <p>Maintaining angiogenesis inhibition and switching the chemotherapy backbone represent the current second-line therapy in patients with <em>RAS</em> mutant metastatic colorectal cancer (mCRC).</p> <p>Regorafenib, an oral multikinase inhibitor, prolonged overall survival (OS) in chemorefractory setting.</p> <p><strong>Methods</strong></p> <p>STREAM was an academic, multicenter, single-arm phase 2 trial, evaluating the activity of regorafenib in <em>RAS</em> mutant mCRC, in terms of the rate of patients who were progression-free after 6months from study entry (6mo-PF). Patients were pretreated with fluoropyrimidine, oxaliplatin and bevacizumab. According to Simon’s two-stage design, ≥ 18 patients 6mo-PF were needed in the overall population (N=46). Secondary endpoints were safety, objective response rate (ORR), progression-free survival (PFS) and OS. Early metabolic response by [18F]-FDG PET/CT scan was an exploratory endpoint. EudraCT Number:2015-001105-13</p> <p><strong>Results</strong></p> <p>The number of patients 6mo-PF was 8/22 at the first stage and 14/46 in the overall population. ORR was 10.9%, Disease Control Rate 54.6%, median (m)PFS 3.6 months (mo) (95%CI 1.9-6.7), mOS 18.9 mo (95%CI 10.3-35.3), mPFS2 (from study entry to subsequent-line progression) was 13.3mo (95%CI=8.4-19.7). Long responders patients (>6mo-PF) significantly more often had a single metastatic site and lung-limited disease. No unexpected toxicity was reported. Grade≥3 events occurred in 39.1% patients, mostly hand-foot syndrome (13%), fatigue and hyperbilirubinemia (6.5%). Baseline metabolic assessment was associated with OS in multivariate analysis, while early metabolic response was not associated with clinical outcomes. </p> <p><strong>Conclusion</strong></p> <p>The study did not meet its primary endpoint. However, regorafenib was well tolerated and did not preclude subsequent treatments. Patients with good prognostic features (single metastatic site and lung-limited disease) reported clinical benefit with regorafenib. The exploratory metabolic analysis suggests that baseline [18F]-FDG PET/CT might be useful to select patients with favorable outcome.</p> <p>A chemotherapy-free interval with regorafenib might be worth of further studies as second-line treatment in selected patients with RAS mutant mCRC.</p> <p> </p>
Altered mRNA splicing by mutant p53 activates oncogenic RAS in pancreatic cancer
GEO Series GSE114502. Mus musculus; Homo sapiens. 36 samples. Type: Expression profiling by high throughput sequencing.
Abrogation of Oncogenic RAS Signaling by a RAS(ON) Inhibitor Doublet Primes Immune-refractory KRASG12C-mutant NSCLC for Immune Checkpoint Blockade
GEO Series GSE315010. Homo sapiens; Mus musculus. 44 samples. Type: Expression profiling by high throughput sequencing.
RAS(ON) multi-selective inhibition drives anti-tumor immunity in preclinical models of NRAS-mutant melanoma
GEO Series GSE300712. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
Gene expression levels in colon cancer cells with mutant K-ras under hypoxic conditions
GEO Series GSE35973. Homo sapiens. 8 samples. Type: Expression profiling by array.
Dataset (II) related to publication: A cancer-associated K-RAS mutant protein that preferentially binds GDP displays gain-of-function and atypical signaling
<p>Dataset (II) related to publication:</p> <blockquote> <p>A cancer-associated K-RAS mutant protein that preferentially binds GDP displays gain-of-function and atypical signaling</p> </blockquote> <p>Includes raw trajectories of MD-simulations: K-RAS(M67L)+GDP replicas 11–20 (each replica 10 micros.)</p> <ul> <li>Individual .zip files contain raw-desmond trajectories (-out.cms files and trj-files)</li> </ul> <p>Other datasets related to this publication: 10.5281/zenodo.5506845 and 10.5281/zenodo.5507131</p>
Dataset (III) related to publication: A cancer-associated K-RAS mutant protein that preferentially binds GDP displays gain-of-function and atypical signaling
<p>Dataset (III) related to publication:</p> <blockquote> <p>A cancer-associated K-RAS mutant protein that preferentially binds GDP displays gain-of-function and atypical signaling</p> </blockquote> <p>Includes raw trajectories of MD-simulations: K-RAS(WT)+GDP replicas 1–10 (each replica 10 micros.)</p> <ul> <li>Individual .zip files contain raw-desmond trajectories (-out.cms files and trj-files)</li> </ul> <p>Other datasets related to this publication: 10.5281/zenodo.5506845 and 10.5281/zenodo.5507212</p>
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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.